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Author Topic:   How novel features evolve #2
Percy
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Posts: 22391
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


(1)
Message 256 of 402 (674631)
10-01-2012 9:51 AM
Reply to: Message 254 by zaius137
10-01-2012 12:53 AM


Re: On topic news
zaius137 writes:
The definition you can use does not exist. Fins evolving into legs are complete and utter fantasy. Now you need to make scientific arguments that support your speculation.
The question isn't whether fins evolving into legs is a fantasy. The question is how you're defining novel. You need to provide a definition of novel that is acceptable to you so that we can focus on novelty that you actually accept as novelty, and that allows we people that you're discussing with to identify features that are *not* novel to you (citrate digestion in the presence of oxygen) versus features that *are* novel to you (and which evidently doesn't include fins evolving into legs).
If in your mind nothing could ever be novel then there's really no point in you're contributing to a thread on novelty, so if you're actually participating in this thread in good faith then could you maybe provide a few examples of innovations you would consider novel?
--Percy

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Taq
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Posts: 9972
Joined: 03-06-2009
Member Rating: 5.5


(1)
Message 257 of 402 (674656)
10-01-2012 1:27 PM
Reply to: Message 250 by zaius137
09-30-2012 12:34 AM


Re: On topic news
By definition, I showed that the transport of citrate trough the cell wall of E. coli was not a novel innovation because under anaerobic conditions it could already take place.
However, E. coli were not able to transport citrate in aerobic conditions. After many generations, they were able to transport citrate in aerobic conditions, a phenotype that they previously did not have. Therefore, it is a novel trait by definition. Also, this trait came about through random mutations and was then selected for. So this is an example of a novel trait coming about through random mutation and selection.
This is because the transport of citrate through the cell wall under anaerobic conditions was adapted to aerobic conditions via a newly promoted recessive gene.
E. coli do not have recessive genes. The new phenotype came about through mutations.
The transport of citrate already occurred but was enhanced (adapted),
Aerobic transport of citrate did not occur previous to the mutations.
It is noteworthy that this silent transporter was in the genome all along never being pruned by evolution.
There was nothing silent about it. The transporter was changed through mutation, and those mutations led to a new and novel phenotype.

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 Message 250 by zaius137, posted 09-30-2012 12:34 AM zaius137 has not replied

  
Taq
Member
Posts: 9972
Joined: 03-06-2009
Member Rating: 5.5


(1)
Message 258 of 402 (674657)
10-01-2012 1:36 PM
Reply to: Message 217 by zaius137
09-25-2012 2:08 AM


Re: Really?
Even accepting there are many species of bacteria with the same morphology (dubious claim). You can claim speciation only when biologists use 24 separate definitions of a species not necessarily dependent on aligning morphology.
We are claiming that aerobic citrate transport is a novel feature that came about through random mutation and selection.
The only question is if the phenotypes are front loaded.
Perhaps you could try to answer that question?
Give me an example
I looked up a random human HOX gene which was Homo sapiens homeobox A1 (HOXA1) found here:
Homo sapiens homeobox A1 (HOXA1), RefSeqGene on chromosome 7 - Nucleotide - NCBI
If you click on the BLAST search on the right it will do a similarity search. You will find that human HOXA1 differs from both chimp and orangutan HOXA1 at several sites. HOX genes are different between species.
Single point mutations are not new gene sequences.
Yes, they are. Mutations produce gene sequence that is not found in the ancestor. That is the very definition of mutation.

This message is a reply to:
 Message 217 by zaius137, posted 09-25-2012 2:08 AM zaius137 has replied

Replies to this message:
 Message 263 by zaius137, posted 10-01-2012 2:05 PM Taq has replied

  
zaius137
Member (Idle past 3409 days)
Posts: 407
Joined: 05-08-2012


Message 259 of 402 (674658)
10-01-2012 1:36 PM
Reply to: Message 255 by Tangle
10-01-2012 3:27 AM


Re: On topic news
Tangle,
So your contribution to this entire thread has been a sham. You've ruled out all changes as impossible before you even started.
I am not ruling out changes, but to what degree and the mechanism for them. As to the last part of the preceding sentence, science still lacks understanding.
Maybe my drift of this post is possibly all wrong. I thought there might be two sides to a debate. I am not contributing to the evolution view of new novel traits; although there are scientific arguments to make, (P.S. I have not found one that is convincing to me). Do you want me to debate myself? Seems a bit psychotic.
Now lets talk evidence.

