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Thread: Alternate theories to the theory of evolution?

  1. #1 Alternate theories to the theory of evolution? 
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    Are there any scientific alternatives to the theory of evolution, even if they are not well-established? Someone once told me that Kimura's theory is an alternative, but I am not sure.


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    No, no scientific theories. Quite a lot of creationism/ID theories, but these are not scientific.


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    there is no such thing as "the" theory of evolution
    there are various theories that explain certain aspects of evolution better than others, and they or may not be in competition with one another - they may even complement each other

    off the top of my head i can think of the following theories that still carry some weight today : natural selection, sexual selection, neutral drift, punctuated equilibrium
    there may be others, but i can't think of any right now (i purposely have disregarded discredited theories such as orthogenesis or saltational mutations)
    "Reality is that which, when you stop believing in it, doesn't go away." (Philip K. Dick)
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  5. #4 Re: Alternate theories to the theory of evolution? 
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    Quote Originally Posted by ufcarazy
    Are there any scientific alternatives to the theory of evolution, even if they are not well-established? Someone once told me that Kimura's theory is an alternative, but I am not sure.
    This is like asking for alternative 'scientific theories' for general relativity, which by the way would be a bit easier to do (string theory comes to mind, but I wouldn't call it scientific, yet).

    As of yet there aren't any alternative theories to 'evolution', maybe in the future someone will think of something but I doubt it will be very much different from it (considering the fossil record).

    Also (if you're religiously motivated, I'm not going to assume that though), materialists I think would like an alternative, since it might explain the origin of life or maybe even the anthropic principle. Evolution doesn't do that.
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    Quote Originally Posted by marnixR
    there is no such thing as "the" theory of evolution
    there are various theories that explain certain aspects of evolution better than others, and they or may not be in competition with one another - they may even complement each other

    off the top of my head i can think of the following theories that still carry some weight today : natural selection, sexual selection, neutral drift, punctuated equilibrium
    there may be others, but i can't think of any right now (i purposely have disregarded discredited theories such as orthogenesis or saltational mutations)
    Are these different theories because they are different mechanisms, and the mechanism pretty much defines the theory?
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    I think what he's saying is that the only things really in dispute about evolution are the finer points of how the specifics of it work, not whether or not it occurs at all. That is an undeniable fact of biology.
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    Quote Originally Posted by ufcarazy
    Quote Originally Posted by marnixR
    there is no such thing as "the" theory of evolution
    there are various theories that explain certain aspects of evolution better than others, and they or may not be in competition with one another - they may even complement each other

    off the top of my head i can think of the following theories that still carry some weight today : natural selection, sexual selection, neutral drift, punctuated equilibrium
    there may be others, but i can't think of any right now (i purposely have disregarded discredited theories such as orthogenesis or saltational mutations)
    Are these different theories because they are different mechanisms, and the mechanism pretty much defines the theory?
    Evolution means that life changes over time. These are possible mechanisms for how this change came about, so I'd say a part of evolution. I think most biologists say they all occur but disagree on their importance.
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  9. #8 Re: Alternate theories to the theory of evolution? 
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    Quote Originally Posted by ufcarazy
    Are there any scientific alternatives to the theory of evolution, even if they are not well-established? Someone once told me that Kimura's theory is an alternative, but I am not sure.
    There are no viable alternatives. No.
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    Quote Originally Posted by ufcarazy
    Are these different theories because they are different mechanisms, and the mechanism pretty much defines the theory?
    natural selection : usually the preferred explanation for adaptation through differential survival and reproductive success
    sexual selection : stresses the fact that access to females is a crucial part of passing your genes on, and may lead to characters that initially appear counter-adaptive
    neutral drift : indicates that not all evolutionary change has to be adaptive
    punctuated equilibrium : explains how rates of evolutionary change may vary over geological time

    in essence, the debate of whether evolution happens is over, which makes evolution a fact - the various theories try to explain various aspects of HOW evolution happens
    "Reality is that which, when you stop believing in it, doesn't go away." (Philip K. Dick)
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    Quote Originally Posted by marnixR
    Quote Originally Posted by ufcarazy
    Are these different theories because they are different mechanisms, and the mechanism pretty much defines the theory?
    natural selection : usually the preferred explanation for adaptation through differential survival and reproductive success
    sexual selection : stresses the fact that access to females is a crucial part of passing your genes on, and may lead to characters that initially appear counter-adaptive
    neutral drift : indicates that not all evolutionary change has to be adaptive
    punctuated equilibrium : explains how rates of evolutionary change may vary over geological time

    in essence, the debate of whether evolution happens is over, which makes evolution a fact - the various theories try to explain various aspects of HOW evolution happens
    I am not clear on your answer. It seemed like you were saying that there is more than one theory that explains how life has developed, and I asked if the reason there is more than one theory is because there is more than one mechanism when the mechanism is what defines a theory.

    I have never heard anyone else say that there is not only one theory explaining life, but several. Does anyone else agree that there is more than one theory explaining how life has developed?
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    Quote Originally Posted by Finger
    I think what he's saying is that the only things really in dispute about evolution are the finer points of how the specifics of it work, not whether or not it occurs at all. That is an undeniable fact of biology.
    Aren't the specifics of how a thing works what makes a theory a theory? Theories don't explain by simply saying THAT something happens, but by stating HOW. If there is disputation about the HOW, then wouldn't that mean there is disputation about the theory?
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    Quote Originally Posted by ufcarazy
    I have never heard anyone else say that there is not only one theory explaining life, but several. Does anyone else agree that there is more than one theory explaining how life has developed?
    different aspects of evolution are addressed by different varieties of evolutionary theory, because they were developed to address specific evolutionary conundrums

    they are not necessarily mutually exclusive, so i suppose that taken together they might form what you might want to call "the" theory of evolution, should you feel so inclined - personally i don't have such a monolithic view of how scientific theories develop
    "Reality is that which, when you stop believing in it, doesn't go away." (Philip K. Dick)
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    Quote Originally Posted by drowsy turtle
    No, no scientific theories. Quite a lot of creationism/ID theories, but these are not scientific.
    ...nor even theoretical but merely hypothetical.
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  15. #14  
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    Quote Originally Posted by ufcarazy
    Aren't the specifics of how a thing works what makes a theory a theory?
    Not necessarily, Newton's theory of gravity may have made sense mathematically, but it hardly explained why things attract or why G is constant thoughout the universe.
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    Quote Originally Posted by Finger
    I think what he's saying is that the only things really in dispute about evolution are the finer points of how the specifics of it work, not whether or not it occurs at all. That is an undeniable fact of biology.
    If evolution means change over time by known processes then that is of couse a fact. I think what the original poster meant by evolutionary theory was the idea that all diversity of life is accounted for by observed evolutionary processes in operation today.

    This of couse is not an undeniable fact. There are many observed biological features in existence that cannot be accounted for by the claimed processes. Biologists are forced to speculate about cooption or coevolving molecular components and developmental control mechanisms to name just a couple unobserved processes. The debate is not simply what processes account for what effect, the debate is about whether or not any process can account for dramatic changes in form and funtion.

    Twenty years ago when I took undergraduate biology, cell chemistry was still considered to be fairly simple so the theory made sense then. Recent studies demonstrate that most cellular processes involve ten or more protein components that are fitted together by shape and chemical afinity. Many are aided by specific organized transport, inventory, control, assembly and repair subsystems. Changes to these kinds of systems generally seem to require multiple coordinated alterations of several genes and gene control sequences. The challenge for modern experimental and molecular biologists is to identify the processes that can account for these observations.

    The changes we see in experiments are single and rarely dual alterations that change performance of individual proteins. Most weaken the function to prevent a chemical from exploiting the protein for a targeted purpose like antibiotics and pesticides for example. So far we have no example of stepwise alterations leading to a new function where the steps are greater than three or four steps. The processes named by another poster don't seem to be able to accomplish this kind of thing in any reasonable time scale that can account for the rate of changes indicated by the fossil record and molecular homology studies. And this raises the question; exactly what process can accomplish this?
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    Parahomology of proteins gives us insight into this. We can look at proteins present in mammals, and see that they share strong sequence homology with some bacterial proteins that have completely different functions, this is strong evidence of exaptation. Moreover, if you take into account that genes are often found in duplicates or triplets within eukaryotic genomes, it isn't necessarily important that one mutation may reduce functionality because there are other genes present so that the functional protein isn't lost.

    Edit: For example there are 20 nonfunctional copies of G3DH in humans.

    Edit2: http://www.ncbi.nlm.nih.gov/pubmed/6...?dopt=Abstract
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  18. #17  
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    Quote Originally Posted by cypress
    Twenty years ago when I took undergraduate biology, cell chemistry was still considered to be fairly simple so the theory made sense then. Recent studies demonstrate that most cellular processes involve ten or more protein components that are fitted together by shape and chemical afinity. Many are aided by specific organized transport, inventory, control, assembly and repair subsystems. Changes to these kinds of systems generally seem to require multiple coordinated alterations of several genes and gene control sequences.
    What sort of half-assed Biology course did you take 20 years ago? We knew about some remarkably complex cascades long before 1989. Classical and alternative complement cascades, for example. Clotting cascade. I'm sure there's more.

    Far from assuming that cellular processes and genetics were simple, I can recall as late as 2000 (which is when I was doing my undergrad) it being fully expected that the human genome ought to yield some 100,000-200,000 genes. I'm sure that expectation goes back much further than a mere 20 years. When the results gave a mere 25,000 genes everyone was rather surprised. So we certainly haven't been labouring under the illusion that things were simpler than we know them to be now.

    Quote Originally Posted by cypress
    The challenge for modern experimental and molecular biologists is to identify the processes that can account for these observations.
    The complexity we observe has been well-known about for some time, indeed even over-anticipated, and it certainly hasn't demanded that we invoke processes outside of evolutionary theory to get an explanation. That's wishful thinking on your part.
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    It's the artificial gap between "microevolution" and "macroevolution" cropping up.
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    Quote Originally Posted by cypress
    Quote Originally Posted by Finger
    I think what he's saying is that the only things really in dispute about evolution are the finer points of how the specifics of it work, not whether or not it occurs at all. That is an undeniable fact of biology.
    If evolution means change over time by known processes then that is of couse a fact. I think what the original poster meant by evolutionary theory was the idea that all diversity of life is accounted for by observed evolutionary processes in operation today.

    This of couse is not an undeniable fact. There are many observed biological features in existence that cannot be accounted for by the claimed processes. Biologists are forced to speculate about cooption or coevolving molecular components and developmental control mechanisms to name just a couple unobserved processes. The debate is not simply what processes account for what effect, the debate is about whether or not any process can account for dramatic changes in form and funtion.

    Twenty years ago when I took undergraduate biology, cell chemistry was still considered to be fairly simple so the theory made sense then. Recent studies demonstrate that most cellular processes involve ten or more protein components that are fitted together by shape and chemical afinity. Many are aided by specific organized transport, inventory, control, assembly and repair subsystems. Changes to these kinds of systems generally seem to require multiple coordinated alterations of several genes and gene control sequences. The challenge for modern experimental and molecular biologists is to identify the processes that can account for these observations.

    The changes we see in experiments are single and rarely dual alterations that change performance of individual proteins. Most weaken the function to prevent a chemical from exploiting the protein for a targeted purpose like antibiotics and pesticides for example. So far we have no example of stepwise alterations leading to a new function where the steps are greater than three or four steps. The processes named by another poster don't seem to be able to accomplish this kind of thing in any reasonable time scale that can account for the rate of changes indicated by the fossil record and molecular homology studies. And this raises the question; exactly what process can accomplish this?
    I hate to rock your boat but a lot happened in 20 years. Why don't you read up a bit before you claim something.
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  21. #20  
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    Quote Originally Posted by spuriousmonkey
    I hate to rock your boat but a lot happened in 20 years. Why don't you read up a bit before you claim something.
    Cypress states "Twenty years ago when I took undergraduate biology, cell chemistry was still considered to be fairly simple so the theory made sense then. Recent studies demonstrate that most cellular processes involve ten or more protein components that are fitted together by shape and chemical afinity."
    This suggests he has done some reading on the matter. Would you like to pinpoint where he is hopelessly out of date?
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    Quote Originally Posted by Ophiolite
    Quote Originally Posted by spuriousmonkey
    I hate to rock your boat but a lot happened in 20 years. Why don't you read up a bit before you claim something.
    Cypress states "Twenty years ago when I took undergraduate biology, cell chemistry was still considered to be fairly simple so the theory made sense then. Recent studies demonstrate that most cellular processes involve ten or more protein components that are fitted together by shape and chemical afinity."
    This suggests he has done some reading on the matter. Would you like to pinpoint where he is hopelessly out of date?
    One example:

    Complement receptor is an inhibitor of the complement cascade

    A paper in JEM from 1981 in which discusses the role of CR1 in the complement cascade. A quick scan through the paper reveals that the author's knowledge of the cascade is already rather detailed. For a degree course not to have similar understanding some 8 years later seems very unlikely. If it did, then fair enough but not reflective of scientific opinion on complexity greater than 20 years ago. It was not held that molecular biology was simple by any means.
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  23. #22  
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    Quote Originally Posted by Ophiolite
    Quote Originally Posted by spuriousmonkey
    I hate to rock your boat but a lot happened in 20 years. Why don't you read up a bit before you claim something.
    Cypress states "Twenty years ago when I took undergraduate biology, cell chemistry was still considered to be fairly simple so the theory made sense then. Recent studies demonstrate that most cellular processes involve ten or more protein components that are fitted together by shape and chemical afinity."
    This suggests he has done some reading on the matter. Would you like to pinpoint where he is hopelessly out of date?
    I am quite sure when you would look up this 'presumed read material, which existence is unproven' they would not state that the complexities reported in any way danger the theory of evolution since evolution cannot explain the complexity.

    But let's have this literature list then. I hope it is primary literature and not some website because otherwise the discussion has already ended before it started.

    So far we have no example of stepwise alterations leading to a new function where the steps are greater than three or four steps.
    We have not? In the mouse there are 22 FGF genes, all derived from duplication events. While some can rescue some others to some degree or in total, mostly they are often not even co-expressed in a temporal and spatial manner, and act through different receptors, executing radically different functions.

    A totally different function isn't a big step? are we going to discuss what are three or four steps?

    Lobed fins are changed into legs, into arms, into wings, back into fins again.

    Individual miRNAs are duplicated, reversed in orientation, given a new function etc. time after time during evolution.

    The genome is full of a rich history of modification of function and the generation of new function.

    All you need to do is open up a text book.
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    Quote Originally Posted by TheBiologista
    Quote Originally Posted by cypress
    Twenty years ago when I took undergraduate biology, cell chemistry was still considered to be fairly simple so the theory made sense then. Recent studies demonstrate that most cellular processes involve ten or more protein components that are fitted together by shape and chemical afinity. Many are aided by specific organized transport, inventory, control, assembly and repair subsystems. Changes to these kinds of systems generally seem to require multiple coordinated alterations of several genes and gene control sequences.
    What sort of half-assed Biology course did you take 20 years ago? We knew about some remarkably complex cascades long before 1989. Classical and alternative complement cascades, for example. Clotting cascade. I'm sure there's more.
    But you have changed the context and point of my general comment. And worse you provided an example equally out of context, namely one that is not intracellular. You are attacking credibility rather than addressing the argument. You do this by cherry picking fine points, changing the substance and then attacking the altered point.

