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Thread: "Natural selection" is it for real ?

  1. #1 "Natural selection" is it for real ? 
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    Can somebody explain me how is it possible to have on one hand "Natural selection", on the othrer hand knowing that every possible gene has it's "unique number" ?


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    I am not dextrous enough to determine quite what you mean by every possible gene has its unique number. Could you elaborate on that.

    I certainly see nothing sinister in the notion that Natural Selection is acting on phenotypes arising from specific gene combinations.


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    Getting the 3codons before ATG and the 3codons after the TGA, together makes uniquie indentifyer for every gene.
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    Are you referring to the start and stop sequences and the "TaaTaa" sequence?
    *Welcome, my friends, to the show that never ends*
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    no
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    I am not a geneticist, therefore please clarify each specific point below.

    Is this 'unique identifier' for each gene:

    1. Widely recognised as present by most or all researchers in this field?
    a) If so, could you cite some references that describe it?
    b) If not, could you explain and justify your claim for it in detail?

    2. Present in all phyla? Present in Prokaryotes and Eukaryotes?
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    Present in Viral, Bacteria, Archeaa, Eucariota.

    If you have good broadband you could see for yourself, just download those perl scripts ...
    http://www.cyber-indian.com/gene_index/conv_1.pl - For downloading GenBank Genome files form NCBI
    http://www.cyber-indian.com/gene_index/rep_2.pl - For generating sorted list of 'unique identifiers'
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  9. #8  
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    Hi cyber_indian,

    you ask,

    Can somebody explain me how is it possible to have on one hand "Natural selection", on the othrer hand knowing that every possible gene has it's "unique number" ?
    'Uniqeness' itself, is logically defined. No two things can be identical in every respect. I do not think you have to dissolve into a genetic haystack to ponder this question. The principles are clear. What is not clear to me is why you appear to see 'natural selection' and 'genetic unique numbers' as mutually exclusive.
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    Cyber Indian, I want to echo TBs point. You have posted a couple of threads here (and on other forums if I am not mistaken) where you touch on a hypothesis you have regarding the characteristics of of genes and the structure of DNA.

    Please explain to us, in some detail, what this hypothesis is. At present you seem to be giving hints as to its nature, while taking occasional swipes at current geneticists and asking vague questions as in this present thread.

    I for one find this approach frustrating. It is certainly unscientific. If you are pursuing it deliberately it might also be characterised as rude. Please share your thoughts with us. We may not agree with them, we may grasp them to our bosom, but until we can see them in the light of day it would be precipitate to do either.
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    The problem is that if I reveal the whole idea people get scared and automaticaly reject it - they simply don't what to believe that other way may be possible, that's why I want to discuss only this part "gene_indexes" and after that reveal the rest.
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    In spite of, Gene therapy can't yet deliver fullproof method of delivering working gene without damaging others by placing itself in the middle of existing ones. I believe a little modification of "sticky ends" method and marking the needed gene at the both ends would be the solution of the problem.

    What if I tell you that this might have been done before in much bigger scale.
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    Cyber_Indian, this is a Science forum. It is true that it is not Nature or Bull.Geol.Soc.Am., so posts are not subject to conventional peer review or significant editorial control.

    However, it would seem appropriate to follow the conventions by which scientific ideas are communicated within a research paper i.e. The conclusions are presented at the start, in the form of an abstract. In contrast you are proceeding in a manner that is a cross between a detective novel and a crossword. If I may use a street expression - it's time for you to shit, or get off the pot.
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    What I've done is download as much as possible genomes (about 3GB), having an idea with a perl script I extracted the both ends of every gene (that's what I called "gene_index") and sorted them up to see if there is more than one gene with the same gene_index. What I foud is that two or more genes with the same gene_index woud be matching 96.35%(using ClustalW).

    I gave you the scripts - you can for yourself. Basicaly they are BioPerl script downloading genbanks and sequence all of the CDS in the mather I explained earlier.
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    Quote Originally Posted by cyber_indian
    What I found is that two or more genes with the same gene_index woud be matching 96.35%.
    Thank you fro replying, however this sentence does not make any sense to me, or rather I can generate three or four mutually exclusive interpretations of it. Can you clarify please.
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    The genes that have the same gene_index would have 3.65% difference average.
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    I'm not concern with the gene itself, what I'm working on is the space between the genes.

    I made a list of the genes with same gene_index and did ClustalW aligment with genes with same gene_index. After that I made average calculation which turn out to be 96.35%.

