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Author Topic:   molecular genetic evidence for a multipurpose genome
derwood
Member (Idle past 1876 days)
Posts: 1457
Joined: 12-27-2001


Message 256 of 317 (22878)
11-15-2002 1:54 PM
Reply to: Message 249 by peter borger
11-14-2002 11:04 PM


quote:
Originally posted by peter borger:
dear Dr Page,
In reponse to:
quote:

What monkenstick said...
You are really out there...

This message is a reply to:
 Message 249 by peter borger, posted 11-14-2002 11:04 PM peter borger has replied

Replies to this message:
 Message 257 by peter borger, posted 11-15-2002 4:49 PM derwood has replied

  
peter borger
Member (Idle past 7666 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 257 of 317 (22887)
11-15-2002 4:49 PM
Reply to: Message 256 by derwood
11-15-2002 1:54 PM


Dear Dr Page,
In mail #10 (thread: molecular genetic proof against random mutations) you wrote:
I believe you have make an entirely unwarranted and somewhat bizarre extrapolation.
"a comparison between fixed and polymorphic sites between the two species shows also no significant deviation from the assumption of a neutral evolution in this region.
Apparently, you have never heard of the Neutral Theory?
MY RESPONSE:
From your response above it is immediately clear that it is YOU who apparently never heard of neutral theory since you attacked the authors of the paper (!!).
The sentence you quote above is a quote of Karl J. Schmid and Diethard Tautz in their paper A screen for fast evolving genes from Drosophila.
Your responses get sloppier and more inconsistent. If you have nothing to contribute to the discussion, why do you mail me this non-sense? It really puzzles me.
Best wishes,
Peter

This message is a reply to:
 Message 256 by derwood, posted 11-15-2002 1:54 PM derwood has replied

Replies to this message:
 Message 276 by derwood, posted 11-19-2002 9:05 AM peter borger has not replied

  
peter borger
Member (Idle past 7666 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 258 of 317 (22888)
11-15-2002 5:01 PM
Reply to: Message 251 by Mammuthus
11-15-2002 3:15 AM


Dear Mammuthus,
PB:However, if introns are not neutral --as Mammuthus claims, and I agree-- the major part of evolutionary papers on this topic can be considered useless.
M: Read what I said. I never said that introns are not neutral. I said that not every site in an intron is neutral. Did you ever learn anything about intron splicing?
PB: What sites (in addition to sensible sites involved in splicing) do you mean? How do you determine these sites? It is non-coding DNA, remember.
Best wishes,
Peter

This message is a reply to:
 Message 251 by Mammuthus, posted 11-15-2002 3:15 AM Mammuthus has replied

Replies to this message:
 Message 263 by Mammuthus, posted 11-17-2002 12:55 PM peter borger has replied

  
peter borger
Member (Idle past 7666 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 259 of 317 (22889)
11-15-2002 5:07 PM
Reply to: Message 237 by Itzpapalotl
11-14-2002 6:32 AM


Dear Itz,
I was not referring to sensible splicing sites. They are, of course, non-neutral, and we know how the sequences look like.
Best wishes,
Peter

This message is a reply to:
 Message 237 by Itzpapalotl, posted 11-14-2002 6:32 AM Itzpapalotl has not replied

  
Fred Williams
Member (Idle past 4856 days)
Posts: 310
From: Broomfield
Joined: 12-17-2001


Message 260 of 317 (22891)
11-15-2002 5:40 PM
Reply to: Message 253 by Mammuthus
11-15-2002 3:32 AM