This message is a reply to:
 Message 255 by Tangle, posted 10-01-2012 3:27 AM Tangle has replied

Replies to this message:
 Message 261 by Tangle, posted 10-01-2012 1:50 PM zaius137 has not replied
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Taq
Member
Posts: 9972
Joined: 03-06-2009
Member Rating: 5.5


Message 260 of 402 (674659)
10-01-2012 1:37 PM
Reply to: Message 254 by zaius137
10-01-2012 12:53 AM


Re: On topic news
Fins evolving into legs are complete and utter fantasy.
We are not asking if it is a fantasy or not. We are asking if it would be novel or not.

This message is a reply to:
 Message 254 by zaius137, posted 10-01-2012 12:53 AM zaius137 has not replied

  
Tangle
Member
Posts: 9489
From: UK
Joined: 10-07-2011
Member Rating: 4.9


(1)
Message 261 of 402 (674660)
10-01-2012 1:50 PM
Reply to: Message 259 by zaius137
10-01-2012 1:36 PM


Re: On topic news
zaius writes:
(P.S. I have not found one that is convincing to me).
As you've never found a definition of novel that convinces you, it's hardly likely that you ever will.
Now lets talk evidence.
We've done that; we have hard evidence - you just shrug and say it's either not novel or just an adaption. Which is both strange and stupid.

Life, don't talk to me about life - Marvin the Paranoid Android

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Taq
Member
Posts: 9972
Joined: 03-06-2009
Member Rating: 5.5


(1)
Message 262 of 402 (674663)
10-01-2012 2:01 PM
Reply to: Message 259 by zaius137
10-01-2012 1:36 PM


Re: On topic news
I am not ruling out changes, but to what degree and the mechanism for them. As to the last part of the preceding sentence, science still lacks understanding.
What does science not understand about mutations?
I thought there might be two sides to a debate. I am not contributing to the evolution view of new novel traits; although there are scientific arguments to make, (P.S. I have not found one that is convincing to me).
Whether a feature is novel has nothing to do with evolution. It is only a question of comparing descendants to ancestors. Once novel features are discovered, then we ask the question of how they could evolve. So far, you refuse to even participate in the first step, the identification of novel features. What you are pushing is a completely semantic argument that you use to deny the existence of novel features. That isn't an honest way to approach a discussion, which is why Tangle stated "So your contribution to this entire thread has been a sham". I think he is dead on.

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 Message 259 by zaius137, posted 10-01-2012 1:36 PM zaius137 has not replied

  
zaius137
Member (Idle past 3409 days)
Posts: 407
Joined: 05-08-2012


Message 263 of 402 (674664)
10-01-2012 2:05 PM
Reply to: Message 258 by Taq
10-01-2012 1:36 PM


Re: Really?
Taq,
By strict definition, the trait is not novel.
E. coli do not have recessive genes. The new phenotype came about through mutations.
Sorry, genes not expressed, not promoted, silent.
Yes, the new phenotype came about by mutations Your point is.
Aerobic transport of citrate did not occur previous to the mutations.
True, it was adapted to an aerobic condition.
There was nothing silent about it. The transporter was changed through mutation, and those mutations led to a new and novel phenotype.
The expression of that trait was silent it was promoted by a mutation. Please point out your interpretation of the following quotation.
quote:
The Cit+ trait originated in one clade by a tandem duplication that captured an aerobically expressed promoter for the expression of a previously silent citrate transporter. Genomic analysis of a key innovation in an experimental Escherichia coli population | Nature
I looked up a random human HOX gene which was Homo sapiens homeobox A1 (HOXA1) found here:
Homo sapiens homeobox A1 (HOXA1), RefSeqGene on chromosome 7 - Nucleotide - NCBI
If you click on the BLAST search on the right it will do a similarity search. You will find that human HOXA1 differs from both chimp and orangutan HOXA1 at several sites. HOX genes are different between species.
Your point is that we differ from the apes. I might answer yes and claim common descent is not scientifically viable.