    That sound like choice number 2.
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    I understand that, what I don't understand is the meaning of your phrase What I found is that two or more genes with the same gene_index woud be matching 96.35%
    Does this mean:
    1) In 96.35% of cases the genes with the same gene index are the same gene.
    2) In all cases where genes have the same gene index the genes themselves are identical throughout 96.35% of their structure.
    3) Something else.
    Please clarify.
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    So if there is unique numbering it means that it all cames form one place.
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    Hi CI,

    Your style of posting seems unduly enigmatic. If you are looking to use other people here as sounding boards, you will certainly have to give more detail and background. There might be risks regarding protection of any ideas, but there are different ways of asking questions and keeping control of intellectual property at the same time. At the moment the tightness of your cloak threatens to suffocate the idea.
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  21. #20  
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    Quote Originally Posted by cyber_indian
    So if there is unique numbering it means that it all cames form one place.
    This is getting really frustrating. What do you mean? What is the it you refer to? What is the one place it must have come from?
    If that statement was intended as a reply to my previous post I have to tell you it fails utterly to communicate anything of meaning to me. Please make a further attempt to be clear and comprehensive.
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    At first the idea was that it's possible to transfer a whole ecosystem on bacterial level through space regardless of distance and time to other habitable planets. All you do is make library of all common genes label them and make a mechanisam to reconstruct themselfs. Now when I see this gene_indexing I'm starting to think that maybe we have done this to ourselfs already - transfer ourself to another place in order to save our existance.

    For me "Natural selection" is not self explaining enough.
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  23. #22  
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    Point 1:
    (a) I totally agree with you that is plausible that bacteria could be transferred through space from some other point to the Earth, where they could provide the basis for a new ecosystem.
    (b) Saying it is plausible is different from saying it is possible, though there is evidence that tends to support the concept.
    (c) Transferring the basis of an ecosystem is quite different from transferring an ecosystem. You have not yet convinced me that that is plausible.

    Point 2:

    If one has the technology to perform the genetic engineering necessary for the type of project you are proposing then why would you trust to random drift of bacteria through space? Why not target planetary systems that represent good potential 'breeding grounds'? One hundred thousand litte Voyager's all carrying their pre-programmed selection of microbes just waiting for their new freedom.
    This point is not of itself proof that it could not occur as you suggest, but it does need to be accounted for in a logical way.

    Point 3:
    You have not yet clearly explained the labelling you claim to have discovered. You say for example the genes which have the same gene index have a 3.65% difference average. Difference between what and what? What are you averaging? You are still wholly unclear in this critical area of your concept. Again I ask you to be more precise. You clearly know what you are talking about, but we, the readers do not. You need to be very precise, using specific nouns not pronouns, so we know what you are talking about at each point.

    Point 4:

    How would this mechanism, which reconstructs the ecosphere over billenia (is that a word? well, it is now) actually work? Have you any proposals for that?
    Surely, there would have to be genes for later, more advanced forms of life, lying latent in the genetic structure of early, more primitive life. In that case would we not be able to locate such material within the early genomes?

    Point 5:I share with you reservations about the power of Natural Selection (along with genetic drift, etc) to account for everything we observe in evolution, but I there are two possibilities I would consider before I went to your own hypothesis:
    a) Other, unidentified mechanisms are at work in modifying the genetic structure of organisms.
    b) I am mistaken in having reservations.
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    First read this http://www.cyber-indian.com/theory/index.html and I'll answer you more later. I wanted to discuss only the gene_index for now, but since you asked.
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    I never mention "random drift of bacteria through space", my current idea is to use commet to seed planets.
    And second I don't expect we're going to find a live planet, more like favourable factors. And there sould be a process witch will teraform enviroment before the reassemble process begin - reassemble bacteria to run the main cycles(nitrogen, carbon dioxide, sulfur and photosynthesis) and many others.
    And third unlike the conventional thinking (Bacterium is the first source), the base and carrier is the Archaea not Bacterium domain.

    About "Point 3" 3.65% is the percentage two tings:
    -Genes with long chunks of insert and delete mutations.
    -Genes who has mutations over the gene_index itself - who actualy belong to different gene_index.

    The difference is actualy aligment between every gene with the rest of the genes of the same group - genes with the same gene_index.