quote:
You can continue to ignore the reality of what experiments have been done as you have persistently done on this board or you can actually learn about the subject and actually adopt an alternative to your ignorance is bliss tactic.
Proc Natl Acad Sci U S A 2001 Sep 25;98(20):11388-93 Related Articles, Links
Contribution of individual random mutations to genotype-by-environment interactions in Escherichia coli.
Remold SK, Lenski RE.
I looked at this paper, and this is hardly an example of new genetic information. It is pretty much no different than Mark’s nylon muncher. Here’s an important passage from your citation (emphasis mine):
First, the resource dependence could be caused by recent adaptation in response to the 10,000 generations of selection in minimal glucose medium. During this period of adaptation, fitness increased rapidly for the first 2,000 generations but more slowly thereafter (20). This fitness trajectory suggests that the population is nearing a fitness peak in glucose. Theoretically, the closer a genotype is to the peak, the smaller the number of possible mutations that can be beneficial (36). Moreover, in the absence of selection for performance on maltose, the progenitor may have lost fitness in the maltose environment, leaving more opportunities for improvement in maltose. As a result of both of these effects, more mutations should be beneficial in the un-selected maltose environment than in the glucose environment.
What does this all mean? The parent population was near a fitness peak in the glucose environment; in the maltose environment it was in a valley, having lost fitness. The subsequent experiments with the mutant strains only showed selection moving the maltose bacteria back up the maltose peak. There is clearly no new genetic information here.
Informed evolutionists who are aware of the information problem propose gene duplication followed by mutation as the mechanism of increasing information in the genome. Fine. Any observed examples? Scott tried "begging the question" by giving a hypoethetical, unobserved example that allegedly occurred millions of years ago, and then protested after his logic was exposed and declared it an impossible challenge. But if evolution is true, there should be plenty of observed examples of this in the literature. Why can’t you give me even one provocative example?
Evolution, the "impossible dream".

This message is a reply to:
 Message 253 by Mammuthus, posted 11-15-2002 3:32 AM Mammuthus has replied

Replies to this message:
 Message 261 by Itzpapalotl, posted 11-15-2002 6:45 PM Fred Williams has not replied
 Message 262 by Mammuthus, posted 11-17-2002 12:38 PM Fred Williams has not replied

  
Itzpapalotl
Inactive Member


Message 261 of 317 (22895)
11-15-2002 6:45 PM
Reply to: Message 260 by Fred Williams
11-15-2002 5:40 PM


Although the ancient examples are unobserved there is good evidence that they occured, do you disagree with the evidence for the duplications and what are your reasons for this?. The evidence could be inconclusive but that should also be possible show with reference to the evidence.
Your position that "gene duplication followed by mutation" does not happen is in direct conflict with Peter Borger's who used the strong evidence for selection on duplicated genes (a high rate of nonsynonymous mutations, clearly "gene duplication followed by mutation") as evidence for his multipurpose genome theory.

This message is a reply to:
 Message 260 by Fred Williams, posted 11-15-2002 5:40 PM Fred Williams has not replied

Replies to this message:
 Message 265 by peter borger, posted 11-17-2002 9:34 PM Itzpapalotl has replied
 Message 277 by derwood, posted 11-19-2002 9:07 AM Itzpapalotl has not replied

  
Mammuthus
Member (Idle past 6476 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 262 of 317 (22986)
11-17-2002 12:38 PM
Reply to: Message 260 by Fred Williams
11-15-2002 5:40 PM


FW:
I looked at this paper, and this is hardly an example of new genetic information. It is pretty much no different than Mark’s nylon muncher. Here’s an important passage from your citation (emphasis mine):
M: And you clearly did not read the entire paper nor the other paper I cited...your problem...not mine...or evolutions for that matter.
FW:
What does this all mean?
M: We know Fred...you have trouble understanding even the basics...
FW:
The parent population was near a fitness peak in the glucose environment; in the maltose environment it was in a valley, having lost fitness. The subsequent experiments with the mutant strains only showed selection moving the maltose bacteria back up the maltose peak. There is clearly no new genetic information here.
M: Oh, so they were magically shoved up the adaptive peak without selection for specific genotypes...LOL!
FW:
Informed evolutionists who are aware of the information problem propose gene duplication followed by mutation as the mechanism of increasing information in the genome.
M: What would an electrician part time keyboard player who knows nothing about biology know about what "informed" evolutionists propose?
FW:
Fine. Any observed examples? Scott tried "begging the question" by giving a hypoethetical, unobserved example that allegedly occurred millions of years ago, and then protested after his logic was exposed and declared it an impossible challenge. But if evolution is true, there should be plenty of observed examples of this in the literature. Why can’t you give me even one provocative example?
M: You have been given several but just deny them in your complete ignorance. And the two citations were just two of about 20 from one research group alone...so much for what you know about informed evolutionists.
FW:
Evolution, the "impossible dream"....impossible when one is to dense to understand even the basics.

