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Author Topic:   molecular genetic proof against random mutation (1)
Percy
Member
Posts: 22503
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.9


Message 12 of 274 (13498)
07-14-2002 3:09 PM
Reply to: Message 1 by peter borger
07-11-2002 10:27 PM


A link to the paper and to the figure you reference have been added to your original post by the Admin, making it easier to actually comment on the contents of your post.
peter borger writes:

After reading Spetner's book I realised that all it would take to overthrow NDT is molecular genetic evidence against the mechanisms of random mutation...
That mistakes occur in transmitting the genetic code from one generation to the next has been established beyond any reasonable doubt.

Scientifically speaking, we need only one example that is not in accord with NDT. It would question the validity of the concepts.
It would only "question the validity of the concepts" if it were a mechanism contradicting NDT, not merely missing from it.

The first paper I like to discuss with evolutionists is the paper by Schmid and Tautz published in a leading scientific journal (Schmid and K.J. and Tautz, D. A screen for fast evolving genes from Drosophila. Proceeding of the National Academy of Science USA 1997, Volume 94: p9746-9750.).
You draw conclusions from this paper in areas unrelated to the issues it addresses. Certainly the authors wouldn't agree with you.

It should be noted that evolutionists simply add all polymorphisms of the two species of Drosophila, and than they treat them as one species. In other words they compare apples with pears!
If you're talking about the figure, the authors do not add the polymorphisms together, they merely present them in the same table for comparison. Since the two species share a recent common ancestor, genetic similaries are expected, and the table shows this. If the two species were really as different as apples and algae (I can't use your analogy of apples and pears, since they, too, share a recent common ancestor) then they wouldn't even share this 1G5 gene.

They also discriminate between non-fixed (polymorphic) and fixed base substitutions. Obviously, fixed base substitutions are not taken into account. As a result, this biased comparison of distinct species does not say anything about the rate of evolution within one species. All it demonstrates is the difference between two homologous DNA regions of two distinct organisms.
And this is why you shouldn't attempt to draw conclusions outside the specific topic of paper. As the title of the paper clearly states, there were developing a screening technique for identifying fast evolving genes within the Drosophila genome. Their technique evidently requires ignoring base substitutions. You can't draw conclusions about the consistency of the Drosophila genome with mutational theory from this paper.

Similarly, introns in the 1G5 gene found in the subpopulations of D. simulans do not demonstrate variation at all. This is a very peculiar phenomenon, since the theory of neutral evolution says that the highest incidence of mutations is within the intron regions of a gene. It is assumed that intron regions are not subject to selection, and are able to mutate at random. This is not only expected between species, but also within subpopulations of one species. Yet, we do not see variation within the introns of subpopulations!
First, while introns are not expressed in the organisms phenotype, there are still clear limits on permissible mutations. In particular, they have to remain recognizable as introns else they may result in expression, which would be equivilent to a massive multi-nucleotide polymorphism and probably catastrophic to the organism.
Second, and orthogonal to the first point, with a data set of two introns your conclusions have practically zero statistical significance. The authors conclusions are inconclusive for the same reasons. Replication of this process by other scientists using other genes must be performed before, over time and only if congruent results are obtained, the author's results can become generally accepted.

In addition, have a close look at the positions of the mutations in the introns between the species. The intron exhibits 13 mutations; 10 out of 13 are immediately adjacent to each other (numbers 153-162). The chance that 10 mutations occur at random within an intron of 61 units equals 1.4 x 10(exp)-18. In contrast, the chance that a cluster of 10 adjacent mutations occur in the intron equals 2.2 x 10(exp)-14. Therefore, it is reasonable to assume that the cluster of mutations observed in the introns did not arise by a random mechanism. This is a very important observation, since it is molecular evidence evidence against random mutation. It is, of course, neither mentioned in the text nor discussed!
First, and as already mentioned, there are still clear limits on permissible mutations within introns.
Second, it's not mentioned in the paper because it isn't relevant to their goal of identifying a screen for fast evolving genes.

Another remarkable observation is that the 1G5 genes in subpopulations of D. melanogaster, as far apart as Australia, Russia or Canada are completely identical.
But don't forget the relatively local differences, such as between populations in Australia, and between populations in the US. Without speculating as to possible reasons, it doesn't seem like either simple migration or Noah's Ark account for it very well.

Over millions of years only a fraction of variation has been generated within subpopulations of Drosophila melanogaster in the so-called ‘very unstable’ 1G5 gene. In sharp contrast, a lot of variation is observed between the two species.
Uh, nothing else would make sense. Naturally there are fewer genetic differences within a species than between species.

Why does the 1G5 gene within a species stay nearly stable over time, whereas the same genes are highly variable within distinct sibling species?
The paper is about identifying fast evolving genes, and 1G5 was chosen because it is precisely that, a fast evolving gene. As they state in the introduction, the fast evolving genes were identified by comparison with Drosophila virilis, which is thought to have diverged with Drosophila melanogaster some 40-60 million years ago. They then compare the IG5 gene of Drosophila melanogaster with Drosophila yakuba, divergence thought to be 10-15 million years ago, in order to test their hypothesis that "under a neutral model of molecular evolution that a gene that shows a high divergence rate between species should also be polymorphic within a species."
In other words, the identification of fast evolving genes does not derive from the data in Figure 1. If you're trying to figure out how they identified fast evolving genes from this data you are doomed to failure because this is not the data they used. As far as I could tell, they don't actually present this data in the paper.
These misinterpretations suggest that a reassessment of your conclusion that the Drosophila genome is "completely stable" might be appropriate.