    This is the group (gene_index|gene_size|crc|polarity|domain|gene_id| genome_id|gene_description|):

    AAAAGAATAxGTAAAAGAG|1881bp|7453947EF512785B|+|B|S0 114|NC_004741_1|pyruvate dehydrogenase(dihydrolipoyltransacetylase component)|
    AAAAGAATAxGTAAAAGAG|1881bp|B47DAA329495C5D8|+|B|SF 0112|NC_004337_1|pyruvate dehydrogenase(dihydrolipoyltransacetylase component)|
    AAAAGAATAxGTAAAAGAG|1893bp|AB974B233436A948|+|B|EC s0119|NC_002695_1|pyruvate dehydrogenasedihydrolipoyltransacetylase component|
    AAAAGAATAxGTAAAAGAG|1893bp|AB974B233436A948|+|B|Z0 125|NC_002655_2|pyruvate dehydrogenase(dihydrolipoyltransacetylase component)|
    AAAAGAATAxGTAAAAGAG|1893bp|BA85BCB8AA604335|+|B|SS O_0123|NC_007384_1|pyruvate dehydrogenasedihydrolipoyltransacetylase component|

    And this is the aligment (have to mention that where there are two or more genes with same gene_index and crc I represent only one of them - that's why they are represented here only by the crc)

    -AAAAGAATAxGTAAAAGAG-
    7453947EF512785B - pyruvate dehydrogenase(dihydrolipoyltransacetylase component)
    -B47DAA329495C5D8 - 1880/1881, 99.95%
    -AB974B233436A948 - 1848/1881, 98.25%
    -BA85BCB8AA604335 - 1859/1881, 98.83%
    B47DAA329495C5D8 - pyruvate dehydrogenase(dihydrolipoyltransacetylase component)
    -7453947EF512785B - 1880/1881, 99.95%
    -AB974B233436A948 - 1847/1881, 98.19%
    -BA85BCB8AA604335 - 1858/1881, 98.78%
    AB974B233436A948 - pyruvate dehydrogenasedihydrolipoyltransacetylase component
    -7453947EF512785B - 1848/1893, 97.62%
    -B47DAA329495C5D8 - 1847/1893, 97.57%
    -BA85BCB8AA604335 - 1854/1893, 97.94%
    BA85BCB8AA604335 - pyruvate dehydrogenasedihydrolipoyltransacetylase component
    -7453947EF512785B - 1859/1893, 98.20%
    -B47DAA329495C5D8 - 1858/1893, 98.15%
    -AB974B233436A948 - 1854/1893, 97.94%

    This is the list of the most mutated genes I have http://www.cyber-indian.com/theory/doc/c3.txt
    And this is the whole pool of genes I have http://www.cyber-indian.com/theory/d...es_index_0.txt and it's sorted so you can see it better (this one is 83 MB so you must use flashget or be a little patient)


    About "Point 4"
    After succed by gravity off a commet and landing, a sertain type of chemical or set of chemicals probably from volcanoes would triger reassembling mode.
    At first Archaea would trigger viral genes to start producing and get excrete from that cell. Viruses (gene delivering tools) would attack other carrier cells and dragg with them the needed genes and new SUrface protein - guiding it to the needed specie's cell.
    Once inside of the specie's cell genes self insert (after cleaved) into the chromosome acording where is found on the chromosome the same seqience as the gene's gene_index.

    "locate such material within the early genomes" - what kind of material you mean ?
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    I also forgot ... if you've head about "HERV" (Human endogenous retroviruses) this one is verry intresting
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    Sounds more plausible now ?

    come on I gave you what you asked ...
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    Pretty clear what we have here. Someone posting a sort of belief,rather than science, about the creation of earth life, or intelligently done by some kind of panspermia process.

    That's why the obscure posting, the unclear statement of ideas. Because to state the belief clearly would show how not credible or scientific it is.

    There is a real absence of cogent exposition, logical or scientific statement, and basically, shows an underlying 'axe to grind'.

    We are unable to penetrate this vagueness because there's nothing there to find. Went to find a claimed tree and all found the 'will o' the wisp'. And there it is. :wink:
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  29. #28  
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    [quote="cyber_indian"]Sounds more plausible now ?
    quote]No.
    Quote Originally Posted by cyber_indian
    come on I gave you what you asked ...
    I have no doubt that you think you did, but nowhere do I see anything even beginning to approach an answer to my questions, nor any attempt to present your argument in a cogent manner.

    Cyber, I actually think it is entirely plausible that life on Earth was deliberately seeded by an earlier life form. I am certainly a strong advocate of random pan spermia as the source of life on Earth. I am potentially your largest supporter on this site, but you have failed utterly to communicate your idea - and the logic and evidence behind it - in a simple, straightforward, yet comprehensive manner. At the moment I am strongly leaning towards Steve's interpretation. You are running out of opportunities to get your point across.
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    First of all I hope you have read my base article http://www.cyber-indian.com/theory/index.html , second what I've wrote in this thread is a supplement to my article ... also read the "Quotes" in the article (they are extract from internet and some textbooks) which support further ...

