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Author | Topic: Genetic Redundancy and Natural Selection | |||||||||||||||||||||||||||||||||||
BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
I hate to start a new thread at a time when I am already vastly behind in my replies on other threads - but I just read an interesting article by Dr. Peter Borger on the topic of genetic redundancy (Dr. Borger is an inactive member of these forums I believe).
Dr. Borger's primary assertion is that natural selection and gene duplication can not account for the startling level if genetic redundancy found in the genome. He uses the SRC gene family as an example case. Summarizing his explanation, the SRC genes code the family of proteins (8 in total) that activate cellular division. Non-synonymous point mutations in these genes are often lethal because they code proteins that don't "turn-off" leading to cancerous cell division. SRC proteins are not identical (sharing only 60-80% of their sequences), so since these genes are highly selective against mutation it is highly unlikely that they arose as a result of gene duplication - they would have to have evolved separately. While mutation often results in a lethal phenotype knockout experiments on SRC genes show that mice can survive without some SRC genes. Now, Dr. Borger argues this as evidence of a designed system - and initially I agree with his assessment - but I'd like to give my darwinist friends here the opportunity to provide a rational explanation. How is it possible for evolution to generate redundancy within genetic systems?
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: Certainly - sorry for not being more clear.
quote: Assuming I don't have a misunderstanding of the concept myself - a non-synonymous point mutation is a change to the nucleotide sequence (GATC) in a gene that causes a corresponding change to the protein(s) coded by that gene by replacing one amino acid in that protein chance with a different one. Because of the redundancy in the genetic code many mutations are synonymous: they change the DNA nucleotide sequence but do not result in a change to the resulting protein because they still code for the same amino acid.
quote: Design is simply the conclusion that I and the author of the article draw. I could go into detail, but it seems to be beyond the scope of the question. I'm not asking readers to come to the conclusion of design - I am asking readers to demonstrate how darwinian evolution explains genetic redundancy. I ask because I'm curious if a functional hypothesis has been developed yet within the darwinian framework.
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: Good point - here's why I mentioned the conclusion of design: The article I linked is the first in a series. Dr. Borger outlines in subsequent articles a YEC design-oriented baramin-based hypothesis that seems to fit the data rather well. I'm wondering if darwinian evolution has a corresponding hypothesis - and if so how well does that hypothesis fit the data? (I'm not trying to be condescending here - I'd really like to know!)
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: Sorry...I'm not sure I understand. I don't think I've posted the supporting evidence in the Biological classification vs. 'Kind' thread (unless there is a specific post you are referring to?). It was my intention to bring up some of it in responses to posts on that thread - or are you asking me to post the evidence on that thread and then link it from here? I'm happy to comply - just not sure I'm following what your request is.
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: A noble goal indeed.
quote: I don't intend to discuss baraminology in this thread - I was hoping to receive one or more answers to a specific question posed to darwinists. I agree it would be good to define baraminology and its evidence - and I have been and will continue to try and do so in that thread. My only reasoning for mentioning mine and Dr. Borger's conclusion of design here was so that respondants would understand my perspective on the issue. Since it is possible my bias toward YEC thinking is influencing my conclusion I may not have adequately considered possible evolutionary hypotheses to answer the question I posed. I felt disclosing my position would give those who responded a better frame of reference to answer the question. Does that clear things up? If you still disagree I will happily edit out the mention of my conclusion.
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: I don't know Dr. Borger personally - I have no clue about his credentials nor do I really care. Whoever wrote the article in question makes some good points regarding natural selection and genetic redundancy. The point here is not to perform a character assassination on the author of the article. The point is to demonstrate how evolution can account for this problem. I asked a very specific question and am hoping for a very specific answer - neither really has anything to do with Dr. Borger. I wouldn't be surprised if you and others dodge the question and instead attack Dr. Borger's credentials - but that would lead me to suspect that you don't have an answer.... However, if it needs clarified Dr. Borger has defended his credentials here on these forums. Now, would you please approve the thread? *Edit: Sorry, after re-reading the above I may have come across rudely - that was not my intent. I appreciate you pointing out the supposed flaw in Dr. Borger's credentials (now resolved), but didn't find it particularly applicable to the question I posed. Edited by BobTHJ, : Added clarifying note
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: Borger gives this quote:
‘In the redundant gene family of SRC-like proteins, many, perhaps almost all point mutations that damage the protein also cause deleterious phenotypes and kill the organism. The genetic redundancy cannot decay away through the accumulation of point mutations.’ And attributes this source:
Toby, J.G. and Spring, J., Genetic redundancy in vertebrates: polyploidy and persistence of genes encoding multidomain proteins, Trends in Genet. 14:46—49, 1998 Let me know if anyone has access to this paper. I'm curious what it says.
