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Thread: list of beneficial mutations?

  1. #1 list of beneficial mutations? 
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    is there somewhere out there on the net that has a list of all beneficial mutations found by science? that anyone here knows of?


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    Beneficial mutations are dependent on the environment.

    A fish that mutates fins into legs, that lives near shoreline might survive better than the fish it evolved from. Thus it is a beneficial mutation.

    Take that same mutation but put it in the middle of the ocean, not near land, and it would likely be detrimental.

    Please tell me though you are not one of those people who believes that there are no beneficial mutations.


    Always minimize the variables.

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    quite the opposite, i do believe in beneficial mutations, just wanted to know if anyone had made a list of (refracing) obviously beneficial mutations found (for the organism they are studing) or potentially beneficial mutations found (stronger bones, higher muscle mass, ect)
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    Seen in a long perspective, every single feature of a human of today could be seen as a "beneficial mutation".

    But I guess the question was about more recent, and less widely spread mutations.
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    studied mutations... given that the rest counts as morphology of the species....
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    just wanted to know if anyone had made a list of (refracing) obviously beneficial mutations found (for the organism they are studing) or potentially beneficial mutations found (stronger bones, higher muscle mass, ect)
    It is not possible to determine in advance of selection whether a given mutation is "beneficial".
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    seemingly beneficial mutations?
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    With the exception of those genes, elements, chromosomes and sequences that seem to exist for no reason other than to hurt their hosts and continue their own selfish replication, you could argue that most genes are in some sense beneficial. However, I guess your question relates to gene variants that appear to confer a particular advantage to those that carry them. There are many of those, too many to list; I don't know if anyone has put them all on one page or not. Off the top of my head:

    HIV-positive, long-term nonprogressors (elite controllers) - mutation in the CCR5 receptor of T cell lymphocytes
    Duffy antigen gene variants - protection against Plasmodium vivax malaria infetion
    Lipoprotein Lipase mutations - reduced risk of heart disease
    Myostatin gene mutations - increased muscle mass :



    You could look at selection also; how humans have adapted to particular environments, say to high altitude.
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    Quote Originally Posted by scienceguy8888
    studied mutations... given that the rest counts as morphology of the species....
    That is quite a given. It's not one that I could readily accept. As earlier noted the vast majority of mutations still extant in our genes are beneficial mutations.
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    Quote Originally Posted by Zwirko
    HIV-positive, long-term nonprogressors (elite controllers) - mutation in the CCR5 receptor of T cell lymphocytes
    Are you sure? If I'm not mistaken, CCR5 mutation prevents HIV infection.
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    Genetic variant in cows produces more milk.

    Sickle cell anemia wards off malaria.
    Grief is the price we pay for love. (CM Parkes) Our postillion has been struck by lightning. (Unknown) War is always the choice of the chosen who will not have to fight. (Bono) The years tell much what the days never knew. (RW Emerson) Reality is not always probable, or likely. (JL Borges)
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    Evolution of Nylonase in bacteria.

    It is a great example, because it is the evolution of an entirely new gene, with the old one it mutated from completely functional. It did this by gene duplication and then a frameshift mutation of a duplicate.

    Here is a youtube video with explanation. The nylonase bit is about half way through or so, but the whole thing is good even if you know about mutations. Couldn't find the peer reviewed article, but it's out there.

    http://www.youtube.com/watch?v=OfybuMJVWj0

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    Quote Originally Posted by Twit of wit
    Are you sure? If I'm not mistaken, CCR5 mutation prevents HIV infection.
    As I understand it there are many variants of CCR5. You can also, obviously, be homozygous or heterozygous for such alleles. So there are differing degrees to which such mutations can offer protection.

    These patients are termed long-term nonprogressors because although they are infected with HIV, the progression to AIDS is slowed or in rare cases seems to be prevented.
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    Quote Originally Posted by Zwirko
    Quote Originally Posted by Twit of wit
    Are you sure? If I'm not mistaken, CCR5 mutation prevents HIV infection.
    As I understand it there are many variants of CCR5. You can also, obviously, be homozygous or heterozygous for such alleles. So there are differing degrees to which such mutations can offer protection.
    The mutation of CCR5 prevents HIV from entering cells. People who have both alleles with the mutation can't get infected at all.

    Quote Originally Posted by Zwirko
    These patients are termed long-term nonprogressors because although they are infected with HIV, the progression to AIDS is slowed or in rare cases seems to be prevented.
    No, long term nonprogressors are infected, but don't progress to AIDS.
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    Why restrict this pointless detour to homozygous Δ32 deletions in CCR5? Mutations in CCR5 come in many varieties, with differing outcomes of HIV progression. Please recall that you said mutations in this gene prevent HIV gaining entry into cells; clearly some do, many do not - some even lead to faster progression to AIDS. It'd be nice if you were just to agree that you were mistaken, rather than do the old goal-post shifting trick again.