    If haven't read it, there is some of it ...

    What we need is a bacterium (Archaea) which can resist desert environment (extremophilic), find a suitable place and start deploying other simplified bacteria (Eubacteria) with genetically altered functions that can fill up the environment gaps. Later on when the environment mild up, finish up deploying the rest of the species from the world they came from. What we need for the deployment is:

    Scenario 1 - memory units:
    -A blueprint - all the life form's DNA of the previous world ecosystem gathered and reduced it to greatest common factors (example for that is vertebrates - head, body, arms/wings/fins, legs and tail), strategically planned and stored in bacteria as gene module (group of genes working together to fulfill a function) units.
    -A way to keep gene modules stored and suppressed until transplanted (memory bacteria doesn’t transcode these extra genes – probably condense that extra chromosome).
    -A transplanting tool – vector (virus).
    -And a way the transplanting tool to identify only the target specie and specific type of cell (antigen/antibody mechanism).
    At first bacteria secrets a blank virus (a virus with DNA for its own structure only), by infecting a memory bacterium it multiplies and charging itself with the designated gene modules and antigens (a process called “transduction”). Now because of the antigen/antibody mechanism the virus is targeted to fuse/append (new DNA information) only with a specific specie and tissue.

    Scenario 2 - prophage:
    -A blueprint - all the life form's DNA of the previous world ecosystem gathered and reduced it to greatest common factors (example for that is vertebrates - head, body, arms/wings/fins, legs and tail), strategically planned and stored in bacteria as gene module (group of genes working together to fulfill a function) units.
    -Prophage with attached gene modules in bacterium host.
    -A trigering factor for the phage (virus).
    -And a way the phage tool to identify only the target specie and specific type of cell (antigen/antibody mechanism).


    The building from a blueprint begins with the most common and most simple specie, and then we start appending the DNA difference to form new and new type species come out (that’s why evolution is a tree alike). In case of more complex species, they have to be deployed by transition/accumulation (also known as evolution, evidence for that is the junk DNA and pseudogenes). Sexual mechanism makes sure the newly acquired genes have been distributed in between that one genus and as one of the mechanisms clearing unwanted mutations (DNA integrity break up). All species has to find their spot in the ecosystem. That’s why they have to be able to mold their functionality (or the ecosystem would collapse), by means of shuffling/rearranging genes just before cell division of the newborn. Appending the genome and molding specie functionality is what we call natural selection.

    There are tree types of live form:
    -Archaea – Deploying.
    -Eubacteria – A simplified version (prokaryotes) with only the necessary functions, so it can be more efficient servicing the environment.
    -Species – A copy of the previous world.

    ...

    Further worth mentioning HERV a.k.a. Human endogenous retroviruses - viral remains found stuffed in human and many other genomes, presence which scientist try to explain and most connect with evolution.

    Endogenous retrovirus - Retroviruses are viruses that reverse-transcribe their RNA into DNA for integration into the host's genome. Human and other mammalian endogenous retroviruses are retroviruses thought to be derived from ancient infections of germ-cells; as such their proviruses.
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    It appears as though this exploration of natural selection versus genetics is being made unnecessarily complicated.

    The only thing that is important from natural selection is the concept that when genetic mutations occur it is either advantageous, disadventageous, or neither to the living thing that has the mutation. If the mutation is advantageous, the thing will survive and continue to reproduce. Its reproduction leads to more with similar mutations and so on and their population grows and so on and so forth and over time if this population with these mutations begin interbreeding and speciation will eventually occur. When the mutation is disadventageous the thing dies and doesn't reproduce. This mechanism is what leads to why every ecosystem seems to be so well stocked, everything with its dinner table. That was Darwin's observation and that's all it is about. It couldn't be more obvious, and Darwin was in the right place at the right time.

    Anything to do with the genetic code and natural selection are pretty much apples and oranges. Natural selection only concerns itself with realized biological variation.
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    [quote="steve"]Pretty clear what we have here. Someone posting a sort of belief,rather than science, about the creation of earth life, or intelligently done by some kind of panspermia process.
    ... ... ... quote]

    Steve there is no belief here, not ever religion - that what gets you(darvinist) on fire. Don't worry I'm no creatonist or ID-ist - do me a favor and don't compare me to nonscientific ones. All I do is arguing about do we realy know what evolution is and how it works. Natural selection and my theory goes similar way, but which one is the right one is the question.