    Far from assuming that cellular processes and genetics were simple, I can recall as late as 2000 (which is when I was doing my undergrad) it being fully expected that the human genome ought to yield some 100,000-200,000 genes. I'm sure that expectation goes back much further than a mere 20 years. When the results gave a mere 25,000 genes everyone was rather surprised. So we certainly haven't been labouring under the illusion that things were simpler than we know them to be now.
    Again off topic. Gene count does not address the character of intracellular protein interaction.

    Quote Originally Posted by cypress
    The challenge for modern experimental and molecular biologists is to identify the processes that can account for these observations.
    The complexity we observe has been well-known about for some time, indeed even over-anticipated, and it certainly hasn't demanded that we invoke processes outside of evolutionary theory to get an explanation. That's wishful thinking on your part.
    Perhaps now would be a good time for you to provide an example of a known process experimentally observed to have generated the subject observation.
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  25. #24  
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    You guys have NO idea what you are talking about with evolution. You see.. I have a very valid alternative to evolution.
    Instead of millions of mutations happening over a long period of time, I propose that what caused us to be here today was... MAGIC. That's right folks. We poofed here from God's hand and here we are today. MAGIC is what created us!


    *cough*
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    Quote Originally Posted by i_feel_tiredsleepy
    Parahomology of proteins gives us insight into this. We can look at proteins present in mammals, and see that they share strong sequence homology with some bacterial proteins that have completely different functions, this is strong evidence of exaptation. Moreover, if you take into account that genes are often found in duplicates or triplets within eukaryotic genomes, it isn't necessarily important that one mutation may reduce functionality because there are other genes present so that the functional protein isn't lost.

    Edit: For example there are 20 nonfunctional copies of G3DH in humans.

    Edit2: http://www.ncbi.nlm.nih.gov/pubmed/6...?dopt=Abstract
    Sure, homology can provide insight into the changed that have occurred as I indicated previously, but doesn't tell us how those changes occur. There is no need for us to reiterate our points of agreement, since the discussion would be rather boring. We can clearly see that changes occur but we can't demonstrate how known processes account for the kinds of changes I described earlier. Exaptation via gene duplication is interesting speculation no doubt, but without selection pressure what mechanism is there to sift the permutations? Can a proposed process be observed and tested?
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    Quote Originally Posted by TheBiologista
    Quote Originally Posted by Ophiolite
    Quote Originally Posted by spuriousmonkey
    I hate to rock your boat but a lot happened in 20 years. Why don't you read up a bit before you claim something.
    Cypress states "Twenty years ago when I took undergraduate biology, cell chemistry was still considered to be fairly simple so the theory made sense then. Recent studies demonstrate that most cellular processes involve ten or more protein components that are fitted together by shape and chemical afinity."
    This suggests he has done some reading on the matter. Would you like to pinpoint where he is hopelessly out of date?
    One example:

    Complement receptor is an inhibitor of the complement cascade

    A paper in JEM from 1981 in which discusses the role of CR1 in the complement cascade. A quick scan through the paper reveals that the author's knowledge of the cascade is already rather detailed. For a degree course not to have similar understanding some 8 years later seems very unlikely. If it did, then fair enough but not reflective of scientific opinion on complexity greater than 20 years ago. It was not held that molecular biology was simple by any means.
    So I am showing my age. My undergraduate degree was completed in 1983. However once again this is a cell exterior example, and I believe involves single pairs of protein interaction in sequence (six in all if I have that correct) as opposed to the ten or more concurrent interaction I intended to discuss.
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    Quote Originally Posted by spuriousmonkey
    Quote Originally Posted by Ophiolite
    Quote Originally Posted by spuriousmonkey
    I hate to rock your boat but a lot happened in 20 years. Why don't you read up a bit before you claim something.
    Cypress states "Twenty years ago when I took undergraduate biology, cell chemistry was still considered to be fairly simple so the theory made sense then. Recent studies demonstrate that most cellular processes involve ten or more protein components that are fitted together by shape and chemical afinity."
    This suggests he has done some reading on the matter. Would you like to pinpoint where he is hopelessly out of date?
    I am quite sure when you would look up this 'presumed read material, which existence is unproven' they would not state that the complexities reported in any way danger the theory of evolution since evolution cannot explain the complexity.

    But let's have this literature list then. I hope it is primary literature and not some website because otherwise the discussion has already ended before it started.
    Here are two:

    B. Alberts, 1998. "The cell as a collection of protein machines: preparing the next generation of molecular biologits." Cell 92

    S. Woodson 2005. "Biophysics: assembly line inspection." Nature 438

    So far we have no example of stepwise alterations leading to a new function where the steps are greater than three or four steps.
    We have not? In the mouse there are 22 FGF genes, all derived from duplication events. While some can rescue some others to some degree or in total, mostly they are often not even co-expressed in a temporal and spatial manner, and act through different receptors, executing radically different functions.

    A totally different function isn't a big step? are we going to discuss what are three or four steps?

    Lobed fins are changed into legs, into arms, into wings, back into fins again.

    Individual miRNAs are duplicated, reversed in orientation, given a new function etc. time after time during evolution.

    The genome is full of a rich history of modification of function and the generation of new function.

    All you need to do is open up a text book.
    All you need to do is read my post. I accept that these changes occurred. But none of us know how they occurred. Thus far experimental techniques have failed to demonstrate that known evolutionary processes can account for the examples I raised. To the contrary, the most recent experimental work in this area seems to indicate that they cannot, at least not in the amount of time indicated by the fossil record.
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  29. #28  
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    Quote Originally Posted by cypress

    Again off topic. Gene count does not address the character of intracellular protein interaction.

    [q
    Do you know what most genes code for?

    Proteins.

    Do you know what constitutes signaling pathways?

    protein interactions. Intracellular and extracellular.

    And protein-DNA-RNA interactions: intracellular mostly.
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    Oh here we go with the meta argument. Next it'll be all cries of "logical fallacy" and "ad hominem".

    Quote Originally Posted by cypress
    Quote Originally Posted by TheBiologista
    Quote Originally Posted by cypress
    Twenty years ago when I took undergraduate biology, cell chemistry was still considered to be fairly simple so the theory made sense then. Recent studies demonstrate that most cellular processes involve ten or more protein components that are fitted together by shape and chemical afinity. Many are aided by specific organized transport, inventory, control, assembly and repair subsystems. Changes to these kinds of systems generally seem to require multiple coordinated alterations of several genes and gene control sequences.
    What sort of half-assed Biology course did you take 20 years ago? We knew about some remarkably complex cascades long before 1989. Classical and alternative complement cascades, for example. Clotting cascade. I'm sure there's more.
    But you have changed the context and point of my general comment. And worse you provided an example equally out of context, namely one that is not intracellular. You are attacking credibility rather than addressing the argument. You do this by cherry picking fine points, changing the substance and then attacking the altered point.
    I assumed you were making a general point about complexity, in particular " cooption or coevolving molecular components" and using intracellular signalling as an example. Am I wrong? And since you're making a very broad point about the credibility of evolution in the context of changing understanding of complexity, I think my point- that we made no such assumptions about complexity, in general, in the time frame specified by you- is thus quite valid. I used cascades, another example of "cooption or coevolving molecular components" and genetics as my examples merely because I'm ot well versed in intracellular signalling.

    Quote Originally Posted by cypress
    Far from assuming that cellular processes and genetics were simple, I can recall as late as 2000 (which is when I was doing my undergrad) it being fully expected that the human genome ought to yield some 100,000-200,000 genes. I'm sure that expectation goes back much further than a mere 20 years. When the results gave a mere 25,000 genes everyone was rather surprised. So we certainly haven't been labouring under the illusion that things were simpler than we know them to be now.
    Again off topic. Gene count does not address the character of intracellular protein interaction.
    And your argument is surely not so specific as to be worrying about complexity in that sense alone. This is not off topic. You're trying to make out that evolution was credible in the past because we didn't think living systems were that complex, but this is clearly not the case. We didn't know as much, sure. But if anything we assumed greater complexity, by some measures. And we still considered evolution to be valid.

    Quote Originally Posted by cypress
    Quote Originally Posted by cypress
    The challenge for modern experimental and molecular biologists is to identify the processes that can account for these observations.
    The complexity we observe has been well-known about for some time, indeed even over-anticipated, and it certainly hasn't demanded that we invoke processes outside of evolutionary theory to get an explanation. That's wishful thinking on your part.
    Perhaps now would be a good time for you to provide an example of a known process experimentally observed to have generated the subject observation.
    So you accept that a man can walk to his front door. You're just wondering what process he uses to walk to the shops and back again. I suspect this is a waste of time. You accept the processes which may cause diversification just as we do. Our position is that these processes plus geological time equal the observed complexity, an assertion which is made by inference from the known facts and which we can test in various ways. But what you want is the process in a bottle, complete, in human time.

    There's a catch of course. Just as with your arguments on abiogenesis, if we do manage to bottle it, you'll then claim intelligent human intervention was required.

    If you were a homicide cop you'd insist on seeing the murder for yourself with five corroborating witnesses rather than accept the validity of inference from the empirical evidence. And if turned out that the victim just fell off a ladder you'd say it was because you were all watching him.

    Quote Originally Posted by cypress
    Quote Originally Posted by TheBiologista
    Quote Originally Posted by Ophiolite
    Quote Originally Posted by spuriousmonkey
    I hate to rock your boat but a lot happened in 20 years. Why don't you read up a bit before you claim something.
    Cypress states "Twenty years ago when I took undergraduate biology, cell chemistry was still considered to be fairly simple so the theory made sense then. Recent studies demonstrate that most cellular processes involve ten or more protein components that are fitted together by shape and chemical afinity."
    This suggests he has done some reading on the matter. Would you like to pinpoint where he is hopelessly out of date?
    One example:

    Complement receptor is an inhibitor of the complement cascade

    A paper in JEM from 1981 in which discusses the role of CR1 in the complement cascade. A quick scan through the paper reveals that the author's knowledge of the cascade is already rather detailed. For a degree course not to have similar understanding some 8 years later seems very unlikely. If it did, then fair enough but not reflective of scientific opinion on complexity greater than 20 years ago. It was not held that molecular biology was simple by any means.
    So I am showing my age. My undergraduate degree was completed in 1983. However once again this is a cell exterior example, and I believe involves single pairs of protein interaction in sequence (six in all if I have that correct) as opposed to the ten or more concurrent interaction I intended to discuss.
    Then by all means please discuss it with specific examples.

    While we're at it, maybe you could stop beating about the bush and state your hypothesis clearly.
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    Quote Originally Posted by spuriousmonkey
    Quote Originally Posted by cypress
    Again off topic. Gene count does not address the character of intracellular protein interaction.
    Do you know what most genes code for?

    Proteins.

    Do you know what constitutes signaling pathways?

    protein interactions. Intracellular and extracellular.

    And protein-DNA-RNA interactions: intracellular mostly.
    Exactly. The fact that we used to think the genome was some 5-10 times larger than it is reflects our past expectations (or knowledge) about intracellular pathways. Either expecting a roughly 1:1 complexity from the observed or hypothesising something far more complex than reality. Either way, the suggestion that we didn't assume complexity comparable to that now known simply does not hold water.
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    Quote Originally Posted by spuriousmonkey
    Quote Originally Posted by cypress

    Again off topic. Gene count does not address the character of intracellular protein interaction.

    [q
    Do you know what most genes code for?

    Proteins.

    Do you know what constitutes signaling pathways?

    protein interactions. Intracellular and extracellular.

    And protein-DNA-RNA interactions: intracellular mostly.
    Now you too are changing the substance of the issue raised. I guess it is a good debate tactic. When you can't answer the question asked, change the question to and easier one and answer it instead. Nice. You both know what kind in protein structures I am talking about, have a look at the article I referenced. I don't see why you are unwilling to address it. What weakness are you trying to hide?
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    Quote Originally Posted by TheBiologista

    And your argument is surely not so specific as to be worrying about complexity in that sense alone. This is not off topic. You're trying to make out that evolution was credible in the past because we didn't think living systems were that complex, but this is clearly not the case. We didn't know as much, sure. But if anything we assumed greater complexity, by some measures. And we still considered evolution to be valid.
    I don't consider evolution invalid. I question the presumed processes and suggest that there must be others in play Experimental studies indicate the currently identified processes can't accomplished the observed changes.

    So you accept that a man can walk to his front door.
    I accept that a man is at the front door now and wasn't some time earlier.

    You're just wondering what process he uses to walk to the shops and back again. I suspect this is a waste of time. You accept the processes which may cause diversification just as we do.
    right

    Our position is that these processes plus geological time equal the observed complexity, an assertion which is made by inference from the known facts and which we can test in various ways. But what you want is the process in a bottle, complete, in human time.
    No, I ask for evidence that the claimed processes can theoretically achieve what we observe happened at the molecular level. The issue is not with the assertion or the inference. The problem is with the tests. Recent experimentation together with new information about the rarity of workable combinations conspire against the vague tests that have been offered to date. Time is not the problem either. There have been an estimated 10^13 primates leading to humans. There are 10^30 bacteria produced in one year. One year is plenty of time to observe change since dramatic change is possible in just 10^12 organisms.

    There's a catch of course. Just as with your arguments on abiogenesis, if we do manage to bottle it, you'll then claim intelligent human intervention was required.

    If you were a homicide cop you'd insist on seeing the murder for yourself with five corroborating witnesses rather than accept the validity of inference from the empirical evidence. And if turned out that the victim just fell off a ladder you'd say it was because you were all watching him.
    Rather than making me and your assumptions about what I think the focus, how about staying on point? I'm not asking to witness the experiments. I am not asking the I derive the models. I only ask to use the same criteria Charles Darwin advocated for. Namely a known process presently in operation that can be shown capable of theoretically producing the claimed results.
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    B. Alberts, 1998. "The cell as a collection of protein machines: preparing the next generation of molecular biologits." Cell 92

    S. Woodson 2005. "Biophysics: assembly line inspection." Nature 438

    First one:

    it is a frikking review article from 1998. A review article Do you know what that is?

    And when you read it it says nothing shocking. It is all for evolution. It just states that protein machines are more complex than people thought 10-20 years ago.

    Have you even read it yourself?