This message is a reply to:
 Message 260 by Fred Williams, posted 11-15-2002 5:40 PM Fred Williams has not replied

  
Mammuthus
Member (Idle past 6476 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 263 of 317 (22991)
11-17-2002 12:55 PM
Reply to: Message 258 by peter borger
11-15-2002 5:01 PM


quote:
Originally posted by peter borger:
Dear Mammuthus,
PB:However, if introns are not neutral --as Mammuthus claims, and I agree-- the major part of evolutionary papers on this topic can be considered useless.
M: Read what I said. I never said that introns are not neutral. I said that not every site in an intron is neutral. Did you ever learn anything about intron splicing?
PB: What sites (in addition to sensible sites involved in splicing) do you mean? How do you determine these sites? It is non-coding DNA, remember.
Best wishes,
Peter

+++++++++++++++++++++++++
If you don't know how splicing works Peter then you are in more professional trouble than I realized and really need to take a basic biology class.
oh yeah...and what is an unsensible site? Are there coming to their senses sites as well

This message is a reply to:
 Message 258 by peter borger, posted 11-15-2002 5:01 PM peter borger has replied

Replies to this message:
 Message 264 by peter borger, posted 11-17-2002 5:19 PM Mammuthus has replied

  
peter borger
Member (Idle past 7666 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 264 of 317 (23007)
11-17-2002 5:19 PM
Reply to: Message 263 by Mammuthus
11-17-2002 12:55 PM


Dear Mammuthus,
You say:
If you don't know how splicing works Peter then you are in more professional trouble than I realized and really need to take a basic biology class.
oh yeah...and what is an unsensible site? Are there coming to their senses sites as well
I say:
As mentioned before sensible DNA sequences are sequences that have a function, for instance in splicing, gene regulation, stabilisiation of DNA and/or mRNA, etc. The fact that introns demonstrate conserved regions within species points in the direction of 'sensible sequences' involved in gene regulation. As a matter of fact, sometimes I have to invent a term to describe properly what is observed in the genome. Since 'sense-' and 'antisense sequences' already have a well defined meaning, I rather use 'sensible sequences' for DNA sequences that serve a function.
best wishes,
peter

This message is a reply to:
 Message 263 by Mammuthus, posted 11-17-2002 12:55 PM Mammuthus has replied

Replies to this message:
 Message 267 by Mammuthus, posted 11-18-2002 3:56 AM peter borger has replied

  
peter borger
Member (Idle past 7666 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 265 of 317 (23032)
11-17-2002 9:34 PM
Reply to: Message 261 by Itzpapalotl
11-15-2002 6:45 PM


Dear Itz,
You write:
Your position that "gene duplication followed by mutation" does not happen is in direct conflict with Peter Borger's who used the strong evidence for selection on duplicated genes (a high rate of nonsynonymous mutations, clearly "gene duplication followed by mutation") as evidence for his multipurpose genome theory.
My response:
Gene duplication is a observed phenomenon, so I do not dispute it. It is part of the MPG and accounts for rapid drug resistence after extreme selection constraints. The mechanism to duplicate genes is protein mediated. One often sees duplications in cancer cells in patients that become resistent to oncostatic drugs. In the case of extreme selection it can be expected that a counteracting protein is amplified in reponse to the drugs. In cancer cells usually membrane-associated pumps are amplified (mdr's/pgp's).
If (random) duplications played a role in evolutionism we would expect to find them in the genome as genetic redundancies. Thus --according to this scenario-- an association between duplications and genetic redundancies is expected to be found (=evolutionary prediction). However, genetic redundancies and duplications are NOT associated, so the prediction is falsified. In conlusion, duplications do not play a role in evolutionism. Similarly, it has been demonstrated that chromosomal duplications do not play a role in construction of (the human) genome(s) (Huges et al).
Unless strong selective constraints are present, duplications in bacteria are usually selected against (due to a increased DNA synthesis period; they become 'overgrown'). As stated in 'Molecular Biology of th gene' (Watson JD, et al, page 200, ISBN: 0-8053-9614-4): "The moment that such selective pressure is removed, the disadvantage of the unnecessary genetic duplication manifests itself. Then new variants [that is the wild type, nothing new here pb] are selected that eliminate the duplicated DNA through crossing over events [a protein mediated mechanism, pb]."
These actual facts and observations on microorganisms severely limit (bacterial) genome growth and thus evolutionism in general. I really wonder, do evolutionists ever read books on molecular biology?

