Evolution Theory Issue - Great Debate -mindspawn and RAZD only

Suddenly:You can have a duplication of a coding gene, with additional modification in the genome such that the duplicated gene performs a function that the single copy does not perform. Example: the cit+ behavior in E.coli to metabolize citrate in an aerobic environment due to two mutations and the duplication of the citT coding gene.Why does it take two copies for this to work -- if it was a cryptic\hidden\silent gene activated by the mutations, then why doesn't it work with one copy? I would suspect that the transport protein being coded may be folded a different way, affecting how it functions, due to the proximity with each other, as the folding of a protein is as important (if not more so) as the molecular sequence.Slowly:You can have a duplication of a gene that is responsible for two functions in the parent population, which are then divided in the offspring, each copy performing one of the two functions, allowing subsequent modification in following generations of either\both copies for better fitness of the respective single functions to their ecology. Example: the arctic fish bluegenes mentions in the peanut gallery.Notes on some nits:First, "already there" -- when you start with a duplication -- your requirement -- you necessarily start with genetic sequences that were "already there" (cryptic\hidden\silent) and thus your criticism that the gene was "already there" is really a bogus dodge, a ruse you use to convince yourself that this is not new novel behavior\function.The question is not whether those sequences were there, but whether the genetic coding behavior was modified and a function was being performed that was not present in the previous generation for it to be novel: Over 30,000 previous generations did not perform the cit+ behavior in aerobic conditions, ergo this qualifies as novel behavior according to the agreed definition.Second, "duplicated gene was inverted" -- it isn't in this case, but why should this matter? I know you said "which would disable it" but this is not always the case. If you think about it there should be no difference to coding from promoter to terminator, as how would the molecular construction of the protein know? If I look at it from the other side it would look inverted, yes?Enjoy

True You are not understanding the study. It was the new positioning of the duplicated sequence that allowed an aerobic promoter of ANOTHER gene to start working on the Cit gene. Can you see that? The duplication activated a different promoter when normally the gene was silent.So instead of one silent gene, you had a duplication event, followed by one gene being activated in aerobic conditions and becoming Cit+ using another adjacent gene's promoter, the rnk gene (Quote: This duplication immediately conferred the Cit+ trait by creating a new regulatory module in which the normally silent citT gene is placed under the control of a promoter for an adjacent gene called rnk.) I'm not disputing the novel function, the only dispute that I have had with your example, is that it did not add a coding gene, it merely activated an inactive gene. Thus the net number of active genes decreased by one (silent gene) and then increased by one (activated gene) reaching the original number with no net gain. One of the two duplicates remained silent. The fact that it added a novel function whilst being re-activated is in your favour, but it just isn't an additional gene, its a changed gene, which I have already acknowledged.Since then I have another problem with your example, although these mutated e.coli gain temporary fitness in laboratory conditions, they lose fitness in the natural processes of osmosis found in nature. ie the mutation is damaging.Your example would be better if it didn't revolve around silent genes.

One is right after the other -- head to tail -- and not in a different location.So why is the effect only seen once the duplication has occurred -- why doesn't that same promoter act on the single copy?Is it because of the promoter or because of the coding gene? Or does a coding gene activating with a different promoter then produce a different (folded or altered) protein?For the rest I quote Taq from the Peanut Gallery (Message 55):

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So let's go back to the very beginning of the debate. RAZD quoted two statements by mindspawn as the topic of the debate:

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quote:

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"... recent DNA sequencing is not providing enough support for the hypothesis of evolution. (ie increased DNA complexity of new and uniquely functional active coding genes within an organism is not observed to add fitness)."

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and

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"I have been looking ... for some evidence that a gene can duplicate, and then produce a novel function in the duplicated coding gene that adds fitness. Haven't seen it yet, this basic process of evolution remains unproven. Without it we would just have bacteria on earth, mutating and evolving into alternative forms but never gaining in complexity."

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So does the cit+ duplication fit these criteria? Let's take a look.

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First, is the cit gene duplication unique? Yes. The ancestral bacteria did not have two cit genes with different promoters. Not only that, but it produced a novel phenotype which is citrate utilization in aerobic conditions which was beneficial in the given environment. So we have a novel and beneficial phenotype produced by a gene duplication.