    Even when we know the detailed structure of a protein assembly at an atomic level, as we do for the chaparonin GroEL-GroES, much will remain to be studied. As the article by [7] makes clear, any real understanding of the function of a protein machine will require not only its resting structure in atomic detail, but also a knowledge of the kinetics and energetics of each of its reaction intermediates. New techniques will need to be developed to facilitate such research. But, as always in biology, it will be crucial to define the key parameters that need to be determined, since much more can be measured than should be measured. Outstanding prototype investigations that are clearly explained and reexplained in review article and textbooks can help both to shape this exciting new field and to recruit young scientists to it.
    It is my hope that some of the young scientists who read this issue of Cell will come to the realization that much of the great future in biology lies in gaining a detailed understanding of the inner workings of the cell's many marvelous protein machines

    The basic idea of the review is that biology is more complex than many assume and we shouldn't go complacent and apply tools available to us from other sciences to elucidate/understand the complexity.

    I'm not going to bother to read the second paper because clearly you didn't read the first one yourself.

    shame on you.
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    Quote Originally Posted by cypress
    I don't consider evolution invalid. I question the presumed processes and suggest that there must be others in play Experimental studies indicate the currently identified processes can't accomplished the observed changes.
    That's a pretty vague position. What, specifically with examples, cannot be explained by the known process of evolution. What do you propose as an additional mechanism?

    Quote Originally Posted by cypress
    No, I ask for evidence that the claimed processes can theoretically achieve what we observe happened at the molecular level. The issue is not with the assertion or the inference. The problem is with the tests. Recent experimentation together with new information about the rarity of workable combinations conspire against the vague tests that have been offered to date. Time is not the problem either. There have been an estimated 10^13 primates leading to humans. There are 10^30 bacteria produced in one year. One year is plenty of time to observe change since dramatic change is possible in just 10^12 organisms.
    Source for these numbers? Is that figure for bacteria from a single species or for everything vaguely definable as bacteria?

    Quote Originally Posted by cypress
    Rather than making me and your assumptions about what I think the focus, how about staying on point? I'm not asking to witness the experiments. I am not asking the I derive the models. I only ask to use the same criteria Charles Darwin advocated for. Namely a known process presently in operation that can be shown capable of theoretically producing the claimed results.
    No. We have observed and verified processes leading to incremental change. We are satisfied that these account for the complexity currently observed. What you need to do is show us a specific example that cannot be explained by what we have so far observed. You've got a claim that is unusual, so the onus is on you to support it with evidence.

    Ironic that you accuse me of straying from the topic. You claimed that biologists made the assumption some 20 years ago that life was biochemically simpler than we now know it to be. I think we've now shown that point to be invalid, so you simply failed to address it in your last post and instead focused on more meta argument. Do you concede that this claim was an exaggeration?
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    Quote Originally Posted by cypress
    Experimental studies indicate the currently identified processes can't accomplished the observed changes.
    Facts don't make their own "indications" - you are employing an argument to get from the research results to the hypothesis.

    That argument appears to be: that because any of several small changes in the binding site of some functional protein destroy its current known functionality, the protein cannot be the evolutionary consequence of Darwinian process incremental changes in its defining genetic region, which approach the current functionality over time. The argument is that such an incremental approach involves too many unlikely random increments without selection pressure to establish them, that the probability is too low of such a chain of events.

    The argument employs among several others the following two assumptions:

    That you have available a reasonably complete description or comprehensive understanding of all possible functions of the approaching, incrementally different, protein in all of its possible contexts over evolutionary time (that's how you removed selection pressure from the calculation).

    That all the individual incremental changes necessary are independent events, in the evolutionary context involved; that "chunks" of genome are not swapped in and out, that some changes do not affect the likelihood of others, etc (that's how you arrived at the low probability of the lot of them).

    Neither of those assumptions seems reasonable to me, and the entire argument seems therefore completely invalid.

    But I am willing to be persuaded, if you have some reasoning in support of them.
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    Quote Originally Posted by spuriousmonkey
    B. Alberts, 1998. "The cell as a collection of protein machines: preparing the next generation of molecular biologits." Cell 92

    S. Woodson 2005. "Biophysics: assembly line inspection." Nature 438

    First one:

    it is a frikking review article from 1998. A review article Do you know what that is?

    And when you read it it says nothing shocking. It is all for evolution. It just states that protein machines are more complex than people thought 10-20 years ago.

    Have you even read it yourself?
    The articles are an appropriate response to the question asked, namely articles that demonstrate that cellular systems are now understood to be much more complex than presumed in the early '80's. furthermore the they specifically mention protein machines within cells made up of many more than ten parts.


    The basic idea of the review is that biology is more complex than many assume and we shouldn't go complacent and apply tools available to us from other sciences to elucidate/understand the complexity.

    I'm not going to bother to read the second paper because clearly you didn't read the first one yourself.

    shame on you.
    You have no way to know what I have read or not read. You seem to be changing the question then implying that I didn't answer the question when I did answer the question asked as I stated above. My take-away from those two articles is just as you said, that cellular systems are far more complex than many thought. If you intended for me to substantiate a different point you should be more clear.

    Meanwhile you offer nothing to demonstrate my original statements are incorrect though you appear to be trying very hard to make it seem you have.
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    Quote Originally Posted by TheBiologista

    No. We have observed and verified processes leading to incremental change. We are satisfied that these account for the complexity currently observed. What you need to do is show us a specific example that cannot be explained by what we have so far observed. You've got a claim that is unusual, so the onus is on you to support it with evidence.

    Ironic that you accuse me of straying from the topic. You claimed that biologists made the assumption some 20 years ago that life was biochemically simpler than we now know it to be. I think we've now shown that point to be invalid, so you simply failed to address it in your last post and instead focused on more meta argument. Do you concede that this claim was an exaggeration?
    No I do not. My claim about assumptions regarding intracellular components and functions when taken in total, made at the time I attended undergraduate studies, stands and the reference supplied support it.
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    Maybe this will help to clear up misunderstandings for some.

    http://www.youtube.com/watch?v=SeTssvexa9s
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    Quote Originally Posted by cypress
    Quote Originally Posted by spuriousmonkey
    B. Alberts, 1998. "The cell as a collection of protein machines: preparing the next generation of molecular biologits." Cell 92

    S. Woodson 2005. "Biophysics: assembly line inspection." Nature 438

    First one:

    it is a frikking review article from 1998. A review article Do you know what that is?

    And when you read it it says nothing shocking. It is all for evolution. It just states that protein machines are more complex than people thought 10-20 years ago.

    Have you even read it yourself?
    The articles are an appropriate response to the question asked, namely articles that demonstrate that cellular systems are now understood to be much more complex than presumed in the early '80's. furthermore the they specifically mention protein machines within cells made up of many more than ten parts.


    The basic idea of the review is that biology is more complex than many assume and we shouldn't go complacent and apply tools available to us from other sciences to elucidate/understand the complexity.

    I'm not going to bother to read the second paper because clearly you didn't read the first one yourself.

    shame on you.
    You have no way to know what I have read or not read. You seem to be changing the question then implying that I didn't answer the question when I did answer the question asked as I stated above. My take-away from those two articles is just as you said, that cellular systems are far more complex than many thought. If you intended for me to substantiate a different point you should be more clear.

    Meanwhile you offer nothing to demonstrate my original statements are incorrect though you appear to be trying very hard to make it seem you have.
    You are just running around. We provided ample evidence that your ideas are antiquated.

    Then you demand I address the literature you provided.

    I read one of them, and the gist of the article is just that the newfound complexity (in the 90s) requires different tools then used in the 80s and early 90s.

    Quelle surprise?

    Now you provide evidence of your position.

    Since you haven't.

    In fact, I will refer to the 1998 cell paper as evidence for my position since it clearly states that the complexity can be researched with the scientific tools available.

    Please provide evidence that it doesn't.
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    Quote Originally Posted by cypress
    Quote Originally Posted by TheBiologista

    No. We have observed and verified processes leading to incremental change. We are satisfied that these account for the complexity currently observed. What you need to do is show us a specific example that cannot be explained by what we have so far observed. You've got a claim that is unusual, so the onus is on you to support it with evidence.

    Ironic that you accuse me of straying from the topic. You claimed that biologists made the assumption some 20 years ago that life was biochemically simpler than we now know it to be. I think we've now shown that point to be invalid, so you simply failed to address it in your last post and instead focused on more meta argument. Do you concede that this claim was an exaggeration?
    No I do not. My claim about assumptions regarding intracellular components and functions when taken in total, made at the time I attended undergraduate studies, stands and the reference supplied support it.
    The first one supports a contention that we underestimated the complexity of cells during the 1960's, but not really that we were way off base in the 1980's. It's not a very strong point either way. We always know more later than we did before. We're often amazed, surprised by new knowledge. That rarely equals a paradigm shift in our understanding though. Can you show us that this knowledge did? Because that reference expresses amazement, but at no point does it suggest that there's anything in there that changes our understanding of evolution.

    What about the rest of my post? Will you provide specific examples of systems which cannot be explained by the conventional processes of evolution? Will you specify what you consider the missing component or process of the system to be? Or are we just going to select the parts of posts we can answer, on topic or otherwise, and ignore the rest?
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    Quote Originally Posted by TheBiologista
    Quote Originally Posted by cypress

    No I do not. My claim about assumptions regarding intracellular components and functions when taken in total, made at the time I attended undergraduate studies, stands and the reference supplied support it.
    The first one supports a contention that we underestimated the complexity of cells during the 1960's, but not really that we were way off base in the 1980's. It's not a very strong point either way. We always know more later than we did before. We're often amazed, surprised by new knowledge. That rarely equals a paradigm shift in our understanding though. Can you show us that this knowledge did? Because that reference expresses amazement, but at no point does it suggest that there's anything in there that changes our understanding of evolution.
    Surprising that people initially took issue with the statement as it was intended as an introduction to the primary point. Paradigm's change slowly when they are deeply rooted in idealology as this one is. Even when the shift doen't challenge the idealology (as this one seems not to) they often are not well recieved. I suppose because any change could potentially threaten the idealology too.

    What about the rest of my post? Will you provide specific examples of systems which cannot be explained by the conventional processes of evolution? Will you specify what you consider the missing component or process of the system to be? Or are we just going to select the parts of posts we can answer, on topic or otherwise, and ignore the rest?
    I am away from my library so this will have to wait a bit. Also with so many posters with questions, it is difficult to address every point raised.
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    You really want to play the ideology card? That won't get anyone anywhere, since the same claim can be made by both sides. I have to say that your criticisms seem to come down to simple personal incredulity and nothing more.
    Disclaimer: I do not declare myself to be an expert on ANY subject. If I state something as fact that is obviously wrong, please don't hesitate to correct me. I welcome such corrections in an attempt to be as truthful and accurate as possible.

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    Quote Originally Posted by cypress
    Quote Originally Posted by TheBiologista
    Quote Originally Posted by cypress

    No I do not. My claim about assumptions regarding intracellular components and functions when taken in total, made at the time I attended undergraduate studies, stands and the reference supplied support it.
    The first one supports a contention that we underestimated the complexity of cells during the 1960's, but not really that we were way off base in the 1980's. It's not a very strong point either way. We always know more later than we did before. We're often amazed, surprised by new knowledge. That rarely equals a paradigm shift in our understanding though. Can you show us that this knowledge did? Because that reference expresses amazement, but at no point does it suggest that there's anything in there that changes our understanding of evolution.
    Surprising that people initially took issue with the statement as it was intended as an introduction to the primary point. Paradigm's change slowly when they are deeply rooted in idealology as this one is. Even when the shift doen't challenge the idealology (as this one seems not to) they often are not well recieved. I suppose because any change could potentially threaten the idealology too.
    Uhh, Thomas Kuhn. Thing is paradigms only replace old ones (according to Kuhn) if they are better at solving puzzles than the old one. Since ID does not solve puzzles, like where to look for certain fossils, or why there are gene sequences that show a fusion of two chromosomes into one in humans, it cannot replace evolutin, even if it were true. Thus, if one agrees with Kuhn completely ID is a philisophical issue as the scientific establishment is incapable of evaluating it (as scientists are essentially pragmatists and ID violates this philosophy). This agrees with the idea that ID is not science because it is untestable.

    Reading Kuhn, as I am now, would be alot more enjoyable if people stopped misrepresenting his views. As would've been my thermodynamics course.
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    Quote Originally Posted by iceaura
    Quote Originally Posted by cypress
    Experimental studies indicate the currently identified processes can't accomplish the observed changes.
    Facts don't make their own "indications" - you are employing an argument to get from the research results to the hypothesis.

    That argument appears to be: that because any of several small changes in the binding site of some functional protein destroy its current known functionality, the protein cannot be the evolutionary consequence of Darwinian process incremental changes in its defining genetic region, which approach the current functionality over time. The argument is that such an incremental approach involves too many unlikely random increments without selection pressure to establish them, that the probability is too low of such a chain of events.

    The argument employs among several others the following two assumptions:

    That you have available a reasonably complete description or comprehensive understanding of all possible functions of the approaching, incrementally different, protein in all of its possible contexts over evolutionary time (that's how you removed selection pressure from the calculation).
    No sorry that is not my argument. It goes like this:

    Protein machines contain tens and even hundreds of components. (1) In order to properly assemble and remain assembled, they must have specific binding sites that will differentiate between correct partners and the thousands of other proteins in the cell. (2) Not only do the shapes have to match but also the chemical properties of the surface of the proteins must be complementary. If they don't stick together they will drift apart.

    1. S. Woodson 2005, Biophysics: assembly line inspection. Nature 438
    2. I. Nooren and J. Thornton, 2003 Diversity of protein-protein interactions. EMBO J. 22

    Turns out protein shape space has been studied and found to be huge. Conservative estimates obtained by limiting mutations to coherent patches of AA close to each other on the surface of the protein. Even here the numbers were about one in 10^8 binding sites would have to be sampled to find one that binds to a randomly selected protein (3). This study matches nicely with others that indicate a minimum of 5-6 consecutive amino acids are generally involved in binding sites. Thus to generate a new protein binding site would require 5-6 coherent mutational steps. I have already accepted that observed processes can account for single and even rarely two steps. But when three or more steps are required as is the case here, the observed processes have not been shown to be capable of accomplishing this.

    Recent work in experimental molecular biology confirms much of this. One series of studies demonstrates, for the proteins studied, about 1 in 10^70 proteins are functional based on their capacity to form binding sites capable of maintaining a stable tertiary shape. Another study indicates that the number of organisms required to generate a new gene control site where just two changes are required is anywhere from 10^12 to 10^18. In primates, that would be well over 100 million years for one new gene control function, by currently understood processes. Another study confirms that when 4 neutral changes are first required before two functional changes are needed in a protein receptor, stepwise evolutionary processes seem unable to accomplish this.

    3. g. Winter and several others, 1998. Small binding proteins selected from a combinatorial repertoire of knottins displayed on a phage. J. Mol. Bio. 277

    So I am not saying that it there is no incremental functional pathways. You would not accept a demand from me for you to do an exhaustive search, but you seem to think it is reasonable for me to perform one. I am saying that experimental attempts to demonstrate stepwise paths are instead showing that for many specific examples the test demonstrated gaps of several steps.

    That all the individual incremental changes necessary are independent events, in the evolutionary context involved; that "chunks" of genome are not swapped in and out, that some changes do not affect the likelihood of others, etc (that's how you arrived at the low probability of the lot of them).