This message is a reply to:
 Message 261 by Itzpapalotl, posted 11-15-2002 6:45 PM Itzpapalotl has replied

Replies to this message:
 Message 266 by Mammuthus, posted 11-18-2002 3:51 AM peter borger has not replied
 Message 268 by Itzpapalotl, posted 11-18-2002 7:50 AM peter borger has not replied

  
Mammuthus
Member (Idle past 6476 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 266 of 317 (23064)
11-18-2002 3:51 AM
Reply to: Message 265 by peter borger
11-17-2002 9:34 PM


PB:
Similarly, it has been demonstrated that chromosomal duplications do not play a role in construction of (the human) genome(s) (Huges et al).
To bad you are wrong
van Geel M, Eichler EE, Beck AF, Shan Z, Haaf T, van der Maarel SM, Frants RR, de Jong PJ. Related Articles, Links
A cascade of complex subtelomeric duplications during the evolution of the hominoid and Old World monkey genomes.
Am J Hum Genet. 2002 Jan;70(1):269-78.
PMID: 11731935 [PubMed - indexed for MEDLINE]
16: Hughes JF, Coffin JM. Related Articles, Links
Evidence for genomic rearrangements mediated by human endogenous retroviruses during primate evolution.
Nat Genet. 2001 Dec;29(4):487-9.
PB:
These actual facts and observations on microorganisms severely limit (bacterial) genome growth and thus evolutionism in general. I really wonder, do evolutionists ever read books on molecular biology?
M: One has to wonder if you ever have......

This message is a reply to:
 Message 265 by peter borger, posted 11-17-2002 9:34 PM peter borger has not replied

  
Mammuthus
Member (Idle past 6476 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 267 of 317 (23065)
11-18-2002 3:56 AM
Reply to: Message 264 by peter borger
11-17-2002 5:19 PM


PB:
As mentioned before sensible DNA sequences are sequences that have a function, for instance in splicing, gene regulation, stabilisiation of DNA and/or mRNA, etc. The fact that introns demonstrate conserved regions within species points in the direction of 'sensible sequences' involved in gene regulation.
M: Funny, earlier your debate tactic was to say no site was neutral because nobody had excluded a function for every single base pair in the genome..now you are backpedalling.
PB:
As a matter of fact, sometimes I have to invent a term to describe properly what is observed in the genome.
M: You would not have to if you read primary literature..or even textbooks to find out what the sequences are actually called..but if it massages your ego to make up a language to explain long known phenomenon..knock yourself out..
PB:
Since 'sense-' and 'antisense sequences' already have a well defined meaning, I rather use 'sensible sequences' for DNA sequences that serve a function.
M: Which is completely non-descriptive as it does not specificy or even suggest what the function is...and it sounds like a fashion statement like sensible shoes. Or maybe you are advocating sensible shoes in the lab

This message is a reply to:
 Message 264 by peter borger, posted 11-17-2002 5:19 PM peter borger has replied

Replies to this message:
 Message 272 by peter borger, posted 11-18-2002 9:48 PM Mammuthus has replied