This message is a reply to:
 Message 258 by Taq, posted 10-01-2012 1:36 PM Taq has replied

Replies to this message:
 Message 264 by Taq, posted 10-01-2012 2:34 PM zaius137 has replied
 Message 265 by Tangle, posted 10-01-2012 2:39 PM zaius137 has not replied
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Taq
Member
Posts: 9972
Joined: 03-06-2009
Member Rating: 5.5


(1)
Message 264 of 402 (674674)
10-01-2012 2:34 PM
Reply to: Message 263 by zaius137
10-01-2012 2:05 PM


Re: Really?
By strict definition, the trait is not novel.
Yes, it is. The ancestors did not have aerobic citrate transport. Now they do. That is a novel trait by definition.
Sorry, genes not expressed, not promoted, silent.
First it was a gene that did not exist beforehand. Second, the expression of the gene was a result of mutation, more specifically a DNA recombination event:
"It wasn’t a typical mutation at all, where just one base-pair, one letter, in the genome is changed, he said. Instead, part of the genome was copied so that two chunks of DNA were stitched together in a new way. One chunk encoded a protein to get citrate into the cell, and the other chunk caused that protein to be expressed."
http://news.msu.edu/.../evolution-is-as-complicated-as-1-2-3
So it would appear that novel features can evolve through DNA recombination events that result in brand new genes with brand new expression patterns. This result could only come about through mutation.
True, it was adapted to an aerobic condition.
That adaptation occurred through mutation followed by selection, otherwise known as evolution.
The expression of that trait was silent
Prior to the mutations, it did not have this trait so how could it be silent?
Your point is that we differ from the apes. I might answer yes and claim common descent is not scientifically viable.
The point is that HOX genes can differ without being detrimental which is what you were arguing against originally. You like to change your argument midstream, don't you?
I will also note that common descent through evolutionary mechanisms is testable by testing for a nested hierarchy. I guess you are unaware that evolution produces differences in lineages? It is strange that you are unaware of this in a thread that is discussing that very topic.

This message is a reply to:
 Message 263 by zaius137, posted 10-01-2012 2:05 PM zaius137 has replied

Replies to this message:
 Message 267 by zaius137, posted 10-01-2012 7:43 PM Taq has replied

  
Tangle
Member
Posts: 9489
From: UK
Joined: 10-07-2011
Member Rating: 4.9


(1)
Message 265 of 402 (674676)
10-01-2012 2:39 PM
Reply to: Message 263 by zaius137
10-01-2012 2:05 PM


Re: Really?
zaius writes:
By strict definition, the trait is not novel
That'll be the strict definition which you refuse to give. The definition which is within your gift and no-one else's. Useless.

Life, don't talk to me about life - Marvin the Paranoid Android

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Percy
Member
Posts: 22391
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


(2)
Message 266 of 402 (674683)
10-01-2012 3:13 PM
Reply to: Message 263 by zaius137
10-01-2012 2:05 PM


Re: Really?
zaius137 writes:
By strict definition, the trait is not novel.
The truth is that you're still stonewalling about providing a definition. You're being called out on it pretty regularly, I can't see how you could possibly believe you're fooling anyone. You're inventing your arbitrary criteria for novelty as you go along. If you're not interested in discussing how novelty evolves, if you're not even willing to discuss a definition of novelty, then perhaps you should find something else to do.
--Percy

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 Message 263 by zaius137, posted 10-01-2012 2:05 PM zaius137 has not replied

  
zaius137
Member (Idle past 3409 days)
Posts: 407
Joined: 05-08-2012


Message 267 of 402 (674692)
10-01-2012 7:43 PM
Reply to: Message 264 by Taq
10-01-2012 2:34 PM