It should also be realised that only approximately 30% of the D. melanogaster genome is polymorph and only 11 % is heterozygous. These percentages speak for themselves: the major part of Drosophila genes does not vary at all! They are completely stable!
Uh, without rate information the percentages mean nothing, and certainly 30% polymorph implies considerable variability for which you need some kind of source.
--Percy

This message is a reply to:
 Message 1 by peter borger, posted 07-11-2002 10:27 PM peter borger has replied

Replies to this message:
 Message 13 by peter borger, posted 07-14-2002 9:46 PM Percy has replied

Percy
Member
Posts: 22503
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.9


Message 14 of 274 (13529)
07-15-2002 12:01 AM
Reply to: Message 13 by peter borger
07-14-2002 9:46 PM


peter borger writes:

Thanks for you response, but I am not impressed by your rebuttal.
Charmed, I'm sure!

Could you point out where exactly you rebut my observation of "non-randomness of mutations in the 1G5 gene" in the above sentence?
You're referring to the continguous set of nucleotide differences in the intron of 1G5? If so, you made a lot of points, and I addressed a lot of points. Is this one you feel is key?
The possibility I mentioned previously was that you don't know what the requirements of the intron are. There may be limitations on where changes can be made in the intron without causing disruption of its very behavior as an intron.
There are of course other possibilities. Heads *can* come up ten times in a row. The substitution may have been a single, large replication error. I'm sure there are other possibilities. You can't conclude non-randomness from the data available. This was not a topic the paper even remotely addressed, you're just using it to mine data.
It appeared to me that your primary claim was that the 1G5 gene exhibited relative stability between Drosophila melanogaster with Drosophila yakuba, when in reality the paper used that gene because it exhibited fast evolution when Drosophila melanogaster and Drosophila virilis were compared. The data for that comparison isn't present in the paper.
--Percy

This message is a reply to:
 Message 13 by peter borger, posted 07-14-2002 9:46 PM peter borger has replied

Replies to this message:
 Message 16 by peter borger, posted 07-15-2002 12:28 AM Percy has replied

Percy
Member
Posts: 22503
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.9


Message 19 of 274 (13555)
07-15-2002 11:05 AM
Reply to: Message 16 by peter borger
07-15-2002 12:28 AM


You believe that the sequence of ten differing nucleotides within the intron of the 1g5 gene in Drosophila melanogaster and Drosophila yakuba could not have arisen randomly. I offered several possible random sources, but that doesn't mean you are wrong, only that you were leaving out some possibilities.
Perhaps some non-random sources *are* responsible. What do you think they could be?
--Percy

This message is a reply to:
 Message 16 by peter borger, posted 07-15-2002 12:28 AM peter borger has replied

Replies to this message:
 Message 21 by peter borger, posted 07-16-2002 4:07 AM Percy has replied

Percy
Member
Posts: 22503
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.9


Message 23 of 274 (13625)
07-16-2002 10:30 AM
Reply to: Message 21 by peter borger
07-16-2002 4:07 AM


peter borger writes:

I have the impression that you avoid my question.
Sorry, Peter, didn't mean to seem like I was ignoring your question, but it was *you* who assigned me the viewpoint of neutral selection, not me. Neutral selection isn't a possibility I would have considered. If you want to make "answer my question" demands, then me first, you addressed almost none of the points in my first post.
Your opening post claimed proof against random mutation in the form of consecutive nucleotide differences in the intron of the 1G5 gene of two closely related Drosophila species. I've pointed out the statistical insignificance of small data sets, suggested possible sources, at least one of which was non-random, and in my previous post I granted that perhaps the source *was* non-random, and inquired what you thought the possible sources might be.
There's something about the paper that I wasn't able to figure out, and maybe you know the answer. Table 3 has a AF005851 link for the MEL-1G5 gene. I expected it to contain the full base sequence for the 1G5 gene, but it doesn't come close to matching the sequence segments from Figure 1. Do you know what the sequence represents?
--Percy

This message is a reply to:
 Message 21 by peter borger, posted 07-16-2002 4:07 AM peter borger has replied

Replies to this message:
 Message 30 by peter borger, posted 07-16-2002 8:25 PM Percy has replied

Percy
Member
Posts: 22503
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.9


Message 31 of 274 (13680)
07-16-2002 10:11 PM
Reply to: Message 30 by peter borger
07-16-2002 8:25 PM


What'd I say, what'd I say!! (so I can remember for next time -
)
--Percy

This message is a reply to:
 Message 30 by peter borger, posted 07-16-2002 8:25 PM peter borger has not replied

Replies to this message:
 Message 33 by wj, posted 07-16-2002 11:28 PM Percy has not replied

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