    And please stop with this "mutations are the main key to evolution" - you sound lame, exactly like the religious believers.
    Every scpecie have some sort of DNA mutation repair - don't they what to evelolve ???

    Here is intresting Quote for you:
    -DiRuggiero's team has learned that when it comes to DNA repair, Halobacterium is something of a "Renaissance bug." It dabbles in a bit of everything. Its genome of only 2,400 genes contains several distinct sets of DNA-repair mechanisms. Some of these sets of tools are like the DNA-repair tools found in plants and animals, other sets are more like those of bacteria, and still others are characteristic of a lesser-known group of life called "Archaea" (the group that Halobacterium belongs to). Halobacterium has them all. Beyond even that, Halobacterium has a few novel DNA-repair mechanisms that no one has ever seen before!
    - Halobacteria can repair badly damaged DNA. "We have completely fragmented their DNA. ...And they can reassemble their entire chromosome and put it back into working order within several hours," says Adrienne Kish, a member of the research group studying Halobacteria at the University of Maryland. These Archaea can also survive extreme dryness, a hard vacuum, and of course, high salt concentrations. We are not the only ones to notice that Halobacteria could use these capabilities to survive in space.

    http://science.nasa.gov/headlines/y2...radmicrobe.htm
    (by NASA-funded researchers at the University of Maryland )
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    Hi folks, I'm new here so I thought I'd start with the perpetual topic.

    Quote Originally Posted by cyber_indian
    And please stop with this "mutations are the main key to evolution" - you sound lame, exactly like the religious believers.
    Every scpecie have some sort of DNA mutation repair - don't they what to evelolve ???
    Mutation repair is one of natures wonders, but it isn't perfect. If it was perfect, there would be no evolution and we wouldn't be here today. It's a game of numbers, a mutation repair system that was 99.999999% efficient would still lead to hundreds of base changes each generation - simply because of the 3 billion bases in our DNA, This slight infidelity in DNA mutation repair allows for the generation of new genotypes each generation, (and therefore evolution) however the natural consequence of evolution is cancer.

    This is something I'd written for some of my students, I know it will be a little simplistic for most of you, but I'm too lazy to rewrite it for a more experienced audience

    • I teach cancer biology here in Malaysia, and I use the analongy of evolution to explain to the students how tumours arise (it gets a bit dificult when some say they dont believe in it!).

      Tumours evolve in the same way species are thought to have, through random mutations followed by natural selection/survival of the fittest. Cancers are inititally triggered by mutations in certain genes (oncogenes and tumour suppressor genes). The function of these genes are very varied, but include many of those gene which are repsonsible for repairing the natural DNA damage, and monitoring DNA replication during cell division. If a cell loses these protective functions, it begins to accumulate mutations. This is essentially a random process, but natural selection/survival of the fittest 'selects' the cells with the set of mutations required for tumour development.

      Cancer is simple uncontrolled cell growth, they evolve as a group of competing clones (cells with the same genetic make up all derived from a common ancestor cell). If a breast cell has a mutation in the gene for heamoglobin, then nothing happens, but if the breast cell has a mutation of the gene for a growth factor receptor, it can trigger the cell to grow and divide more than it's neighbouring cells (on its way to becoming cancerous). Basically we only see the cells that were succesful (ie able to form a tumour), in the same way we only see the succesfull species (and in my view, the only reason we are the ones asking about evolution is because our species was the succesful one and not the neanderthals!)

      Natural selection in the tumour microenvironment works exactly the same way as in the world of biology: tumour cells with a collection of mutations that increase their growth rate out-compete the other tumour cell clones and become the domionant clone. That's what I do - proflie the genetic mutations present in cancers to try and predict the biological behaviour of a tumour.

      So why did I bore you all with this??

      Well, cancer is a natural consequence of evolution. If our DNA, our DNA repair systems, and our cellular mutation detection systems were perfect we would never get cancer; however we would also never have evolved!

      The fact that our systems are not 100% perfect means that mutations do occur (and accumulate) during our lifetime. This has been the driving force in evolution but the price we have paid for this is that about a third of us will get cancer.
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  34. #33  
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    Jashuk, thank you for that perspective. This is slightly off-topic, but may I nitpick on one point. You say that the mutations we suffer due to copying errors are the price we pay for evolution. I just want to quibble with your "that's why one third of us will get cancer". Surely a significant proportion of those who get cancer do so as a result of external environmental factors - smoking, diet, radiation exposure, etc. That doesn't invalidate your basic point, but it alters the actual figures somewhat.
    Wellcome to the forum by the way.
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    ??? quote "tumour cells with a collection of mutations that increase their growth rate out-compete the other tumour cell clones and become the domionant clone." - I don't concider myself a peace of tumor.
    ??? quote "This is essentially a random process, but natural selection/survival of the fittest 'selects' the cells with the set of mutations required for tumour development."

    quote "Cancer is simple uncontrolled cell growth" - corrosion of my car radiator is also a "cancer", but it will not turn my car into a Porsche!!!