    Neither of those assumptions seems reasonable to me, and the entire argument seems therefore completely invalid.

    But I am willing to be persuaded, if you have some reasoning in support of them.
    So you see I am not making assumptions, I am observing what experimentation is placing in front of us. However when you chose to believe that observed processes have generated all observed diversity, it is you who are making assumptions. Can you provide experimental results that demonstrate how observed evolutionary processes do overcome these hurdles? Remember I do not dispute that change has occurred, so please do not show me homology examples since they only demonstrate that changes occur without telling us how they occurred. If you can't provide this for me then please admit that it is you and not me that are making assumptions.
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    Quote Originally Posted by cypress
    So you see I am not making assumptions, I am observing what experimentation is placing in front of us. However when you chose to believe that observed processes have generated all observed diversity, it is you who are making assumptions. Can you provide experimental results that demonstrate how observed evolutionary processes do overcome these hurdles? Remember I do not dispute that change has occurred, so please do not show me homology examples since they only demonstrate that changes occur without telling us how they occurred. If you can't provide this for me then please admit that it is you and not me that are making assumptions.
    Not evolution per se, but the immune system creates variations with unique binding sites all the time, so many that even if we came into contact with a completely foreign antigen we would have at least one cell to fight it (this cell then reproduces to make a large number of these cells). Since the immune system seems to have evolved from transposons, these may provide a hint.

    Transposons code copy proteins throughout the genome. So that we all have many copies of the same gene. Some variation doesn't hurt (b/c we have many other copies to do the job anyways). So many possible binding sites are possible (and since there are many proteins it probably binds to at least one other protein). Eventually the binding site allows the protein to bind to another with a different function, this can create either systems that do harm, nothing, or create a new useful function. The binding could also get stronger over time through gradual evolution. This idea is supported by said homologies, since the proteins would need there own functions. This idea would allow the new system to be integrated into an even more complex system.

    But, while this is testable (by looking for functions of individual proteins), it is not fully testable yet, as we cannot look at homologies or evolution of binding sites (which I believe you are focusing on). Though we could test the amount of variation between transposon copies to see how long it would take for enough variation to be present to form a binding site.

    Maybe natural selection didn't create complex systems, but I don't think natural selection is incapable of making them. Since evolution is consistent with everything injecting another solution for certain systems seems pointless to me. Plus development, for which there is much evidence for evolution, probably is rooted in complex molecular machines, so if development evolved it did so because complex molecular systems did to.

    By the way I think complexity is not the only factor effecting evolution. Given enough time and variation natural selection could create anything. So it is not enough to say that things are too complex for natural selection, one must show that there is not enough variation and time.
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    Quote Originally Posted by cypress
    Quote Originally Posted by TheBiologista
    Quote Originally Posted by cypress

    No I do not. My claim about assumptions regarding intracellular components and functions when taken in total, made at the time I attended undergraduate studies, stands and the reference supplied support it.
    The first one supports a contention that we underestimated the complexity of cells during the 1960's, but not really that we were way off base in the 1980's. It's not a very strong point either way. We always know more later than we did before. We're often amazed, surprised by new knowledge. That rarely equals a paradigm shift in our understanding though. Can you show us that this knowledge did? Because that reference expresses amazement, but at no point does it suggest that there's anything in there that changes our understanding of evolution.
    Surprising that people initially took issue with the statement as it was intended as an introduction to the primary point. Paradigm's change slowly when they are deeply rooted in idealology as this one is. Even when the shift doen't challenge the idealology (as this one seems not to) they often are not well recieved. I suppose because any change could potentially threaten the idealology too.
    Paradigms also change slowly when they're well-rooted in evidence and/or the contradictory evidence is weak. Or absent in this case. Hope you get to your library soon. Or just figure out Pubmed.

    Resistence to change is always appropriate. That's scepticism. It prevents us from credulously accepting every half-formed idea that is proposed. The alternative is to go in circles. Science has progressed just fine by maintaining scepticism towards new ideas. Indeed it has progressed so fast that generation gaps seem wider than ever before, and mostly on the basis of things like technology uptake and bioethics.

    When a proposed change is sweeping, strong resistance is warranted. When it also fails to fill a gap in our understanding, fails to predict new data and is based upon neither evidence nor clear hypothesis, it's quite appropriate to be dismissive pending some change to that situation.

    Quote Originally Posted by cypress
    Quote Originally Posted by TheBiologista
    What about the rest of my post? Will you provide specific examples of systems which cannot be explained by the conventional processes of evolution? Will you specify what you consider the missing component or process of the system to be? Or are we just going to select the parts of posts we can answer, on topic or otherwise, and ignore the rest?
    I am away from my library so this will have to wait a bit. Also with so many posters with questions, it is difficult to address every point raised.
    You don't need to go to a library to state your hypothesis clearly, to detail its implications, to explain the predictions it would make and specify how it might be falsified.
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    Quote Originally Posted by TheBiologista

    You don't need to go to a library to state your hypothesis clearly, to detail its implications, to explain the predictions it would make and specify how it might be falsified.
    I posted my argument last night in my last post. Guess you missed it.

    Paradigms also change slowly when they're well-rooted in evidence and/or the contradictory evidence is weak. Or absent in this case.
    The evidence is piling up that observed processes at the molecular level don't account for development of new and unique binding sites. The processes are demonstrably too slow to search shape space for the rare coherent, functional, well fitted combinations required to construct molecular components made up of the tens and hundreds of proteins. The evidence is demonstrating that without selection to drive a stepwise process, several neutral but necessary mutations required prior to a key functional change effectively makes the alteration out of reach in any reasonable timeframe except for the very rare chance occurrence. We can allow one or two rare cases, but observed diversity demands millions.

    Where is this well-rooted evidence that the evolutionary processes actually do accomplish these feats? Please don't offer studies of similarities and homologous structures as we both agree that changes occurred. I want to see evidence that evolutionary processes are in fact capable of accomplishing the observed changes. Let's see just how sound your supposed evidence is. Is it evidence or presumption?
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    Quote Originally Posted by Golkarian
    Quote Originally Posted by cypress
    So you see I am not making assumptions, I am observing what experimentation is placing in front of us. However when you chose to believe that observed processes have generated all observed diversity, it is you who are making assumptions. Can you provide experimental results that demonstrate how observed evolutionary processes do overcome these hurdles? Remember I do not dispute that change has occurred, so please do not show me homology examples since they only demonstrate that changes occur without telling us how they occurred. If you can't provide this for me then please admit that it is you and not me that are making assumptions.
    Not evolution per se, but the immune system creates variations with unique binding sites all the time, so many that even if we came into contact with a completely foreign antigen we would have at least one cell to fight it (this cell then reproduces to make a large number of these cells). Since the immune system seems to have evolved from transposons, these may provide a hint.
    Quite right it is not an evolutionary process. It is however good research. It is these studies that lead to awareness of the size and diversity of protein shape space and binding sites. This is the line of research used to derive the estimates I provided. Early hypothesis were that immune system gene mutation might account for derivation of the near endless capability to derive unique shapes and binding sites. Unfortunately it turns out not to be the case. There seem only to be a couple hundred genes involved.

    It would be an interesting assumption to presume this reactive (not random) process or one similar to this is involved. So your first response is an assumption.

    Transposons code copy proteins throughout the genome. So that we all have many copies of the same gene. Some variation doesn't hurt (b/c we have many other copies to do the job anyways). So many possible binding sites are possible (and since there are many proteins it probably binds to at least one other protein).
    Assumption number 2. Not bad assumptions, but not evidence.

    Eventually the binding site allows the protein to bind to another with a different function, this can create either systems that do harm, nothing, or create a new useful function.
    Assumption 3.

    The binding could also get stronger over time through gradual evolution.
    Assumption 4

    This idea is supported by said homologies, since the proteins would need there own functions. This idea would allow the new system to be integrated into an even more complex system.
    Assumption 5. Now becoming a just so story. Remember, similarity is evidence for change but it tells us nothing about how the change occurred.

    But, while this is testable (by looking for functions of individual proteins), it is not fully testable yet, as we cannot look at homologies or evolution of binding sites (which I believe you are focusing on). Though we could test the amount of variation between transposon copies to see how long it would take for enough variation to be present to form a binding site.
    Yes, current research is doing exactly this. The research I mention is and it is deriving results that take too long or don't happen at all. The door is beginning to close on this avenue.

    Maybe natural selection didn't create complex systems, but I don't think natural selection is incapable of making them.
    Assumption 6.

    Since evolution is consistent with everything
    Assumption 7.

    injecting another solution for certain systems seems pointless to me. Plus development, for which there is much evidence for evolution, probably is rooted in complex molecular machines, so if development evolved it did so because complex molecular systems did to.
    Assumption 8.

    By the way I think complexity is not the only factor effecting evolution. Given enough time and variation natural selection could create anything.
    Assumption 9. A well described and coherent story. Interesting no doubt, and perhaps even partially correct. Please don't belittle one by accusing them of making assumptions when you are quite happy to string together some of your own.

    So it is not enough to say that things are too complex for natural selection, one must show that there is not enough variation and time.
    Right. The two modification gene control example indicates that 4 million years is far too short of time for humans to evolve from a primate common ancestor by known evolutionary processes. The fossil record indicates most phyla were derived during the early cambrian in a period of less than 20 million years. Again this is way to short of time to derive the vast array of new proteins, protein combinations, developmental controls, gene controls, etc. etc. These changes involve derivation of millions of new components that are also well fitted together. But studies indicate that for three or more key changes by evolutionary processes, well over 10^18 organism would be required. (1) When several neutral changes are required prior to one or more key alteration, conventional evolutionary processes appear to fail navigating the pathway (2) in any reasonable time, instead, as expected, it gets hopelessly lost in other neutral alteration making the distance even further out of reach.

    edit to add references.

    1) R. Durrett, & D. Schmidt, 2008. Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution. Genetics 180.

    2) J. Bridgham, E. Ortlund, and J. Thornton, 2009. An epistatic ratchet constrains the direction of glucocorticoid receptor evolution. Nature 461.

    J. Bridgham, Carroll, and J. Thornton, 2006. Evolution of hormone-receptor complexity by molecular exploitation. Science 312.
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    Forum Cosmic Wizard spuriousmonkey's Avatar
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    They have observed a lizard speciation event in less than 30 years in the wild.

    Why would 4 millions years be too short?
    "Kill them all and let God sort them out."

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    Quote Originally Posted by spuriousmonkey
    They have observed a lizard speciation event in less than 30 years in the wild.

    Why would 4 millions years be too short?
    4 million years is too short of time to derive a new gene control binding site when two alterations are required and the gene pool is limited to 10^8 organisms. See the reference I added in the edit of my last post. Humans seem to have large numbers of gene control and developmental control differences with greater than two alterations compared to other primates.

    What molecular level alterations were observed in your example? What new protein binding sites, gene control sites, and developmental pathways were derived? What new form and function was generated?
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    Quote Originally Posted by cypress
    Transposons code copy proteins throughout the genome. So that we all have many copies of the same gene. Some variation doesn't hurt (b/c we have many other copies to do the job anyways). So many possible binding sites are possible (and since there are many proteins it probably binds to at least one other protein).
    Assumption number 2. Not bad assumptions, but not evidence.
    Assumption if I say it accounts for evolution, but it does actually happen.

    Quote Originally Posted by cypress
    Eventually the binding site allows the protein to bind to another with a different function, this can create either systems that do harm, nothing, or create a new useful function.
    Assumption 3.
    The binding could also get stronger over time through gradual evolution.
    Assumption 4

    This idea is supported by said homologies, since the proteins would need there own functions. This idea would allow the new system to be integrated into an even more complex system.
    Assumption 5. Now becoming a just so story. Remember, similarity is evidence for change but it tells us nothing about how the change occurred.
    It's still a hypothesis, all hypotheses have assumptions, that's what makes them testable. Homologies support natural selection, in my opinion, because random chance alone cannot create this kind of complexity and intelligent design could start it from scratch (no similarities necessary). So while they don't imply natural selection they make other alternatives less likely.

    Add a reference for tranposon -->immune system hypothesis:

    http://www.plosbiology.org/article/i...0E1113BC86C08F

    Quote Originally Posted by cypress
    Maybe natural selection didn't create complex systems, but I don't think natural selection is incapable of making them.
    Assumption 6.
    Based on the other assumptions, if the others allow for natural selection, this assumption it true as well.

    Quote Originally Posted by cypress
    By the way I think complexity is not the only factor effecting evolution. Given enough time and variation natural selection could create anything.
    Assumption 9. A well described and coherent story. Interesting no doubt, and perhaps even partially correct. Please don't belittle one by accusing them of making assumptions when you are quite happy to string together some of your own.
    One I would like to say that evolution is capable of making anything within energy restraints. Plus I never (to my knowledge) accused you of making assumptions. Assumptions are what make hypotheses testable.

    Quote Originally Posted by cypress
    So it is not enough to say that things are too complex for natural selection, one must show that there is not enough variation and time.
    Right. The two modification gene control example indicates that 4 million years is far too short of time for humans to evolve from a primate common ancestor by known evolutionary processes. The fossil record indicates most phyla were derived during the early cambrian in a period of less than 20 million years. Again this is way to short of time to derive the vast array of new proteins, protein combinations, developmental controls, gene controls, etc. etc. These changes involve derivation of millions of new components that are also well fitted together. But studies indicate that for three or more key changes by evolutionary processes, well over 10^18 organism would be required. (1) When several neutral changes are required prior to one or more key alteration, conventional evolutionary processes appear to fail navigating the pathway (2) in any reasonable time, instead, as expected, it gets hopelessly lost in other neutral alteration making the distance even further out of reach.

    edit to add references.

    1) R. Durrett, & D. Schmidt, 2008. Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution. Genetics 180.

    2) J. Bridgham, E. Ortlund, and J. Thornton, 2009. An epistatic ratchet constrains the direction of glucocorticoid receptor evolution. Nature 461.

    J. Bridgham, Carroll, and J. Thornton, 2006. Evolution of hormone-receptor complexity by molecular exploitation. Science 312.
    While I can see where some examples could support your hypthesis I think these fail, development of all major phyla after the Cambrian are regulated by the same set of genes (the Hox genes), once this system is in place new proteins aren't really necessary, just duplication and slight variations of preexisting proteins, if you want to show that natural selection is incapable of making certain systems I'd look before the Cambrian.

    http://nro.sagepub.com/cgi/reprint/5/3/164

    Also at an anatomical level large changes are possible in short periods of time (much larger than in the fossil record):

    http://www.sciencemag.org/cgi/conten.../275/5308/1934

    But I guess I'll need a study similar to this but at the genetic level to convince you?
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    Cypress, I think another diffiulty is that binding sites are neutral but that is only a small part of the protein itself, everything else can be derived from old functions. Also binding sites could have been weaker and less specific in the past (just a speculative counter-example) this would mean that they developed via natural selection. It could be tested by creating weak binding sites in the lab which are subsets of the modern ones.
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  54. #53  
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    Quote Originally Posted by cypress
    Quote Originally Posted by spuriousmonkey
    They have observed a lizard speciation event in less than 30 years in the wild.