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Second, does this qualify as an increase in DNA complexity as it relates to the evolution of morphological complexity such as the transition from unicellular to multicellular? Again, the answer is yes. The basic advancement needed for bridging the gap between unicellular and multicellular life is the ability to control gene regulation. Increasing the number of genes under different promoters is essential for increasing the types of tissues and functions that a multicellular organism can have. That is the entire basis for homeobox genes and their importance in metazoan evolution through duplication and divergence of function. Hox genes are transcription factors that bind to gene promoters, and increasing the genes under the influence of different promoters is an increase in genome complexity.

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So I would say that the cit+ example fits all of the mindspawn's criteria.

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Seems to me that this covers it.EnjoyEdited by RAZD, : link

As far as I can see its the same protein produced, its own promoter did not activate the protein production. The new promoter activated the gene to produce proteins. Its affect is only seen after the duplication event, because the event involved more than just the duplication of that particular gene. Somehow the gene came under the influence of another gene's promoter. the studt does not give details how this occurred.RAZD I want to explain my position so there is no confusion. My position is based on the assumption that the first prokaryote type organism had about 1000 coding genes as observed in modern prokaryotes. The figure "1000" isn't as important as the concept that most organisms have increased in number of coding genes over time, whatever the starting number was. This assumption does appear to be a strawman argument for you, because you have indicated its possible for the first organism to have had many coding genes, but it seems to be a discussion we are continuing with.In essence I want to see how a 1000 coding gene organism can become a 1001 coding gene organism. Or a 21000 coding gene organism can become a 21001 coding gene organism. Now evolutionary theory does not require consistent additions, any organism can evolve decreases as well as increases in protein coding genes depending on what would improve fitness at that time. Thus a 1000 gene organism can become 999 genes. Then go back to 1000 genes. This still does not explain how evolution can claim additional coding genes over time.This is why I believe your example is not good enough, to illustrate this , let's assume that region of the genome had ten genes:CCCCCCCCCC (ten coding genes)Then due to a lack of promotion, the one gene goes silent:
CCCCCSCCCC (9 coding genes and one silent gene)Then there is a mutation event in which the silent gene is duplicated:
CCCCCSSCCCC (9 coding genes, two silent genes)However we know this isn't exactly what happened because the one copy was activated due to an adjacent promoter from another gene now affecting it:
CCCCCSCCCCC (10 coding genes, one silent gene)The net result is that the organism has returned to 10 coding genes, its original state before that original gene went silent. One of these genes has a changed promoter , it still produces proteins for nitrates, but is activated in different circumstances than before, so the organism has undergone a novel change, but has not increased in the number of novel genes. The great test is when the original silent gene also activates maybe under another set of environmental conditions, will the doubled protein production destroy the E.Coli? We do not know if the double up will kill it, because there has been NO increase in protein coding genes, there were ten, then nine, then ten in that region. Eleven coding genes could kill it, because a duplicated gene when both copies code for proteins often kills an organism. Or even a loss of fitness could occur, which seems to be the case anyway, because this organism lost its ability to survive during osmosis which always occurs in nature.So your example is unrelated to the gain of additional coding genes over time, a process acknowledged as fundamental to most evolutionists.ps , I'm really curious how they determined that the initial 12 populations of E.Coli were identical, this seems like a very strong statement for 1988 when full genome sequencing of E.Coli only occurred in 1997? Any lack of uniformity back then would change the entire interpretation of the evidence.Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.

There are two issues here:

• are you asking for proof of a mechanism (ie - having a entire new gene made de novo) that does not exist -- and that is not necessary for evolution to work, or
• are you asking for how evolution can develop a new coding gene from existing genes

The first doesn't require an answer other than "evolution does not work that way" and your expectation is at fault.The answer to the second is that the easiest way is via gene duplication and then modification, as was seen in the E.coli experiment.This provides two coding genes that operate in different environments, one in the old environment and the new copy in the new environment. Environment is important to the process because of selection. Moving into and adapting to a new environment opens up more possibilities for survival of that population, which can then evolve further adaptations in that environment that would not be selected in the previous environment. Duplication and then modification then selection.Over time we would expect those two copies of the protein to diverge further as they get adapted to different behaviors and eventually they could show barely any relation but act as completely different coding genes. This is seen in some studies as having occurred in the past:Stepwise evolution of essential centromere function in a Drosophila neogene - PubMed (fruit flies) and
Low copy repeats - Wikipedia (humans) Cloning of asexual single cell bacteria is not difficult, and if they were able to compare the gene sequences to find the locations of the duplications they had the ability to check.Enjoy.Edited by RAZD, : clrty