    I have not doubt about that cancer is a result of change in the DNA, but I do believe that change in DNA ("mutation") has two totally different meanings - constructional and damaging. And I do believe that you do know "cancerogenous" material very well, but wrongfully connect it to a different subject.

    Example is a earlier thread couple of guys said that computers "have logic and therefore can think", in the same light computer processors have "prediction logic" and therefore can read your horoscope.

    That's what happens when we don’t have enough information on certain subject and that's how we end up blaming the "evolution" on this so abused word "mutation".
    I think is time to draw a line between "damaging mutations" and "evolution".

    Damaging in cells is like car engine:
    -Malnutrition-
    They need certain types of nutrients, once one or more of those nutrients stop reaching the needed processes those processes goes wrong.
    Equivalent is engine's oil - if it leeks out or sludge forms, the lack of oil there causes the engine to fail. (Leading to disturbance of the normal processes)
    -Cancerogeninc-
    Easies examples radiation(energy) or chemical, first one leads to direct destruction of the working infrastructure and second one - certain chemicals may neutralize or block certain type of process.
    Equivalent examples to have a crash, flying object, magnetic force surges the electrical equipment(energy) or chemical examples water in the oil, corrosion of parts, sugar in the gas, rust blockage in the cooling system.

    There is nothing random in damage, it's just a unfortunate outcome.
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  36. #35  
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    Hi Ophiolite, thanks for the welcome!

    You are correct about smoking, this dramatically increases mutation rates and I have heard estimates that 'banning' smoking would reduce cancer incidence by 50%. Not all mutations are caused by environmental compounds though, the background rate of DNA damage (i.e. mutations caused by natural, endogenous compounds, such as free radicals) has been estimated (through in vitro experiments) as between 100,000 and 500,000 molecular 'lesions' per cell per day (or about 1 base per every 6000 bases of DNA). Without a very efficient repair system this would be catastrophic! Obviously the rate of these 'mutations' will be raised in the lung cells of a smoker, and the skin cells of a sunbather. Even by just walking outside into the sun, the DNA of the your skin will be undergoing millions of mutations (base changes), this is particularly relevant to me as a Yorkshire man living in the intense sun of Malaysia! These mutations are constantly being repaired by our cells DNA repair system, which are incredibly efficient, and most never get passed on because the majority of cells in our body are differentiated and not dividing.

    The kind of mutations that are relevant to 'non-environmental cancer' are those errors made during the copying of the DNA in dividing cells (if the dividing cell is a germ cell then these are relevant to evolution). Our DNA copying, proof reading, and error repair enzymes are also amazing in their efficiency, traditional (and very conservative) calculations put the error rate at around 1 per 10exp9 errors per base (i.e. about 3 errors each time any cell in the body divides). These mutations will accumulate during the lifetime of an individual, with each additional cell division additional errors occur and the chance of a mutation occurring in a cancer related gene increase (cancer is naturally a disease of the elderly, and the incidence has a linear relationship with age).

    Smoking also dramatically increases the 'turnover' of lung cells, as many are killed by apoptosis due to high levels of DNA damage. These are replaced by division, so a 30 year old smoker will have cells which have divided as many times as a 70 year old non-smoker (guesstimate figures!). So the smoker has a double whammy, an increased cancer risk from the greater mutation rate, and an increased risk associated with the number of divisions his cells have made (i.e. by the time he is 50, his lungs are actually '90'!). Increasing life span will always mean that cancer is a major killer, even in the cleanest living of folk, due simply to the accumulation of 'natural' mutations with time and each cell division.

    Sorry to go off topic! I'll rectify that now.....
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  37. #36  
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    Hi cyber,

    Quote Originally Posted by cyber_indian
    Every scpecie have some sort of DNA mutation repair - don't they what to evelolve ???
    Sorry if I misunderstood you, I thought you were saying that mutations (and therefore evolution) would not occur in organisms with DNA repair systems so I was giving an example of how even the best DNA damage repair systems still allow mutations to slip thorough.