quote: Thank you, you did present some possibilities. However, consider there are 8 (or 9) genes in this family. So - not only would the gene have to be duplicated the appropriate number of times (a reasonable assumption) but then each of those variants would have to undergo either:1) A series of non-fatal mutations. Apart from point mutations, these would be what - insertions and deletions? Assuming Dr. Borger's assertion is correct I'm not sure how that would result in a less lethal phenotype. 2) a deactivation, followed by mutations into a different functional protein, followed by a reactivation (improbable). Your third option is a possibility - though without knowing if SRC mutations are lethal in all known organisms it is difficult to know if this is a reasonable option. Let's assume for a moment that one of the methods you posited was sufficient to create the redundancy in the SRC genes. How does redundancy occur across a large portion of the genome. I could see (given adequate time) this event occurring once - but repeatedly hundreds or thousands of times? What mechanism does evolution have to preserve a redundancy? Natural selection works against it.
quote: Funny you should mention that - because that is exactly what we see at the cellular level. Intensely complex machinery working in synchronization, operating from a set of coded instructions that code multiple tasks simultaneously, and a self-regulating self-repairing, redundant system to carry it all out. The complexity far exceeds the limits of mechanics or computer science. But the random, imperfect nature of the evolutionary process explains it perfectly, right?
quote: You mean, other than the irreducible complexity I eluded to above? Nope that's it. See what you want to see.
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: No, no....try and understand the YEC model. Creation was perfect. God created a variety of genomes that had the ability to modify themselves and adapt to a wide variety of situations. Mutation is a product of the fall - of sin entering the world. Now the once perfect genome is deteriorating: losing large chunks of information and mutating to degenerate or fatal phenotypes. If the YEC model is correct we should see more degeneration of the genome (ie a higher rate of disease, cancer, loss of function, declining lifespans etc.) as time progresses. The semi-recent revolution in medicine has staved this off to some extent, but in the end it will succumb to the crumbling genome (unless technology is developed to repair/restore it, which is a possibility).
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: Thank you. Out of curiosity, could you provide me a link to a paper detailing some of the other functions of SRC-family genes?
quote: Agree. Borger does need to provide the data to back this claim.
quote: A darwinian approach would assume the chimp SRC gene to be compatible with humans - an ID approach not so much. Though it would be interesting to know....
quote: Winzeler, E.A. et al., Functional characterization of the S. cerevisiae genome by gene deletion and parallel analysis, Science 285: 901—906, 1999 shows that gene duplication can not account for even half of the cases of genetic redundancy. Let's step back from the SRC gene and look at the big picture for a minute: The moment a gene is duplicated mutation begins to act upon it, modifying it from its twin. As long as the gene remains functionally redundant to its paralogue then there is no positive selective pressure to maintain that gene (it does not add to the fitness of the organism). Thus natural selection has no method of retaining redundancy. It lasts only for the short (relatively speaking) duration until mutation drives it away from functional redundance. Yet we see a remarkable level of redundance in the genome - far more than can be accounted for by recently duplicated genes. We also see dormant genes that code for functions not normally expressed. These cryptic genes are activated by extreme environmental pressures on the organism. How does natural selection preserve these dormant/cryptic genes when they are not typically expressed and therefore provide no fitness benefit to the organism (except under certain extreme conditions)?
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: Try reading what I wrote again. Note the words "...at the cellular level." As to the genetic bottleneck, the baranome hypothesis accounts for this. Baranomes are pluripotent. They contain a host of dormant genes to allow the organism to thrive in a wide variety of environments and contain the genetic machinery to induce rapid variation and speciation.
quote: Your logic is flawed. I could see you arguing this line of reasoning if you could demonstrate piece by piece the reversal of a process without the destruction of the functionary (still not sure I'd agree - but at least you'd have a logical argument). However, you are suggesting that since a single piece of a system can be removed and the system will still function then it must not be irreducibly complex - this argument has no merit.
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: If this is a case of mis-quoting (and it appears it is) then Borger should have been more careful to notate his modification to the quote.
quote: It is doubtful Borger is trying to mislead. Based on the context it is clear Borger is speaking about non-synonymous mutations. And what makes you think that Gibson, T.J. and Spring, J are referring to a subset of non-synonymous mutations? All non-synonymous mutations "damage" the protein (though in many cases for non-SRC genes this still results in a valid phenotype). Maybe I'm wrong though - I can't read the article myself so perhaps they specify this more clearly. I'm not sure why you think Borger should address a polyploidy origin. It seems a pretty weak hypothesis considering the SRC genes are located at different spots on different chromosomes. Again, I don't have access to the cited article - so maybe they explain this?
quote: Thanks - I'm reading through it and finding it interesting. I'm a bit disappointed by Borger's arrogant and wild claims at the start - but it seems he shapes up a bit once you get a little further into the conversation. Edited by BobTHJ, : a bunch of typographical goofs
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: Because you said so it must be true?
quote: I'm sorry you disagree. I find the notion that humans are wise and good enough to divorce themselves from their Creator to be arrogant, unhealthy, and foolish.
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BobTHJ Member (Idle past 5024 days) Posts: 119 Joined: |
quote: I'm not sure how you got from my statement regarding a degenerating genome to this. Care to explain? What does fast replication have to do with my statement? And no - I don't have evidence - but I'm sure somewhere someone is keeping statistics on this stuff. This is a prediction for the baranome hypothesis - and it can likely be proven true or false to some degree of accuracy within the next 50 years or so (though environmental agents such as carcinogens as well as medical efforts to prevent disease do rather complicate the recordkeeping).
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