    Your definition of what a long term nonprogressor is is not accurate. My definition is accurate and mirrors typical examples that a 5 minute search of the literature will find. If you think otherwise, then please provide a credible source.
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    Quote Originally Posted by Zwirko
    Why restrict this pointless detour to homozygous Δ32 deletions in CCR5? Mutations in CCR5 come in many varieties, with differing outcomes of HIV progression. Please recall that you said mutations in this gene prevent HIV gaining entry into cells; clearly some do, many do not - some even lead to faster progression to AIDS. It'd be nice if you were just to agree that you were mistaken, rather than do the old goal-post shifting trick again.
    I have no idea what you are talking about. It seemed clear we are talking about the delta32 deletion that prevents infection. Where exactly I was wrong?

    Quote Originally Posted by Zwirko
    Your definition of what a long term nonprogressor is is not accurate. My definition is accurate and mirrors typical examples that a 5 minute search of the literature will find. If you think otherwise, then please provide a credible source.
    Again, I have no idea what are you talking about. You said that long term nonprogressors are people with the ccr5 gene preventing infection. I said they are not, they are infected, but something keeps them from progressing to aids.
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  18. #17  
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    CCR5 variants - in the context of HIV infection - are associated with the clinical description known as long-term nonprogressor. Carriers of mutant CCR5 alleles are often HIV+ and exhibit slowed/delayed progression to AIDS. You asked if I was sure. I'm telling you, yes I am sure CCR5 mutations are involved in this phenomenon. Since there are many CCR5 variants and other co-receptors involved, as well as other strains of HIV and many other host-encoded and viral-encoded factors involved in HIV infection then why would you assume I'm referring solely to CCR5-Δ32 homozygotes? The homozygous condition doesn't necessarily prevent infection either: people that are homozygous for the CCR5-Δ32 allele have strongly reduced susceptibility to R5-dependent HIV-1 infection. It's not 100% immunity.
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  19. #18  
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    Quote Originally Posted by Zwirko
    The homozygous condition doesn't necessarily prevent infection either: people that are homozygous for the CCR5-Δ32 allele have strongly reduced susceptibility to R5-dependent HIV-1 infection. It's not 100% immunity.
    Do you have any sources mentioning infected people with both alleles with the mutation?
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  20. #19  
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    Sure, I can give sources.

    Some strains of the HIV virus utilise the CXCR4 co-receptor:

    Michael NL et al (1998)
    Exclusive and persistent use of the entry coreceptor CXCR4 by human immunodeficiency virus type 1 from a subject homozygous for CCR5 delta32.
    J Virol. 1998;72:60406047

    Kuipers H et al (1999)
    An HIV-1-infected individual homozygous for the CCR-5 delta32 allele and the SDF-1 3'A. allele.
    AIDS. 1999;13:433434. doi: 10.1097/00002030-199902250-00025

    Balotta C et al (1997)
    Homozygous delta 32 deletion of the CCR-5 chemokine receptor gene in an HIV-1-infected patient.
    AIDS. 1997;11:F6771. doi: 10.1097/00002030-199710000-00001

    O'Brien TR et al (1997)
    2nd HIV-1 infection in a man homozygous for CCR5 delta 32.
    Lancet. 1997;349:1219. doi: 10.1016/S0140-6736(97)24017-1

    Theodorou I et al (1997)
    HIV-1 infection in an individual homozygous for CCR5 delta 32. Seroco Study Group.
    Lancet. 1997;349:12191220. doi: 10.1016/S0140-6736(05)62411-7

    Homozygotes for the Δ32 allele are very rare. Individuals like those mentioned in the papers above are even rarer.
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  21. #20  
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    Quote Originally Posted by Zwirko
    Sure, I can give sources.

    Some strains of the HIV virus utilise the CXCR4 co-receptor
    So they can be infected with other strains of HIV. There is no disagreement between us.

    http://www.mcld.co.uk/hiv/?q=R5
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  22. #21  
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    mutations occur randomly, it is also a part of natural selection.... natural selection refers to 1) survivial of the fittest 2) mutations etcccc........... as haamus said the beneficial mutations happen due to the enviornemnt.... it might not be as useful b/c of the enviornment but it will occur one way or another..... now to lamarcks theory its is passed on if it used and it will not devolope if it is not used.. at the end i have no idea if there is a list... if there is pleasee contact me i would like to see it 2
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