    Quote Originally Posted by cyber_indian
    ??? quote "tumour cells with a collection of mutations that increase their growth rate out-compete the other tumour cell clones and become the domionant clone." - I don't concider myself a peace of tumor.
    I was using cancer as an example of genetic change followed by selection. Obviously a tumour is not an independent life form, but its growth is dependant on exactly the same principle as evolution (i.e. beneficial genetic changes followed by selection - 'clonal evolution'). I wasn't suggesting that you were a piece of tumour, however the human species does fit the definition of a cancer surprisingly well

    Quote Originally Posted by cyber_indian
    quote "Cancer is simple uncontrolled cell growth" - corrosion of my car radiator is also a "cancer", but it will not turn my car into a Porsche!!!
    The analogy of a car is irrelevant, a car does not fit the most fundamental requirement of evolution - self replication (the other being variation between generations).



    I would like to go back to your original hypothesis about gene-indices, as I am fascinated by the patterns in our genome (and also the similarities between hard drives - but I will start another thread on that one!). I have read your posts and find them a little too cryptic to understand fully so hopefully you can clarify a few things.

    If I understand you correctly, you propose that each gene has a unique 'tag' before and after the coding sequence of the gene, and you seem to be alluding to the possibility that these 'tags' were designed intelligently to promote the self assembly of organisms? You also suggest that genes which are highly conserved between species are more likely to share the same tags.

    • Why would these tags be located at the start and end of the coding sequence? The promotor sequence (located upstream) of the gene is just as important as the coding sequence, and different genes have different promotor sequences (to control individual gene expression) so how would the correct promotor sequences be assembled next to the tagged coding sequences. The same applies to the particular enhancer/suppressor sequences located upstream/downstream of the gene.

      It is the gene that is the unit of inheritance (and thus evolution) and not the coding sequence, why would the tags not include the whole gene?

      How can you distinguish your theory from the current understanding that the coding sequence is surrounded by essentially random nucleotide sequences? (a particularly short sequence between ATG and the promotor). A random sequence of 9 bases before and after a gene may be enough to be statistically unique.

      In your list of most mutated genes, many of the genes sharing a 'gene-index' appear unrelated, could this not mean that the nine bases are simply random and that some genes share them by chance? (ie possibly 9 bases are not enough to be unique for each gene - I haven't done the maths!).

      You suggest that highly conserved genes (i.e. pyruvate dehydrogenase in your example) have highly conserved sequences before and after the gene, is this not to be expected? As the gene is inherited as a 'chunk' of chromosome, the sequences up and downstream will be carried with it. This has been know and used for a long time now E.g. for PCR/sequencing of genes identified in one species in an attempt to find them in another. We can design primers based on sequences just upstream and downstream of one species coding region in the hope that these will be conserved in another.

      In the example of pyruvate dehydrogenase, you show a few strains of three species of bacteria that share this particular 'gene-index'. Is that just a small proportion of the data you have or do you mean that out of the thousands of species of bacteria only a few share these up/downstream sequences?

      Finally, and the most important question!
      What is the mechanism that allows a 'tag' to be targeted to a specific genetic locus (or to self assemble)? Obviously this would be very valuable and yes, you would have solved the problem of gene therapy!


    I think in order to establish your theory you need to provide evidence of these 'gene-indices' maintaining the same level of conservation as the gene they mark, particularly with respect to the essential highly conserved genes (I can't give you any examples for bacteria, but something along the lines of the ubiquitin gene in higher mammals). In other words, they have a function that needs to be preserved (unless you are suggesting they were only needed to assemble the first organism on the planet). Current theory would suggest that highly conserved genes would not necessarily maintain highly conserved 'gene-indices' as it we currently do not think these sequences have a functional role (and mutations in these sequences would propagate without any penalty to the organism).


    If you could expand on these points I may understand your idea more, at present it looks like you are reading something into random sequences of nucleotides that closely follow the inheritance of the genes they flank. I would have guessed that anyway.
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  38. #37  
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    I’m happy that there is somebody finally to talk about this matter seriously.
    I will ask you not to compare me to nonscientific groups by saying things like "designed intelligently" - I'm sorry for the remark, but from what I read there is ugly war between Darwinist and religious groups. And as a third parity I prefer to be excluded. Again I'm sorry for this remark.

    The first question indeed is very important - does the promoter and etc. goes in between the gene_index or out, but because of the complexity for now I prefer to ignore it and work on non-prokaryotes mainly. But still there is possible scenario that in reassembly promoter and etc. might have already been on the blank chromosome. Also the gene_index is not of much importance after the reassembly because it's use is only once.