    Why would 4 millions years be too short?
    4 million years is too short of time to derive a new gene control binding site when two alterations are required and the gene pool is limited to 10^8 organisms. See the reference I added in the edit of my last post. Humans seem to have large numbers of gene control and developmental control differences with greater than two alterations compared to other primates.

    What molecular level alterations were observed in your example? What new protein binding sites, gene control sites, and developmental pathways were derived? What new form and function was generated?
    You are deluded. We didn't evolve from extant apes. We shared an ancestor.

    Modern apes have evolved the same distance from the ancestor as we have.

    Giving random references isn't going to work any more. I checked one of your references and it was supporting evolution and the concept that complexity could be understood.

    You will have to quote exactly from your references where the papers support your notions. I am not going to fall for your cheap tricks any more.

    Last reference for instance is a clear case of supporting evolution as it is.
    A frikking quote from the abstract for crying out loud:

    Our results indicate that tight interactions can evolve by molecular exploitationrecruitment of an older molecule, previously constrained for a different role, into a new functional complex.
    How does that support your delusions?

    Another quote from the article that is supposed to support your delusions:

    Our findings demonstrate that the MR-aldosterone partnership evolved in a stepwise fashion consistent with Darwinian theory, but the functions being selected for changed over time
    Do you understand the words "consistent with Darwinian theory"?

    The article is actually opposed to your ideas and explains how complexity is no problem:

    The puzzle that complex systems pose for Darwinian evolution depends on the premise that each part has no functionand therefore cannot be selected foruntil the entire system is present. This puzzle might indeed cause Darwin's theory to "break down" if the functions of the parts must remain static for all time. But virtually all molecules can and do participate in more than one process or interaction, so a complex's elements may have been selected in the past for unrelated functions. Our work indicates that tightly integrated systems can be assembled by combining old molecules with different ancestral roles together with new onesgenerated by gene duplication or elaboration of enzymatic pathwaysthat represent slight structural variants on older elements. We propose that molecular exploitation will be a predominant theme in evolution, one that may provide a general explanation for how the molecular interactions critical for life's complexity emerged in Darwinian fashion.

    So I now add this article to the literature opposing your ideas.

    I will await your deconstruction of the article. Unless you are a git and continue trolling.
    reference
    http://www.sciencemag.org/cgi/content/full/312/5770/97
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    Quote Originally Posted by spuriousmonkey
    Quote Originally Posted by cypress
    Quote Originally Posted by spuriousmonkey
    They have observed a lizard speciation event in less than 30 years in the wild.

    Why would 4 millions years be too short?
    4 million years is too short of time to derive a new gene control binding site when two alterations are required and the gene pool is limited to 10^8 organisms. See the reference I added in the edit of my last post. Humans seem to have large numbers of gene control and developmental control differences with greater than two alterations compared to other primates.

    What molecular level alterations were observed in your example? What new protein binding sites, gene control sites, and developmental pathways were derived? What new form and function was generated?
    You are deluded. We didn't evolve from extant apes. We shared an ancestor.

    Modern apes have evolved the same distance from the ancestor as we have.
    Never said humans did. Nice attempt to divert attention away from the fact that you don't and can't address the reality that observed evolutionary processes don't provide a mechanism to account for the majority of cellular protein structures.

    Giving random references isn't going to work any more. I checked one of your references and it was supporting evolution and the concept that complexity could be understood.
    An articles writer can support a general idea even as it demonstrates in a different way the points I am focusing on. The first reference you took issue with was provided to demonstrate that our understanding of molecular components in the cell is substantially different now vs. 25 years ago. Back then random stepwise modification plus selection made sense in light of what we understood. That was the only point of the first reference. I never claimed the writer was arguing against evolution. I personally do not argue against evolution. I take issue with the presumed processes.

    You will have to quote exactly from your references where the papers support your notions. I am not going to fall for your cheap tricks any more.
    You just make yourself look bad when you raise red herring arguments. How about demonstrating that known evolutionary processes do generate novel 6 position binding sites and new stable functional tertiary protein structures that fit to multiple complementary proteins. Show us how it is done.

    Last reference for instance is a clear case of supporting evolution as it is.
    A frikking quote from the abstract for crying out loud:

    Our results indicate that tight interactions can evolve by molecular exploitationrecruitment of an older molecule, previously constrained for a different role, into a new functional complex.
    How does that support your delusions?
    The last article was provided for context with the newer one by the same researchers. It demonstrates that while this particular protein hormone receptor may have a stepwise path from a presumed earlier receptor with genera hormone selectivity to the modern one that is quite specific (the second article provides an incomplete glimpse into this pathway), the first article demonstrates that the reverse pathway seems out of reach to known processes because several neutral modifications are first needed before two key modifications can occur and random mutation appears to be unable to navigate the neutral modifications without making sever more that must also be undone. This article is evidence of the situation I referenced that article to support.

    Another quote from the article that is supposed to support your delusions:

    Our findings demonstrate that the MR-aldosterone partnership evolved in a stepwise fashion consistent with Darwinian theory, but the functions being selected for changed over time
    Do you understand the words "consistent with Darwinian theory"?
    Again the second article was used for context with the first. I am an advocate of full disclosure. Perhaps you should focus on demonstrating that the substance of my particular claim is in error rather than attacking my selection of references and the fact that my posts can't address every point raised by the references.

    The article is actually opposed to your ideas and explains how complexity is no problem:

    The puzzle that complex systems pose for Darwinian evolution depends on the premise that each part has no functionand therefore cannot be selected foruntil the entire system is present. This puzzle might indeed cause Darwin's theory to "break down" if the functions of the parts must remain static for all time. But virtually all molecules can and do participate in more than one process or interaction, so a complex's elements may have been selected in the past for unrelated functions. Our work indicates that tightly integrated systems can be assembled by combining old molecules with different ancestral roles together with new onesgenerated by gene duplication or elaboration of enzymatic pathwaysthat represent slight structural variants on older elements. We propose that molecular exploitation will be a predominant theme in evolution, one that may provide a general explanation for how the molecular interactions critical for life's complexity emerged in Darwinian fashion.
    The article provides a specific example where stepwise processes are thought to be able to accomplish a modest alteration in selectivity for a hormone. Furthermore the alterations were not tested in living organisms so we dont even know if these modified receptors have functional selectivity. It is not an example of making a new binding site. It is not an example of new structure. It is not an example of novel multi-protein molecular components. It is not an example of new form or function.

    It is not an example of a counter to my claims in any fashion. Once again you dont address the question posed so you change the question, to one you can answer, throw out a few red herrings to divert attention, and then attack the person all while not addressing the actual question.

    So I now add this article to the literature opposing your ideas.

    I will await your deconstruction of the article. Unless you are a git and continue trolling.
    reference
    http://www.sciencemag.org/cgi/content/full/312/5770/97
    Sorry, no. As I explained above, this article answers an interesting question, but it answers one that known process can easily handle. So really it simply adds slightly to something we already know. The point is, it doesn't in any way address the challenges I raised. The article was for context and completeness. It complements the more recent article by the same researchers.

    Your tactic is tired. Resort to personal attacks to divert from the fact that you dont address the issue raised. When are you going to address the questions posed? Exactly who is trolling, you or me?
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    Quote Originally Posted by cypress
    No sorry that is not my argument. It goes like this:

    Protein machines contain tens and even hundreds of components. (1) In order to properly assemble and remain assembled, they must have specific binding sites that will differentiate between correct partners and the thousands of other proteins in the cell. (2) Not only do the shapes have to match but also the chemical properties of the surface of the proteins must be complementary. If they don't stick together they will drift apart.

    1. S. Woodson 2005, Biophysics: assembly line inspection. Nature 438
    2. I. Nooren and J. Thornton, 2003 Diversity of protein-protein interactions. EMBO J. 22

    Turns out protein shape space has been studied and found to be huge. Conservative estimates obtained by limiting mutations to coherent patches of AA close to each other on the surface of the protein. Even here the numbers were about one in 10^8 binding sites would have to be sampled to find one that binds to a randomly selected protein (3). This study matches nicely with others that indicate a minimum of 5-6 consecutive amino acids are generally involved in binding sites. Thus to generate a new protein binding site would require 5-6 coherent mutational steps. I have already accepted that observed processes can account for single and even rarely two steps. But when three or more steps are required as is the case here, the observed processes have not been shown to be capable of accomplishing this.

    Recent work in experimental molecular biology confirms much of this. One series of studies demonstrates, for the proteins studied, about 1 in 10^70 proteins are functional based on their capacity to form binding sites capable of maintaining a stable tertiary shape. Another study indicates that the number of organisms required to generate a new gene control site where just two changes are required is anywhere from 10^12 to 10^18. In primates, that would be well over 100 million years for one new gene control function, by currently understood processes. Another study confirms that when 4 neutral changes are first required before two functional changes are needed in a protein receptor, stepwise evolutionary processes seem unable to accomplish this.

    3. g. Winter and several others, 1998. Small binding proteins selected from a combinatorial repertoire of knottins displayed on a phage. J. Mol. Bio. 277
    One problem I see with your theory is that you are talking of the space of total proteins available. Usable proteins, as developed by organisms, cluster around similar groups of shapes in general, and can be rather easily modified to 'match' receptor sutes - that's why snake venom is so dangerous, for instance.

    The argument merely that there are large numbers of possible proteins and very few of them match given receptors is rather meaningless - like the hoary old quotation from Fred Hoyle about a whilrwind in a junkyard creating a 747.

    If, for instance, your recent study says that only 1:10^70 proteins studied were functional, surely the question is "Which proteins were they studying?", or were they taking other structural proteins that have nothing to do with the catalytic nature of proteins, and site-binding? Were they, for instance, using entirely the wrong statistical sample?

    The idea of irreducible protein machines was floated by Michael Behe a while ago, and demonstrated to be a lot of nonsense by scientists (who had to take time out from serious work just because Behe became, for a while, a poster boy for the Creationist brigade).

    Your interpretations of various studies is one matter. Have you found a single current piece of properly peer-reviewed research (published, that is, in a respectable science journal and not subsequently refuted) in which any scientists claim that the known evolutionary mechanisms are inadequate to explain the variety of life?
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    1. I am an evolutionist through and through. Cut me and my blood has the same salinity as the ocean off of the Galapagos islands.
    2. Forty years ago I thought there was a great deal of handwaving, assumption making, closing of eyes to inconvenient observations and the like, in accounting for the origin of diversity amongst eukaryotes.
    3. Forty years later and hox genes, evo-devo and the like, notwithstanding, I see the same presumptiveness.
    4. There are likely still mechanisms central to evolution that we have not recognised and certainly not understood. We shall discern them, but not if we deny the need to look for them.

    Now Cypress, are you now, or have you ever been a member of the Intelligent Design movement?
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    Forum Cosmic Wizard spuriousmonkey's Avatar
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    Quote Originally Posted by cypress
    Quote Originally Posted by spuriousmonkey
    Quote Originally Posted by cypress
    Quote Originally Posted by spuriousmonkey
    They have observed a lizard speciation event in less than 30 years in the wild.

    Why would 4 millions years be too short?
    4 million years is too short of time to derive a new gene control binding site when two alterations are required and the gene pool is limited to 10^8 organisms. See the reference I added in the edit of my last post. Humans seem to have large numbers of gene control and developmental control differences with greater than two alterations compared to other primates.

    What molecular level alterations were observed in your example? What new protein binding sites, gene control sites, and developmental pathways were derived? What new form and function was generated?
    You are deluded. We didn't evolve from extant apes. We shared an ancestor.

    Modern apes have evolved the same distance from the ancestor as we have.
    Never said humans did. Nice attempt to divert attention away from the fact that you don't and can't address the reality that observed evolutionary processes don't provide a mechanism to account for the majority of cellular protein structures.

    Giving random references isn't going to work any more. I checked one of your references and it was supporting evolution and the concept that complexity could be understood.
    An articles writer can support a general idea even as it demonstrates in a different way the points I am focusing on. The first reference you took issue with was provided to demonstrate that our understanding of molecular components in the cell is substantially different now vs. 25 years ago. Back then random stepwise modification plus selection made sense in light of what we understood. That was the only point of the first reference. I never claimed the writer was arguing against evolution. I personally do not argue against evolution. I take issue with the presumed processes.

    You will have to quote exactly from your references where the papers support your notions. I am not going to fall for your cheap tricks any more.
    You just make yourself look bad when you raise red herring arguments. How about demonstrating that known evolutionary processes do generate novel 6 position binding sites and new stable functional tertiary protein structures that fit to multiple complementary proteins. Show us how it is done.

    Last reference for instance is a clear case of supporting evolution as it is.
    A frikking quote from the abstract for crying out loud:

    Our results indicate that tight interactions can evolve by molecular exploitationrecruitment of an older molecule, previously constrained for a different role, into a new functional complex.
    How does that support your delusions?
    The last article was provided for context with the newer one by the same researchers. It demonstrates that while this particular protein hormone receptor may have a stepwise path from a presumed earlier receptor with genera hormone selectivity to the modern one that is quite specific (the second article provides an incomplete glimpse into this pathway), the first article demonstrates that the reverse pathway seems out of reach to known processes because several neutral modifications are first needed before two key modifications can occur and random mutation appears to be unable to navigate the neutral modifications without making sever more that must also be undone. This article is evidence of the situation I referenced that article to support.

    Another quote from the article that is supposed to support your delusions:

    Our findings demonstrate that the MR-aldosterone partnership evolved in a stepwise fashion consistent with Darwinian theory, but the functions being selected for changed over time
    Do you understand the words "consistent with Darwinian theory"?
    Again the second article was used for context with the first. I am an advocate of full disclosure. Perhaps you should focus on demonstrating that the substance of my particular claim is in error rather than attacking my selection of references and the fact that my posts can't address every point raised by the references.

    The article is actually opposed to your ideas and explains how complexity is no problem:

    The puzzle that complex systems pose for Darwinian evolution depends on the premise that each part has no functionand therefore cannot be selected foruntil the entire system is present. This puzzle might indeed cause Darwin's theory to "break down" if the functions of the parts must remain static for all time. But virtually all molecules can and do participate in more than one process or interaction, so a complex's elements may have been selected in the past for unrelated functions. Our work indicates that tightly integrated systems can be assembled by combining old molecules with different ancestral roles together with new onesgenerated by gene duplication or elaboration of enzymatic pathwaysthat represent slight structural variants on older elements. We propose that molecular exploitation will be a predominant theme in evolution, one that may provide a general explanation for how the molecular interactions critical for life's complexity emerged in Darwinian fashion.
    The article provides a specific example where stepwise processes are thought to be able to accomplish a modest alteration in selectivity for a hormone. Furthermore the alterations were not tested in living organisms so we dont even know if these modified receptors have functional selectivity. It is not an example of making a new binding site. It is not an example of new structure. It is not an example of novel multi-protein molecular components. It is not an example of new form or function.