Re: Really?
Taq,
First it was a gene that did not exist beforehand.
The sequence that tandem duplicated did exist beforehand and the Cit+ was promoted by that duplication. That is why Lenski said a previously silent transporter. Cit+ was already present in the three clades described in his experiment; the Cit+ promoter was captured by that duplication event. As I have stated before, long coding Sequences never appear by random chance. The difficulty exposed by probability opposes such a suggestion.
The Cit+ trait originated in one clade by a tandem duplication that captured an aerobically expressed promoter for the expression of a previously silent citrate transporter.
Second, the expression of the gene was a result of mutation, more specifically a DNA recombination event:
quote:
"It wasn’t a typical mutation at all, where just one base-pair, one letter, in the genome is changed, he said. Instead, part of the genome was copied so that two chunks of DNA were stitched together in a new way.
A quote from the Wiki:
quote:
Major genome duplication events can be quite common. Gene duplication - Wikipedia
I have no idea why Lenski would pose such a prevarication.
quote:
One chunk encoded a protein to get citrate into the cell, and the other chunk caused that protein to be expressed."
http://news.msu.edu/.../evolution-is-as-complicated-as-1-2-3
Looks like a single mutation event to me.

This message is a reply to:
 Message 264 by Taq, posted 10-01-2012 2:34 PM Taq has replied

Replies to this message:
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Meddle
Member (Idle past 1270 days)
Posts: 179
From: Scotland
Joined: 05-08-2006


(3)
Message 268 of 402 (674694)
10-01-2012 7:50 PM
Reply to: Message 221 by zaius137
09-26-2012 1:43 AM


Re: On topic news
You may be right when talking about heterozygosity in diploids but heterozygosity per capita is also expressible in general populations of bacteria. This is not strange to biology, as I understand it (I am not a biologist though). Here is an example study of such a usage.
I can see how it could be used in that way, however it is not the commonly used definition. There is a risk in non-biologists, not necessarily yourself but others reading this, in equivocating the heterozygosity of a bacterial population with the heterozygosity of an individual diploid organism.
The other reason the bacteria in this experiment should not be referred to as heterozygous is that all the bacteria originated from a single bacterial cell so are there was no genetic variation between or within populations.
In addition, you might note that the plasmid or plasmids within the E. coli retains its diversification per capita in a general population of E. coli. If you know if that was directly addressed by the Lenski experiment please elaborate (I would like additional information on this).
Here is the initial paper where Lenski described the establishment of his long term experiment.
As I mentioned above all subsequent populations originated from a single common ancestor of an E.coli B clone. This carried no plasmids, harboured no bacteriophages and was asexual so could not form pilli to exchange genetic material. In other words any changes seen in the cells are solely the result of mutations. This initial population was used to seed 12 daughter populations, 6 were arabinose negative and 6 were arabinose positive after a spontaneous mutation.
I believe you are building a straw man out of this E. coli as a species is identifiable. Although, no longer very reliably by its citrate uptake.
Well you did refer to morpholological stasis in E.coli showing lack of speciation, so I thought it worthwhile pointing out that morphology was just one aspect of defining a bacterial species. Citrate uptake is probably better defined as part of the phenotype.
As for E.coli being an identifiable species, it is not that straight forward. It has been found there is a great deal of variation amongst E.coli strains, in fact one comparison of 61 sequenced genomes showed only 20% homology. This study also indicated the related Genus Shigella should be classified as strains of E.coli, and conversely E.coli O157 is more closely related to Shigella than it is to other E.coli.
But this topic isn't about speciation, so I don't really want to carry on with this line of discussion. I just find it fascinating since I work in a hospital microbiology lab and we do hundreds of bacterial identifications on a daily basis.
If you read some of the citations, some gene block rearrangements provided the functionality (no new gene material spontaneously appeared). I would be curious to know if you accept that this new functionality was something other than an improvement upon existing genes (beneficial adaptation of an existing mechanism).
I have read the citations, and yes it does involve the manipulation of pre-existing genes, but I think you are paying too much attention to what the gene does and not enough on how it accomplished it. The rearrangements of the genome described in the citations are fairly significant with the potential of these changes inserting into an essential gene rather than next to a useful promoter region. What I find interesting is that the rearrangements described are similar to hypothesised rearrangements for the evolution of the bacterial flagellum which is usually referred to by creationists/IDists as impossible.
About the hox gene not being involved in limb development, I believe you need to be specific about which hox you are talking about. Generally global statements like yours are inevitably wrong.
As I said the hox genes define the layout of the segments in the developing embryo. This in turn affects which genes are expressed depending on which section they find themselves in. So genes that are involved in leg development will be expressed if they find themselves in the right section of the embryo. As an example, consider antennapedia in Drosophila. A mutation in a hox gene has caused legs to form in place of the antennae, because the mutation has caused those cells to think they are part of the thorax, so have expressed genes for structures found in the thorax.
From Message 231:
A transition from a hand to a fin (macroevolution) by what we understand and observe is scientifically impossible.
You keep on saying it is 'scientifically impossible' but don't say how. Look back to the image I posted in Message 228 showing the blob of cells destined to become a human hand and arm. We have identified the pattern of gene expression that accomplishes this, so we can see with a change in gene expression during development the controlled cell death between the digits may not happen and tissue can elongate to form a fin, just as you'd normally have elongation to form the arm. And all this is accomplished without any new genes or rearrangement of gene 'blocks', just adaptation of already established gene pathways.
Not even the studied cases of Fruit flies have ever shown to exhibit any form of macroevolution. In fact, no matter what selective pressure is applied to fruit flies they stubbornly stay fruit flies and only adapt. This statement also applies to E. coli and the evidence only confirms adaptation and not species modification.
All I will say to this is to point out that experiments involving fruit flies or E.coli as models to identify the functions of specific genes, not to induce speciation.
About the transition of humans to eating meat, that happened when Adam and Eve were expelled from the garden. Decidedly a significant event.
Sorry what?! I was sort of thinking of the transition to an omnivorous diet in terms of gene expression influencing development of the gastrointestinal tract.