    I do believe that there is nothing random between the genes and this nonsense is of even more importance than the genes themselves - for instance higher organisms are just a complex sum of different variants(types) of cell colonies, who are arranged precisely - what cause the arrangment. I's just that genes are more obvious then this so called junk - example is computer binary file that you can read the inserted text lines, but if you don't know the assebley language the rest of the file is just monkey simbols for you.
    After I ran a script to list the gene_indexes, I've distinguished tree groups:
    -One - Non-related genes.
    -Two - gene_index related who match the same size +/- I think it was 20bp
    -Tree - gene_index related with possible mutation over the gene_index itself leading to non-relation at all, or related genes with just bigger deletion/insertion or too many changes.
    I ran a second script to a file including the two and tree groups executing CulustalW alignment and the result was match of 97.14% for group two and 74.05% for group tree. And total match of 96.4% for both groups.
    Also group two shows remarkable resemblance and I was stunned when I saw it the first time.
    And I noticed a huge pile of genes that are still "hypothetical protein" and can be easily pointed out by arranging the gene_indexes.

    Here is an example of related genes with SNPs over the gene_index or the gene itself(most probably the original gene is the one with CRC of 006E2EB920021BF5):
    CATTATCCTxCCACTTCAA|840bp|006E2EB920021BF5|-|B|SF2427|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAA|840bp|006F8A8080021BF5|+|B|SF4 223|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAA|840bp|1E902059CE0CE5E5|-|B|S0234|NC_004741_1|IS911 orfB|
    CATTATCCTxCCACTTCAC|840bp|17CE56081304A831|+|B|SSO _4458|NC_007384_1|IS911 ORF2|
    CATTATCCTxCCACTTCAC|840bp|17CE56081304A831|-|B|SSO_3904|NC_007384_1|IS911 ORF2|
    CATTATCCTxCCACTTCAC|840bp|4A016589C4D1DAEE|+|B|SF1 052|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAC|840bp|6A9C1A8536C7101B|-|B|SF0516|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|006E2EB920021BF5|+|B|SSO _2298|NC_007384_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|006E2EB920021BF5|-|B|SF1907|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|006E2EB920021BF5|-|B|SF1925|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|006E2EB920021BF5|-|B|SSO_0730|NC_007384_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|17CE56081304A831|-|B|SSO_2038|NC_007384_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|17CE56081304A831|-|B|SSO_2452|NC_007384_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|17CE56081304A831|-|B|SSO_3607|NC_007384_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|1E902059CE0CE5E5|+|B|SF0 678|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|1E902059CE0CE5E5|+|B|SF1 800|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|1E902059CE0CE5E5|-|B|SF1605|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|1E902059CE0CE5E5|-|B|SF2048|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|6A9C1A8536C7101B|-|B|SF1838|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAG|840bp|74621465D8C9EE0B|-|B|SF2306|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAT|840bp|006E2EB920021BF5|+|B|CP0 269|NC_004851_1|IS911 ORF2|
    CATTATCCTxCCACTTCAT|840bp|006E2EB920021BF5|-|B|SF0683|NC_004337_1|IS911 ORF2|
    CATTATCCTxCCACTTCAT|840bp|1E902059CE0CE5E5|-|B|SF0862|NC_004337_1|IS911 ORF2|

    You can see that list at this address:
    http://www.cyber-indian.com/gene_ind...es_index_0.zip - contains all tree groups
    http://www.cyber-indian.com/gene_ind...es_index_1.zip - contains the two and tree groups
    or you can use the "Search genes" on the http://www.cyber-indian.com/bioperl/index.html - this will do the search in the big file genes_index_0.

    About the "chunk" question I had some thoughts too, but haven’t found time yet to do more research. It's an interesting question, but right now I'm focused on parsing bigger databases for more fine results.

    Pyruvate dehydrogenase was nothing, but just the first choice I picked to show the patterns between genes.

    The targeting as the most mechanisms in cell do, is by match between the target location and needed substance which floats freely around - "Sticky Ends" and "DNA ligase". Meaning that locus will match the gene_index.
    Quote of ligase definition - "DNA ligases have become an indispensable tool in modern molecular biology research for generating recombinant DNA sequences. For example, it is possible mix cut plasmids (with sticky ends), free-floating genes (with complementary sticky ends), and ligase to insert the gene into the plasmid."
    And can give another similar and existing example with the protein sequence also known as protein targeting.

    And finally just open the genes_index_0.txt or genes_index_1.txt and just look at the resemblance.
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