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

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

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