    It is not an example of a counter to my claims in any fashion. Once again you dont address the question posed so you change the question, to one you can answer, throw out a few red herrings to divert attention, and then attack the person all while not addressing the actual question.

    So I now add this article to the literature opposing your ideas.

    I will await your deconstruction of the article. Unless you are a git and continue trolling.
    reference
    http://www.sciencemag.org/cgi/content/full/312/5770/97
    Sorry, no. As I explained above, this article answers an interesting question, but it answers one that known process can easily handle. So really it simply adds slightly to something we already know. The point is, it doesn't in any way address the challenges I raised. The article was for context and completeness. It complements the more recent article by the same researchers.

    Your tactic is tired. Resort to personal attacks to divert from the fact that you dont address the issue raised. When are you going to address the questions posed? Exactly who is trolling, you or me?
    Maybe your little games impress the braindead. But you are just one vast troll.

    an article that contradicts your viewpoint provides context?

    Are you simply insane or just a religious nutter?
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    This reminds me of people like Kent Hovind using fancy words like "Polonium Halos", while the crowd sits transfixed with self-righteous glee on their faces. It won't fly here. These people can think for themselves.
    Disclaimer: I do not declare myself to be an expert on ANY subject. If I state something as fact that is obviously wrong, please don't hesitate to correct me. I welcome such corrections in an attempt to be as truthful and accurate as possible.

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    Quote Originally Posted by Ophiolite
    1. I am an evolutionist through and through. Cut me and my blood has the same salinity as the ocean off of the Galapagos islands.
    2. Forty years ago I thought there was a great deal of handwaving, assumption making, closing of eyes to inconvenient observations and the like, in accounting for the origin of diversity amongst eukaryotes.
    3. Forty years later and hox genes, evo-devo and the like, notwithstanding, I see the same presumptiveness.
    4. There are likely still mechanisms central to evolution that we have not recognised and certainly not understood. We shall discern them, but not if we deny the need to look for them.
    Well stated.

    Now Cypress, are you now, or have you ever been a member of the Intelligent Design movement?
    Nope.
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    Quote Originally Posted by Golkarian
    While I can see where some examples could support your hypthesis I think these fail, development of all major phyla after the Cambrian are regulated by the same set of genes (the Hox genes), once this system is in place new proteins aren't really necessary,
    I don't think I understand your point. Are you suggesting that Hox genes by managing developmental controls somehow account for observed diversity? Or are you suggesting Hox genes and the developmental processes drive alterations in other genes to produce the observed protein variations including novel binding sites and stable functional shapes?

    just duplication and slight variations of preexisting proteins,
    Many proteins don't have homologous precursors. Furthermore the scarcity of stable folding structures (estimated at about 1 in 10^70 for modest sized proteins) argues directly against the notion that duplication and stepwise variation can account for the proteins with similar sequences but completely different structure and function. You will have to do more than assume the process. Please provide a specific example that demonstrates your assumption is valid.

    if you want to show that natural selection is incapable of making certain systems I'd look before the Cambrian.
    Trouble is there are no precursors to examine. The precambrian organisms have no line forward (except bacteria).

    On your final point, the fossils show us what changed but say nothing about how the changes occurred.
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    Quote Originally Posted by cypress
    Quote Originally Posted by Golkarian
    While I can see where some examples could support your hypthesis I think these fail, development of all major phyla after the Cambrian are regulated by the same set of genes (the Hox genes), once this system is in place new proteins aren't really necessary,
    I don't think I understand your point. Are you suggesting that Hox genes by managing developmental controls somehow account for observed diversity? Or are you suggesting Hox genes and the developmental processes drive alterations in other genes to produce the observed protein variations including novel binding sites and stable functional shapes?
    I am saying they explain the diversity. Most complex system are present in all phyla, their diversity can be accounted by the fact that slight variations, not novel proteins and binding sites, can create a huge amount of anatomical diversity.

    Quote Originally Posted by cypress
    just duplication and slight variations of preexisting proteins,
    Many proteins don't have homologous precursors. Furthermore the scarcity of stable folding structures (estimated at about 1 in 10^70 for modest sized proteins) argues directly against the notion that duplication and stepwise variation can account for the proteins with similar sequences but completely different structure and function. You will have to do more than assume the process. Please provide a specific example that demonstrates your assumption is valid.
    This would be true, I think, for proteins that evolved before the Cambrian, most multicellular organisms have proteins that common to them all. A possibility is that some disappeared or that we have not found the precursors yet, since much work has begun on finding the origins of these proteins, but only for a short while, the difficulty with saying that there are no precursors is that it is based on an argument from ignorance.

    Quote Originally Posted by cypress
    if you want to show that natural selection is incapable of making certain systems I'd look before the Cambrian.
    Trouble is there are no precursors to examine. The precambrian organisms have no line forward (except bacteria).

    On your final point, the fossils show us what changed but say nothing about how the changes occurred.
    Not bacteria but unicellular eukaryotes, these probably have many precursors, including photosynthesis, cell-cell communications (precursors to hox genes probably come from these), and the ability to differentiate between cells that are similar or different from self (an essential precursor to our immune system, unicellular eukaryotes use this so they don't eat their offspring). Also primitive worms probably existed before the cambrian (but they would've had hox genes).

    We cannot see it from fossils but we can look at essential genes for anatomy, look where they appeared in the fossil record. I think it's a safe assumption that these genes wouldn't have changed much if the anatomy hasn't changed much. These genes would not always show the mechanism, but they would show which mechanisms are possible.
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    Quote Originally Posted by sunshinewarrior
    Quote Originally Posted by cypress
    No sorry that is not my argument. It goes like this:

    Protein machines contain tens and even hundreds of components. (1) In order to properly assemble and remain assembled, they must have specific binding sites that will differentiate between correct partners and the thousands of other proteins in the cell. (2) Not only do the shapes have to match but also the chemical properties of the surface of the proteins must be complementary. If they don't stick together they will drift apart.

    1. S. Woodson 2005, Biophysics: assembly line inspection. Nature 438
    2. I. Nooren and J. Thornton, 2003 Diversity of protein-protein interactions. EMBO J. 22

    Turns out protein shape space has been studied and found to be huge. Conservative estimates obtained by limiting mutations to coherent patches of AA close to each other on the surface of the protein. Even here the numbers were about one in 10^8 binding sites would have to be sampled to find one that binds to a randomly selected protein (3). This study matches nicely with others that indicate a minimum of 5-6 consecutive amino acids are generally involved in binding sites. Thus to generate a new protein binding site would require 5-6 coherent mutational steps. I have already accepted that observed processes can account for single and even rarely two steps. But when three or more steps are required as is the case here, the observed processes have not been shown to be capable of accomplishing this.

    Recent work in experimental molecular biology confirms much of this. One series of studies demonstrates, for the proteins studied, about 1 in 10^70 proteins are functional based on their capacity to form binding sites capable of maintaining a stable tertiary shape. Another study indicates that the number of organisms required to generate a new gene control site where just two changes are required is anywhere from 10^12 to 10^18. In primates, that would be well over 100 million years for one new gene control function, by currently understood processes. Another study confirms that when 4 neutral changes are first required before two functional changes are needed in a protein receptor, stepwise evolutionary processes seem unable to accomplish this.

    3. g. Winter and several others, 1998. Small binding proteins selected from a combinatorial repertoire of knottins displayed on a phage. J. Mol. Bio. 277
    One problem I see with your theory is that you are talking of the space of total proteins available. Usable proteins, as developed by organisms, cluster around similar groups of shapes in general, and can be rather easily modified to 'match' receptor sutes - that's why snake venom is so dangerous, for instance.
    Some do and these examples are frequently cited to demonstrate what observed processes can accomplish. However, recent studies are uncovering whole groups that don't. Also protein shapes are not reducible to primary structure where mutations occur so shape clustering is not analogous to AA sequence. Suitable combinations of consecutive amino acids involved in binding and folding generally differ by 3-10 bases at key locations according to studies mentioned earlier. It would be cherry picking to cite a few examples and presume that it is true for all. Far more reliable would be to show how observed processes account for the cases that are offered as a challenge. One challenge comes from D. Axe in his studies of beta-lactamase.

    Even when a particular 300 subunit protein can tolerate 10% total variation for function and 20% variation for structural identity then we still have fewer than 1 in 10^39 of a similar sized protein functionally binding to it. (if you are familiar with estimating probability of overlapping perturbations this might make sense, if you are not, forgive me for not explaining it).

    The argument merely that there are large numbers of possible proteins and very few of them match given receptors is rather meaningless - like the hoary old quotation from Fred Hoyle about a whilrwind in a junkyard creating a 747.
    It is inappropriate to brush these odds off as nonsense. Instead one must demonstrate how mutation and selection overcomes these odds to produce workable systems. If each stepwise change is independently selectable, with sufficient time and gene pool size, sure this can be accomplished, but the examples turning up through experimental work are uncovering both structural and enzymatic proteins that don't fit this model. The task at hand is not to cherry pick working examples, rather it is to demonstrate how these challenges are overcome or can be overcome using observed processes.

    If, for instance, your recent study says that only 1:10^70 proteins studied were functional, surely the question is "Which proteins were they studying?", or were they taking other structural proteins that have nothing to do with the catalytic nature of proteins, and site-binding? Were they, for instance, using entirely the wrong statistical sample?
    One enzyme studied was TEM beta-Lactamase. D. Axe 2004, Estimating the prevalence of protein sequences adopting functional enzyme folds, J Mol Bio. 341. In this study, sequence was varied to identify the tolerance of folding stability in a key area of the protein. The conclusion was that fewer than 1 in 10^64 combinations would obtain a stable fold enabling function of lactamase.

    The idea of irreducible protein machines was floated by Michael Behe a while ago, and demonstrated to be a lot of nonsense by scientists (who had to take time out from serious work just because Behe became, for a while, a poster boy for the Creationist brigade).

    Your interpretations of various studies is one matter. Have you found a single current piece of properly peer-reviewed research (published, that is, in a respectable science journal and not subsequently refuted) in which any scientists claim that the known evolutionary mechanisms are inadequate to explain the variety of life?
    I don't mind that you don't take this challenge seriously enough to address the substance of it and show how observed processes navigate these obstacles.

    However, if the challenge could be demonstrably addressed then you would not need to launch off on red herrings, introduce non-sequiturs or beg the question. I will conclude that you too are unable to address the questions posed.
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    Quote Originally Posted by sunshinewarrior
    The idea of irreducible protein machines was floated by Michael Behe a while ago, and demonstrated to be a lot of nonsense by scientists (who had to take time out from serious work just because Behe became, for a while, a poster boy for the Creationist brigade).
    I think his ideas had merit for a while, Behe states why he thought his ideas had more merit than Paley's:

    "Paley appeals to no principle that would prevent incremental development,"

    But once scientists showed that irreducibly complex systems could evolve Behe's ideas collapsed into person incredulity. Whether you consider that nonsense is up to you. Obviously none of his examples are completely explained.
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    Quote Originally Posted by cypress

    I don't mind that you don't take this challenge seriously enough to address the substance of it and show how observed processes navigate these obstacles.

    However, if the challenge could be demonstrably addressed then you would not need to launch off on red herrings, introduce non-sequiturs or beg the question. I will conclude that you too are unable to address the questions posed.
    A: It's hardly challenging, just strident.

    B: You did not address my serious objection regarding sample space.
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    Quote Originally Posted by Golkarian
    Quote Originally Posted by sunshinewarrior
    The idea of irreducible protein machines was floated by Michael Behe a while ago, and demonstrated to be a lot of nonsense by scientists (who had to take time out from serious work just because Behe became, for a while, a poster boy for the Creationist brigade).
    I think his ideas had merit for a while, Behe states why he thought his ideas had more merit than Paley's:

    "Paley appeals to no principle that would prevent incremental development,"

    But once scientists showed that irreducibly complex systems could evolve Behe's ideas collapsed into person incredulity. Whether you consider that nonsense is up to you. Obviously none of his examples are completely explained.
    Wether or not one views his concept to be nonsense, nobody to date has actually demonstrated that his examples could have evolved entirely by observed processes. Each explanation offered cites presumed but unobserved processes and only offer modest partial solutions. It's a lot of hand-waving from both parties, and even if one doesn't accept Behe's alternative ideas, the challenge to existing processes remains largely unanswered. It's been 10 or so years and still no firm solution using known processes.
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    Quote Originally Posted by Golkarian
    Quote Originally Posted by cypress

    I don't think I understand your point. Are you suggesting that Hox genes by managing developmental controls somehow account for observed diversity? Or are you suggesting Hox genes and the developmental processes drive alterations in other genes to produce the observed protein variations including novel binding sites and stable functional shapes?
    I am saying they explain the diversity. Most complex system are present in all phyla, their diversity can be accounted by the fact that slight variations, not novel proteins and binding sites, can create a huge amount of anatomical diversity.
    Hox genes (as well as many many other genes) have been heavily modified and substituted in fruit flies and to date we have obtained one of three outcome...

    1) Fruit flies
    2) deformed, weak and incapacitated fruit flies
    3) dead fruit flies.

    Perhaps I am missing something but I don't know of anything that might substantiate your speculation. Can you help me understand this better?


    This would be true, I think, for proteins that evolved before the Cambrian, most multicellular organisms have proteins that common to them all. A possibility is that some disappeared or that we have not found the precursors yet, since much work has begun on finding the origins of these proteins, but only for a short while, the difficulty with saying that there are no precursors is that it is based on an argument from ignorance.
    We have been looking very hard for these precursors for over one hundred years but they are nowhere to be found even as we have found abundant soft bodied fossils where these precursors should have been. The most reasonable conclusion based on our 100 year search is that they don't exist.

    We cannot see it from fossils but we can look at essential genes for anatomy, look where they appeared in the fossil record. I think it's a safe assumption that these genes wouldn't have changed much if the anatomy hasn't changed much. These genes would not always show the mechanism, but they would show which mechanisms are possible.
    I have no clue how one would test these assumptions. These kinds of things should be happening today if ever. We simply don't observe this stuff occurring.
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    Quote Originally Posted by sunshinewarrior
    Quote Originally Posted by cypress

    I don't mind that you don't take this challenge seriously enough to address the substance of it and show how observed processes navigate these obstacles.

    However, if the challenge could be demonstrably addressed then you would not need to launch off on red herrings, introduce non-sequiturs or beg the question. I will conclude that you too are unable to address the questions posed.
    A: It's hardly challenging, just strident.