This message is a reply to:
 Message 221 by zaius137, posted 09-26-2012 1:43 AM zaius137 has replied

Replies to this message:
 Message 270 by zaius137, posted 10-02-2012 2:56 AM Meddle has replied

  
Meddle
Member (Idle past 1270 days)
Posts: 179
From: Scotland
Joined: 05-08-2006


(1)
Message 269 of 402 (674704)
10-01-2012 11:04 PM
Reply to: Message 267 by zaius137
10-01-2012 7:43 PM


Re: Really?
The sequence that tandem duplicated did exist beforehand and the Cit+ was promoted by that duplication. That is why Lenski said a previously silent transporter. Cit+ was already present in the three clades described in his experiment; the Cit+ promoter was captured by that duplication event. As I have stated before, long coding Sequences never appear by random chance. The difficulty exposed by probability opposes such a suggestion.
The Cit+ trait originated in one clade by a tandem duplication that captured an aerobically expressed promoter for the expression of a previously silent citrate transporter.
You are correct that CitT was already present, and with the duplication of this gene created a second copy next to a promoter that would activate associated genes in the presence of oxygen. This occurred at 31,500 generations which coincides with the ability to uptake citrate albeit poorly, and subsequent duplications improved this effect. But this isn't the most interesting part. They resurrected earlier generations of the e.coli from frozen stores and inserted plasmids multiple duplicates of the new promoter-gene complex. What they found was that adding the plasmid the bacteria would evolve the ability to uptake citrate, but only after generation 20,000.
Therefore other mutations must have occurred at or before 20,000 generations to allow citrate uptake to later evolve, even although these earlier mutations did not have a direct effect on citrate uptake. I'm sure we'll see more on this research in the future.
Anyway you can read more about it in this arcticle that gives some more details about the research.
Edited by Malcolm, : No reason given.