    B: You did not address my serious objection regarding sample space.
    I disagree. I believe I addressed it rather well, unless I misunderstand. In either case it is not much of an objection since it in no way demonstrates how conventional evolutionary problems find pathways from one cluster of functional sequences to another. It is universally understood that these clusters are islands of function isolated by vast seas of non-viability. Your task is to demonstrate either that there are land bridges from island to island or show how biological systems actually do hop from island to island. So far only goal driven genetic engineering has been successful at hopping from place to place. What we need to do is find a natural process that does do the same.
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    Quote Originally Posted by cypress
    Quote Originally Posted by Golkarian
    Quote Originally Posted by sunshinewarrior
    The idea of irreducible protein machines was floated by Michael Behe a while ago, and demonstrated to be a lot of nonsense by scientists (who had to take time out from serious work just because Behe became, for a while, a poster boy for the Creationist brigade).
    I think his ideas had merit for a while, Behe states why he thought his ideas had more merit than Paley's:

    "Paley appeals to no principle that would prevent incremental development,"

    But once scientists showed that irreducibly complex systems could evolve Behe's ideas collapsed into person incredulity. Whether you consider that nonsense is up to you. Obviously none of his examples are completely explained.
    Wether or not one views his concept to be nonsense, nobody to date has actually demonstrated that his examples could have evolved entirely by observed processes. Each explanation offered cites presumed but unobserved processes and only offer modest partial solutions. It's a lot of hand-waving from both parties, and even if one doesn't accept Behe's alternative ideas, the challenge to existing processes remains largely unanswered. It's been 10 or so years and still no firm solution using known processes.
    I think they have demonstrated a way in which they could have evolved, by adding on systems onto other systems, there seems to be no barrier. They just haven't shown every step, and they certainly haven't proven that this is how it happened. Behe fails in that he hasn't shown a way in which those systems are inherently unevolvable.

    http://www.millerandlevine.com/km/ev...1/article.html
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    Quote Originally Posted by cypress
    Quote Originally Posted by Golkarian
    Quote Originally Posted by cypress

    I don't think I understand your point. Are you suggesting that Hox genes by managing developmental controls somehow account for observed diversity? Or are you suggesting Hox genes and the developmental processes drive alterations in other genes to produce the observed protein variations including novel binding sites and stable functional shapes?
    I am saying they explain the diversity. Most complex system are present in all phyla, their diversity can be accounted by the fact that slight variations, not novel proteins and binding sites, can create a huge amount of anatomical diversity.
    Hox genes (as well as many many other genes) have been heavily modified and substituted in fruit flies and to date we have obtained one of three outcome...

    1) Fruit flies
    2) deformed, weak and incapacitated fruit flies
    3) dead fruit flies.

    Perhaps I am missing something but I don't know of anything that might substantiate your speculation. Can you help me understand this better?
    I think the problems with these tests is that they change too much, this is understandable since they are trying to find out what hox genes affect what, bigger the change the easier it is to see this. Evolution works better with gradual change.

    Quote Originally Posted by cypress

    This would be true, I think, for proteins that evolved before the Cambrian, most multicellular organisms have proteins that common to them all. A possibility is that some disappeared or that we have not found the precursors yet, since much work has begun on finding the origins of these proteins, but only for a short while, the difficulty with saying that there are no precursors is that it is based on an argument from ignorance.
    We have been looking very hard for these precursors for over one hundred years but they are nowhere to be found even as we have found abundant soft bodied fossils where these precursors should have been. The most reasonable conclusion based on our 100 year search is that they don't exist.
    For the last 100 years? As you yourself have stated molecular and cellular biology, where we would find these precursors, is in its infancy. Also some systems have been found which are descent precursors like self/non-self differentiation in unicellular organisms (immune system) and cell-cell communication among bacteria that form slime moulds (development).

    Quote Originally Posted by cypress
    We cannot see it from fossils but we can look at essential genes for anatomy, look where they appeared in the fossil record. I think it's a safe assumption that these genes wouldn't have changed much if the anatomy hasn't changed much. These genes would not always show the mechanism, but they would show which mechanisms are possible.
    I have no clue how one would test these assumptions. These kinds of things should be happening today if ever. We simply don't observe this stuff occurring.
    By testing that changes in certain genes affect anatomy, I think its an assumption that has pretty much been verified. Of course it only applies to certain sets of genes.
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    We simply don't observe this stuff occurring.
    Yes we do. It has been documented in the literature several times.
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    the classic creationist ploy : first demand proof beyond what is reasonable, and when that proof turns up, deny that it is the sort of proof that you find convincing
    "Reality is that which, when you stop believing in it, doesn't go away." (Philip K. Dick)
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    Quote Originally Posted by marnixR
    the classic creationist ploy : first demand proof beyond what is reasonable, and when that proof turns up, deny that it is the sort of proof that you find convincing
    Except I'm not a creationist. Is it unreasonable for a for a scientific explanation to include experimental results, repeatable tests, and citation to a process that is in operation today? And where is this proof you speak of?

    Edit: Can we agree that conclusions that include assumptions as a primary component are not proof?
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    Quote Originally Posted by spuriousmonkey
    We simply don't observe this stuff occurring.
    Yes we do. It has been documented in the literature several times.
    You must be changing the context again.

    So you say you have documented observations of modified genes that express different funtion and different binding sites derived by a multistep process whereby the nature of the changes clearly demonstrate without ambiguity what process obtained the change?

    No, sorry you don't. You don't because despite the efforts of many experimental biologists, the tested processes have not derived these kinds of changes. In the longest continuous experiment with bacteria cultures, 30,000 plus generations under continuous selection pressure, nothing out of the ordinary has been obtained.

    30,000 human generations is nearly a million years.
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    Quote Originally Posted by Golkarian
    Quote Originally Posted by cypress

    Wether or not one views his concept to be nonsense, nobody to date has actually demonstrated that his examples could have evolved entirely by observed processes. Each explanation offered cites presumed but unobserved processes and only offer modest partial solutions. It's a lot of hand-waving from both parties, and even if one doesn't accept Behe's alternative ideas, the challenge to existing processes remains largely unanswered. It's been 10 or so years and still no firm solution using known processes.
    I think they have demonstrated a way in which they could have evolved, by adding on systems onto other systems, there seems to be no barrier. They just haven't shown every step, and they certainly haven't proven that this is how it happened. Behe fails in that he hasn't shown a way in which those systems are inherently unevolvable.

    I agree Behe has not yet shown that they are not inherently evolvable. At the same time Miller and others have not demonstrated any way that they could have evolved. They fall short because they must assume processes that are not currently known or observed in operation today. They may as well claim the flying spaghetti monster directed the processes they presume exist. From where I sit, it looks more like a stalemate.
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    Quote Originally Posted by cypress
    Quote Originally Posted by Golkarian
    Quote Originally Posted by cypress

    Wether or not one views his concept to be nonsense, nobody to date has actually demonstrated that his examples could have evolved entirely by observed processes. Each explanation offered cites presumed but unobserved processes and only offer modest partial solutions. It's a lot of hand-waving from both parties, and even if one doesn't accept Behe's alternative ideas, the challenge to existing processes remains largely unanswered. It's been 10 or so years and still no firm solution using known processes.
    I think they have demonstrated a way in which they could have evolved, by adding on systems onto other systems, there seems to be no barrier. They just haven't shown every step, and they certainly haven't proven that this is how it happened. Behe fails in that he hasn't shown a way in which those systems are inherently unevolvable.

    I agree Behe has not yet shown that they are not inherently evolvable. At the same time Miller and others have not demonstrated any way that they could have evolved. They fall short because they must assume processes that are not currently known or observed in operation today. They may as well claim the flying spaghetti monster directed the processes they presume exist. From where I sit, it looks more like a stalemate.
    I disagree, they Miller et al. have shown that there is no barrier to natural selection, and natural selection has been observed creating complexity, the flying spaghetti monster has not. I suppose it is difficult though since the increase in complexity seen is different, e.g. it builds on top of old systems, while the suggested mechanism links formed parts together.
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    Quote Originally Posted by cypress
    Quote Originally Posted by spuriousmonkey
    We simply don't observe this stuff occurring.
    Yes we do. It has been documented in the literature several times.
    You must be changing the context again.

    So you say you have documented observations of modified genes that express different funtion and different binding sites derived by a multistep process whereby the nature of the changes clearly demonstrate without ambiguity what process obtained the change?

    No, sorry you don't. You don't because despite the efforts of many experimental biologists, the tested processes have not derived these kinds of changes. In the longest continuous experiment with bacteria cultures, 30,000 plus generations under continuous selection pressure, nothing out of the ordinary has been obtained.

    30,000 human generations is nearly a million years.
    While I think its reasonable (though I don't think true) to question whether components can come together using binding sites, it should be noted that change, though not the kind you are requesting, has occurred in bacteria under experimental conditions:

    http://aem.asm.org/cgi/reprint/61/5/2020.pdf
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    Also:

    http://www.sciencemag.org/cgi/content/full/319/5860/206

    By this, it seems more likely to me that weak interactions could occur randomly at first, then natural selection could have increased the specificity and strength of the binding.

    "It is also comparatively simple to produce weak contacts randomly, as demonstrated by many examples using surface mutations to induce proteins to crystallize."
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    This might be useful as well (but not peer-reviewed):

    http://pandasthumb.org/archives/2008...ersus-rib.html
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    Quote Originally Posted by cypress
    Edit: Can we agree that conclusions that include assumptions as a primary component are not proof?
    indeed, science does not deal in mathematical proof, but rather along the lines of the judicial concept of "proven beyond reasonable doubt"

    anyone who demands absolute proof outside maths has a hidden agenda (creationist or not - and remember, ID is nothing but creationism that doesn't dare speak its name) because you probably know (or should know) that no such absolute proof can be had

    as for conclusions, can you show me any type of conclusion that doesn't start with initial premises or assumptions ? even mathematical proof starts off with axioms (which in my book are but a fancy word for basic assumptions)
    science usually follows the thread of logic of where the initial assumptions lead and then re-evaluates those assumptions based on whether the outcome of the logic fits the evidence or not - if they do, then the assumptions are validated, if not, then they have been falsified
    "Reality is that which, when you stop believing in it, doesn't go away." (Philip K. Dick)
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    Quote Originally Posted by cypress
    Quote Originally Posted by marnixR
    the classic creationist ploy : first demand proof beyond what is reasonable, and when that proof turns up, deny that it is the sort of proof that you find convincing
    Except I'm not a creationist. Is it unreasonable for a for a scientific explanation to include experimental results, repeatable tests, and citation to a process that is in operation today? And where is this proof you speak of?

    Edit: Can we agree that conclusions that include assumptions as a primary component are not proof?
    Since when is repeatability a character of evolution?

    Obviously you haven't learned anything.
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    Quote Originally Posted by marnixR
    Quote Originally Posted by cypress
    Edit: Can we agree that conclusions that include assumptions as a primary component are not proof?
    indeed, science does not deal in mathematical proof, but rather along the lines of the judicial concept of "proven beyond reasonable doubt"

    anyone who demands absolute proof outside maths has a hidden agenda (creationist or not - and remember, ID is nothing but creationism that doesn't dare speak its name) because you probably know (or should know) that no such absolute proof can be had.
    maximR, it was you who claimed that proof supporting your assumed position was offered. I, on the other hand, have from the beginning asked only for evidence that known and observed processes, in operation today, actually do account for changes in protein shape, function, and binding sites involving structures with several proteins participating.

    You claimed proof was offered and I had denied that proof. I responded by asking for "the proof" you claim was offered.

    Furthermore, you employ prejudice tactics by introducing non-sequiturs and labeling me without knowledge of my beliefs and without relevance to the discussion point.

    as for conclusions, can you show me any type of conclusion that doesn't start with initial premises or assumptions ? even mathematical proof starts off with axioms (which in my book are but a fancy word for basic assumptions)
    science usually follows the thread of logic of where the initial assumptions lead and then re-evaluates those assumptions based on whether the outcome of the logic fits the evidence or not - if they do, then the assumptions are validated, if not, then they have been falsified
    Once again you are off topic. My reference was to assumptions that are used in place of evidence directly to support a conclusion and not as a starting point as you suggest. In this case, the points offered in this thread and in the community of evolutionary biology as a whole, assumptions about the capability and efficacy of random mutation and natural selection to explain observed diversity are indeed used to support the firm belief and conclusions by many that these processes did as a point of fact cause the changes we are discussing.

    So are you or are you not able to provide evidence that observed processes in operation today are able to and do accomplish the kinds of changes I am asking about? Specifically these changes are in protein, protein binding sites involving many interacting proteins, or involving key folds that determine shape and therefore tertiary structure of interacting proteins.

    Earlier you claimed that evidence (you incorrectly used the word proof) has been provided, and like a creationist (stereotyping me), I denied the evidence (you said proof). I replied that only assumptions have been offered in place of evidence. Even the latest responses including the articles linked use heavy doses of assumption to make the points they attempt to make. They make appeals to similarity to support the claim that certain processes accomplish change when in truth any number of processes could have accomplished the change. Furthermore, the process they claim accomplished the change has never been shown and never been observed to be able to make several of the assumed alterations that would have been involved.

    Now have a look at any of the articles offered in this thread and any of the points offered by the other posters and show me the evidence that a specific process was in operation (your word was proof) that I have dismissed.

    Summary:

    My point of all of this is that current evolutionary theory has serious flaws that will likely not go away by dismissal. Instead they need to be addressed by research that should be focused on other more capable processes. Genetic engineering is now easily accomplishing these kinds of changes through goal directed processes and if the evolutionary community does not offer up a viable natural process, it may soon become hard to deny the implications. Like it or not, design advocates are increasingly demonstrating the capability of design to make changes that observed natural processes seem incapable of making. At some point we have got to stop relying on systems that don't generate the observed events or face loss of credibility.

    I seriously doubt it will be effective to claim that all the key protein shapes were derived prior to the cambrian period as has been advocated here and in a couple articles cited. It is a just so story that cannot be validated and does not match with evidence indicating novel proteins were derived during and after the cambrian. What is needed are studies into reactive or self-ordering or some other processes perhaps derived from non-coding DNA regions.

    The first step is recognition that an issue exists but this pattern of denial seems so pervasive I wonder how much longer it will be before it is addressed. Science was once an institution well trusted by the general community, but by about a two to one margin the US public rejects evolution and the majority now rejects man-made global warming. If the science community does not make its case by demonstrating the efficacy of known processes, reputation will continue to slide.
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    Quote Originally Posted by spuriousmonkey
    Quote Originally Posted by cypress
    Quote Originally Posted by marnixR
    the classic creationist ploy : first demand proof beyond what is reasonable, and when that proof turns up, deny that it is the sort of proof that you find convincing
    Except I'm not a creationist. Is it unreasonable for a for a scientific explanation to include experimental results, repeatable tests, and citation to a process that is in operation today? And where is this proof you speak of?

    Edit: Can we agree that conclusions that include assumptions as a primary component are not proof?
    Since when is repeatability a character of evolution?

    Obviously you haven't learned anything.
    In some ways evolution is repeatable, but you can't get the exact same result every time, but you should be able to get results that are scene over and over in nature, such as protein-protein binding, given enough time.
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    Quote Originally Posted by cypress
    Genetic engineering is now easily accomplishing these kinds of changes through goal directed processes and if the evolutionary community does not offer up a viable natural process, it may soon become hard to deny the implications.
    Problem is, this is human design, from what we know humans weren't around for most of evolutionary history. The process by which God, spirit, or whatever other intelligent designer you propose has never been observed. But natural selection has been shown to be able to produce complexity and to have existed since life began. And you assume that protein-protein binding can only occur by neutral changes, as I look around at the literature I am beginning to doubt that claim, since weak interactions don't require much change in proteins.
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    Quote Originally Posted by cypress
    My point of all of this is that current evolutionary theory has serious flaws that will likely not go away by dismissal.
    name them

    + remember that to claim a theory does not explain everything is merely stating the obvious, and not a serious flaw - just an indication that science's work is never finished
    "Reality is that which, when you stop believing in it, doesn't go away." (Philip K. Dick)
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    Quote Originally Posted by marnixR
    Quote Originally Posted by cypress
    My point of all of this is that current evolutionary theory has serious flaws that will likely not go away by dismissal.
    name them

    + remember that to claim a theory does not explain everything is merely stating the obvious, and not a serious flaw - just an indication that science's work is never finished
    I named them in the post you pulled my quote from. If you don't see them as a problem, then possibly you are as much in denial as those I was speaking of. In that case this discussion won't do much for you and I wouldn't expect you to address the flaws.

    However, when a theory claims to account for observed diversity by change over time through citation of particular named and observed processes, as does modern evolutionary theory, then it must be able to demonstrate what process and how that process actually does account for an observed change. I support the concept of evolution, but I notice quite easily that the cited processes don't account for most of the observed molecular systems within cells. I find that disturbing.

    In the two articles I cited from Thompson's studies in Oregon when evaluated critically can be seen to put significant restrictions on traditional evolutionary processes and the ability of those processes to generate novel protein function.

    The researchers, working with the classical evolutionary framework, specifically designed and constructed a potential precursor to GR and MR steroid hormone receptors. This possible precursor was designed with forethought able to be modified in a stepwise fashion into a receptor with similar sequence, structure and binding strength as the modern GR receptor. They surmised that by gene duplication and sequence modification the modern MR steroid could have been derived. All this seems reasonable and consistent with what known evolutionary processes can accomplish. After all changing a steroid receptor with low selectivity for a particular hormone to one that is more selective should not be too difficult.

    The rather surprising results of the second study shows that known evolutionary processes in this case are not able to accomplish the reverse. The reason is because selection for current function favoring GR hormone selectivity drove several minor changes that first needed to be undone before the protein could undergo two critical changes to obtain the designed protein weak and broad selectivity for several hormones (the problem of having to make several neutral changes prior to making key changes is one issue I have raised against chance mutation and selection). Again the researchers framed the study in a traditional way, and used this as an argument to confirm a version of Dollo's law (that evolution does not regenerate lost traits). But let's examine the implications more carefully.

    They presume that Dollo's law indicates that evolution is asymmetric over time. However there is no reason to assume this. The reason they were successful at evolving the presumed ancestral hormone receptor forward is because they specifically designed it to have that capability. But would this occur under selection pressure? No it likely would not. Instead, an actual precursor (as opposed to the presumed one made with forethought and a goal) would also have undergone slight modifications to make it more selectable for current function just as the modern GR version has. These slight modifications are as likely to make the actual ancestor to GR as unevolvable by classical processes in the forward direction as GR was found to be in the reverse direction because no protein in the past would ever be free of selection pressure.

    In short the researchers reconstructed an ancestor from the modern version in such a way as to overcome the barriers that they realized would block known evolutionary processes. They directed events that chance and selection couldn't and in doing so actually and unwittingly built a stronger case against traditional evolutionary theory. These barriers are the barriers I refer to in this thread. These are the kinds of discoveries now occurring that drives the need to find a new process.
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    Quote Originally Posted by cypress
    The reason is because selection for current function favoring GR hormone selectivity drove several minor changes that first needed to be undone before the protein could undergo two critical changes to obtain the designed protein
    This is the problem I think, evolution shouldn't create the exact same changes every time (by its definition), they should have let it take its course and used several replications to see if any created something similar, like protein-protein binding, but not exactly like what they were looking for. Under selective pressure of course.

    Evolution isn't all randomness, but it's alot more random then you are making it out to be.
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    Quote Originally Posted by Golkarian
    Quote Originally Posted by spuriousmonkey
    Quote Originally Posted by cypress
    Quote Originally Posted by marnixR
    the classic creationist ploy : first demand proof beyond what is reasonable, and when that proof turns up, deny that it is the sort of proof that you find convincing
    Except I'm not a creationist. Is it unreasonable for a for a scientific explanation to include experimental results, repeatable tests, and citation to a process that is in operation today? And where is this proof you speak of?

    Edit: Can we agree that conclusions that include assumptions as a primary component are not proof?
    Since when is repeatability a character of evolution?

    Obviously you haven't learned anything.
    In some ways evolution is repeatable, but you can't get the exact same result every time, but you should be able to get results that are scene over and over in nature, such as protein-protein binding, given enough time.
    well, proteins bind to proteins all the time.

    Just fry an egg.

    What's special about that?
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    Quote Originally Posted by spuriousmonkey
    Quote Originally Posted by Golkarian
    Quote Originally Posted by spuriousmonkey
    Quote Originally Posted by cypress
    Quote Originally Posted by marnixR
    the classic creationist ploy : first demand proof beyond what is reasonable, and when that proof turns up, deny that it is the sort of proof that you find convincing
    Except I'm not a creationist. Is it unreasonable for a for a scientific explanation to include experimental results, repeatable tests, and citation to a process that is in operation today? And where is this proof you speak of?

    Edit: Can we agree that conclusions that include assumptions as a primary component are not proof?
    Since when is repeatability a character of evolution?

    Obviously you haven't learned anything.
    In some ways evolution is repeatable, but you can't get the exact same result every time, but you should be able to get results that are scene over and over in nature, such as protein-protein binding, given enough time.
    well, proteins bind to proteins all the time.

    Just fry an egg.

    What's special about that?
    Nothing, it also doesn't infer a reproductive advantage to the egg.
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  90. #89  
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    It's a fools quest to look for repeatibility in evolution since evolutions really choses its own path dependent on many factors, some of which are history, environmental pressures, chance, and available variation.

    Let's just make small logical steps here. No gaps.

    Proteins bind with each other. It's not really a secret. However, most protein interactions aren't very strong.

    We start calling proteins binding proteins or enzymes, when we can actually measure this kind of interaction in a significant manner.

    This kind of protein interaction is is heavily dependent on the 3D structure of the protein, often resulting in valleys and hills of a specific shape.

    A valley with a specific shape will fit a certain protruding structure best (be it protein, lipid, DNA, or RNA).

    The 3D structure of a protein is directly dependent on the genetic sequence of the gene that corresponds to the protein.

    The genetic sequence varies in a population.

    Variation is introduced all the time.

    Proteins encoded by different alleles will have different levels of functionality.

    Natural selection will select for certain functionality and therefore certain variation depending on many factors (for instance environmental and internal).

    Hence protein form is under the influence of evolution.



    Hence there isn't really a problem here is there?

    Will similar solutions evolve over time? yes, you see for instance that a functional protein only allows for variation in certain domains, or even single amino acids within a conserved region. (so many times published it is nonsense to ask for proof. Just get your lazy ass of the couch and read a text book).

    Can a protein gain a new function?
    Yes of course. Either the gene is duplicated and the new copy (or the old copy) acquires a new function, or a gene just evolves new functionality.

    Has this been shown. Well, yes. Duh. Why didn't you hear about it? Well, let me ask you, when is the last time you spend an hour a day browsing the primary literature each day?

    Never?

    Well, how do you expect to keep up to date with what is really going on? Especially since the boring mundane molecular stuff will never make it to popular science sites.

    I was in a meeting not so recently, where they showed nicely the evolution of microRNA 100 into new microRNAs (10 and 993). And interestingly there was also a switch in strands in drosophila giving the micro RNA a totally new function (since it recognizes a totally different target sit). You have no clue what I am talking about? Shrugs. That's science.

    Type in the proper key words in Pubmed and the publications become available.

    Recent publication.
    Science. 2009 Sep 25;325(5948):1688-92
    Evolution of a novel phenolic pathway for pollen development.

    Metabolic plasticity, which largely relies on the creation of new genes, is an essential feature of plant adaptation and speciation and has led to the evolution of large gene families. A typical example is provided by the diversification of the cytochrome P450 enzymes in plants. We describe here a retroposition, neofunctionalization, and duplication sequence that, via selective and local amino acid replacement, led to the evolution of a novel phenolic pathway in Brassicaceae. This pathway involves a cascade of six successive hydroxylations by two partially redundant cytochromes P450, leading to the formation of N1,N5-di(hydroxyferuloyl)-N10-sinapoylspermidine, a major pollen constituent and so-far-overlooked player in phenylpropanoid metabolism. This example shows how positive Darwinian selection can favor structured clusters of nonsynonymous substitutions that are needed for the transition of enzymes to new functions.

    Wow...what are we really moaning about here? Discussing something that has been published a few thousand times?

    Because someone doesn't believe in it?
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    From the same search:

    Emergence of a new gene from an intergenic region.

    Curr Biol. 2009 Sep 29;19(18):1527-31

    It is generally assumed that new genes would arise by gene duplication mechanisms, because the signals for regulation and transcript processing would be unlikely to evolve in parallel with a new gene function. We have identified here a transcript in the house mouse (Mus musculus) that has arisen within the past 2.5-3.5 million years in a large intergenic region. The region is present in many mammals, including humans, allowing us to exclude the involvement of gene duplication, transposable elements, or other genome rearrangements, which are typically found for other cases of newly evolved genes. The gene has three exons, shows alternative splicing, and is specifically expressed in postmeiotic cells of the testis. The transcript is restricted to species within the genus Mus and its emergence correlates with indel mutations in the 5' regulatory region of the transcript. A recent selective sweep is associated with the transcript region in M. m. musculus populations. A knockout in the laboratory strain BL6 results in reduced sperm motility and reduced testis weight. Our results show that cryptic signals for transcript regulation and processing exist in intergenic regions and can become the basis for the evolution of a new functional gene.

    A new gene from nothing. That means a new protein from nothing. And the protein has a function.

    And people say it cannot happen?
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    Disclaimer: I do not declare myself to be an expert on ANY subject. If I state something as fact that is obviously wrong, please don't hesitate to correct me. I welcome such corrections in an attempt to be as truthful and accurate as possible.

    "Gullibility kills" - Carl Sagan
    "All people know the same truth. Our lives consist of how we chose to distort it." - Harry Block
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    Quote Originally Posted by spuriousmonkey
    From the same search:

    Emergence of a new gene from an intergenic region.

    Curr Biol. 2009 Sep 29;19(18):1527-31

    It is generally assumed that new genes would arise by gene duplication mechanisms, because the signals for regulation and transcript processing would be unlikely to evolve in parallel with a new gene function. We have identified here a transcript in the house mouse (Mus musculus) that has arisen within the past 2.5-3.5 million years in a large intergenic region. The region is present in many mammals, including humans, allowing us to exclude the involvement of gene duplication, transposable elements, or other genome rearrangements, which are typically found for other cases of newly evolved genes. The gene has three exons, shows alternative splicing, and is specifically expressed in postmeiotic cells of the testis. The transcript is restricted to species within the genus Mus and its emergence correlates with indel mutations in the 5' regulatory region of the transcript. A recent selective sweep is associated with the transcript region in M. m. musculus populations. A knockout in the laboratory strain BL6 results in reduced sperm motility and reduced testis weight. Our results show that cryptic signals for transcript regulation and processing exist in intergenic regions and can become the basis for the evolution of a new functional gene.

    A new gene from nothing. That means a new protein from nothing. And the protein has a function.

    And people say it cannot happen?

    Sorry, no. Have a closer look. This example once again makes use of similarity and homology but like all other examples provided it tells us nothing of the actual process that caused the changes. I do not question that change occurs. I am asking how that change occurs and I am asking for examples where the presumed processes are instead verified.

    Once again you can't answer the question asked and so you change the question and hope I don't notice the slight of hand.

    edit: The past few papers are interesting in themselves and answer interesting questions. They just don't directly address the issues I am asking about. There is no shortage of papers pointing to phylogenic studies, homologies and general similarities of genes among similar species. They all tell us something about the relationships and provide evidence about the changes that have occurred and what mechanisms might have or are presumed to have cased the changes. But it takes experimental work to confirm the presumed processes and it is in the experimental area that the issues arise. The attempts to confirm that known processes can and do generate the kinds of changes inferred from phylogenetics have not yielded the results that the theory would have predicted. It does no good to point back to these other studies. What is needed are experimental results that demonstrate the processes actually involved.
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    Once again you can't answer the question asked and so you change the question and hope I don't notice the slight of hand.
    It is because your question is retarded.

    In science we give up on retarded questions once we notice they are retarded. Then we formulate a new question which often turns out to be retarded as well, but the main difference being in retardness is that the new question doesn't seem quite so retarded as the original one at the moment of discovery that the first question is retarded.

    That's called critical thought: being able to ascertain when to drop a question and replace it with one that can lead to new and fertile grounds of insight.

    And it is also false to assume that other people actually care about these kind questions which value is zero once certain facts, insights, theories, arguments have been assimilated into your train of thought.


    Why don't you try to formulate a new question that is based on the knowledge that you should have gained so far in this thread?

    I can help you with it of course, but it is best to try yourself first.
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    I think most readers will see you for what you are.

    The most logical reason that experimentation into the efficacy and capability of evolutionary processes are not yielding the results that are predicted by the theory is that chance and selection are incapable of accomplishing the predicted events.

    I have talked about tertiary shapes and binding sites as two of the difficulties in generating novel protein function in systems of coordinated proteins with many interacting components. In addition though, simple reasoning yields other requirements as well. The components must be inventoried and made available at the right time and transported to the right location in ways that prevent deleterious side reactions. Then they must be properly assembled and then quality controlled. All of this requires substantial coordination and a sophisticated control system to manage the process. These supplementary systems require modification along with the primary components in order to generate new functional systems. I suspect it is for all these reasons that we only see proteins that are currently performing the closest relevant function undergo one and two step alterations that then generate the slight adaptations we do observe from chance and selection. We don't see the tens of thousands of others proteins being co-opted for use to drive evolutionary change.

    It is great to point to homologous genes and speculate about changes over time, but if experimental biology is unable to confirm the speculations by testing and validating the processes, then the theory becomes weak and diluted. It makes no sense to prop up ideas that don't deliver. Instead we need to search for processes that do generate the predicted results.
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    Quote Originally Posted by cypress
    I think most readers will see you for what you are.
    I hope so!
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    Quote Originally Posted by spuriousmonkey
    Quote Originally Posted by cypress
    I think most readers will see you for what you are.
    I hope so!
    from your avatar i'd say you're a BEM
    "Reality is that which, when you stop believing in it, doesn't go away." (Philip K. Dick)
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    Boundary Element Method?
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    bloody ennoying midget
    "Reality is that which, when you stop believing in it, doesn't go away." (Philip K. Dick)
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    midget is a relative concept.
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    and relativity is a midget concept
    "Reality is that which, when you stop believing in it, doesn't go away." (Philip K. Dick)
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