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 Message 267 by zaius137, posted 10-01-2012 7:43 PM zaius137 has not replied

  
zaius137
Member (Idle past 3409 days)
Posts: 407
Joined: 05-08-2012


Message 270 of 402 (674712)
10-02-2012 2:56 AM
Reply to: Message 268 by Meddle
10-01-2012 7:50 PM


Re: On topic news
Malcolm.
Wonderful and thoughtful response my friend. You and your like are the entire reason I attend these forums.
I can see how it could be used in that way, however it is not the commonly used definition. There is a risk in non-biologists, not necessarily yourself but others reading this, in equivocating the heterozygosity of a bacterial population with the heterozygosity of an individual diploid organism.
The other reason the bacteria in this experiment should not be referred to as heterozygous is that all the bacteria originated from a single bacterial cell so are there was no genetic variation between or within populations.
I see your point. The tip at which I believe such a yardstick could be used would be when a population actually fixed a beneficial mutation. At that juncture, if SNP mutations were identified you might ask is there a tendency to reduce heterozygosity to zero at the SNPs flanking the selected site (indications of a classic sweep). So far, there has been no positive evidence I have run across. If there ever turned up such a case and it was unequivocal, it would strengthen the evolution argument immensely. Why I believe the evidence for a classic sweep in this case of E. coli is not likely, is because the findings in studies of fitness seem to level off in a consistent manor that parallels other observations of other organisms; not precluding sexual reproducing populations. Why I even attempt such a comparison is that there seems to be a limit to adaptive changes. The sexually reproducing populations face further challenges in beneficial mutational fixation adding to the uncertainty that a classic sweep is possible.
But this topic isn't about speciation, so I don't really want to carry on with this line of discussion. I just find it fascinating since I work in a hospital microbiology lab and we do hundreds of bacterial identifications on a daily basis.
In addition, I hope given the well-documented genome and well-known homology of E. coli variances you are very successful in identifying it. Of course, you must answer yes.
I have read the citations, and yes it does involve the manipulation of pre-existing genes, but I think you are paying too much attention to what the gene does and not enough on how it accomplished it. The rearrangements of the genome described in the citations are fairly significant with the potential of these changes inserting into an essential gene rather than next to a useful promoter region. What I find interesting is that the rearrangements described are similar to hypothesised rearrangements for the evolution of the bacterial flagellum which is usually referred to by creationists/IDists as impossible.
The entire matter of how a gene accomplices what it does is a matter of much investigation. This is where a programming background may yield some useful insight. As a programmer, I often used controlled random number generators to produce and enhance useful output. Take for example a learning program or a game. Now if these random numbers showed up in the wrong place the consequences would be disastrous. I view somatic hypermutation as a clear example of the use of controlled mutation and a similar mechanism should not be discounted as a possible mechanism in adaptation.
As I said the hox genes define the layout of the segments in the developing embryo.
I see the example you quoted and there is a lot going here In the case of digit placement and organization I can not see how you could claim that anything except massive changes to hox gene would work in defining a change from a fin to a hand. I still must refer to the newly discovered larger organization of the hox gene in determining things like digit morphological identity.
quote:
When the Hox code of the of the anlage of the chicken hind limb digit I is altered to match that of digit II, the resulting foot has two similar toes both resembling digit II in morphology. This suggests that the misexpressed gene, Hox-4.6, plays a role in controlling digit morphological identity. Other phenotypes observed in the proximal parts of the hind limb and in similar experiments in the wing also lend support to this interpretation. The role of Hox genes in limb development - PubMed
About a fin turning into a hand.
You keep on saying it is 'scientifically impossible' but don't say how.
I should say that all observable evidence says it is scientifically impossible. Given the experiments with E. coli and Fruit flies there is just not enough change in the genome to produce a comparative event. As I have gone threw before and I know I will probably get chastised for it New structures require new information they do not arise from SNPs. Small adaptive changes do not a limb make.
All I will say to this is to point out that experiments involving fruit flies or E.coli as models to identify the functions of specific genes, not to induce speciation.
I really would like to talk about this one but it defiantly does not fit into this thread. Let us see if we can maybe migrate to another applicable post.
Sorry what?! I was sort of thinking of the transition to an omnivorous diet in terms of gene expression influencing development of the gastrointestinal tract.
I gave the biblical accountIf you supplied an intense selective pressure to a sexually reproducing long generation organism there is not going to be a rapid fixation of this trait I imply the 630k year time frame parallel between humans and E. coli is insufficient.

This message is a reply to:
 Message 268 by Meddle, posted 10-01-2012 7:50 PM Meddle has replied

Replies to this message:
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