  
Itzpapalotl
Inactive Member


Message 268 of 317 (23083)
11-18-2002 7:50 AM
Reply to: Message 265 by peter borger
11-17-2002 9:34 PM


hi Peter B.
I was not saying you believed any specific gene had arisen through duplication just that you were aware of the large amount of research that indicates a high rate of nonsynonymous compared to synonymous mutations in duplicated genes (Kondrashov et al), something which Fred Williams claimed doesn't happen ("gene duplication followed by mutation"). I realise that you are with Fred in beleiving that duplications do not play a role in evolution beyond short term environmental response.
It is clear that the majority of gene duplications are manitained as a transient response to environmental pressures (Kondrashov et al) so when the pressure is removed so is the duplication. But with regards to the antifreeze example the fish still live in cold water so the selective pressure has continued for a long time and continues today and so does the altered duplicated gene. I do not see how an expectation that random duplications are important in evolution must mean they play a role in genetic redundancies. It predicts that duplications occur at random and those that confer a selective advantage are preserved. Again referring back to the fish antifreeze gene just because it was formed from a dulication of the trypsinogen gene does not mean trypsinogen is now redundant nor would there be any expectation of redundancy. A prediction of non random duplication though is that when subject to a particular toxin for example the gene duplication that gives resistance to that toxin should occur at a higher frequency in a population than other duplications, does this happen?. Also more importantly is it an actual prediction of the MPGenome theory, because i wouldn't want to propose a test based on what i assume about MPG rather than what it actually says.
with regards to gene duplication and human evolution this might be of interest:
"An estimated 5% of the human genome consists of interspersed duplications that have arisen over the past 35 million years of evolution. Two categories of such recently duplicated segments can be distinguished: segmental duplications between nonhomologous chromosomes (transchromosomal duplications) and duplications mainly restricted to a particular chromosome (chromosome-specific duplications).Many of these duplications exhibit an extraordinarily high degree of sequence identity at the nucleotide level (>95%)
and span large genomic distances (1—100 kb). Preliminary analyses indicate that these same regions are targets for rapid evolutionary turnover among the genomes of closely related primates. The dynamic nature of these regions because of recurrent chromosomal rearrangement, and their ability to create fusion genes from juxtaposed cassettes suggest that duplicative transposition
was an important force in the evolution of our genome."
Evan E. Eichler. Recent duplication, domain accretion and the dynamic mutation of the human genome. TRENDS in Genetics Vol.17 No.11 November 2001.
F. A. Kondrashov, I. B. Rogozin, Y. I. Wolf, and E. V. Koonin. Selection in the evolution of gene duplications. Genome Biol. 3 (2):RESEARCH0008, 2002.

This message is a reply to:
 Message 265 by peter borger, posted 11-17-2002 9:34 PM peter borger has not replied

Replies to this message:
 Message 269 by Fred Williams, posted 11-18-2002 12:43 PM Itzpapalotl has replied

  
Fred Williams
Member (Idle past 4856 days)
Posts: 310
From: Broomfield
Joined: 12-17-2001


Message 269 of 317 (23101)
11-18-2002 12:43 PM
Reply to: Message 268 by Itzpapalotl
11-18-2002 7:50 AM


quote:
I was not saying you believed any specific gene had arisen through duplication just that you were aware of the large amount of research that indicates a high rate of nonsynonymous compared to synonymous mutations in duplicated genes (Kondrashov et al), something which Fred Williams claimed doesn't happen ("gene duplication followed by mutation").
I never said "gene duplication followed by mutation" doesn't happen. What I did say is that there are no observed examples of "gene duplication followed by mutation" that represent an increase in genetic information. Observed examples often show loss of information since they are associated with some disease.
The only examples given for new, useful genetic information for a species (see Page, Mamuthus) are speculative events that allegedly happened millions of years ago. In other words, there is no evidence for increased genetic information - it's all speculation.

This message is a reply to:
 Message 268 by Itzpapalotl, posted 11-18-2002 7:50 AM Itzpapalotl has replied

Replies to this message:
 Message 270 by Itzpapalotl, posted 11-18-2002 1:41 PM Fred Williams has replied
 Message 278 by derwood, posted 11-19-2002 9:16 AM Fred Williams has not replied
 Message 291 by derwood, posted 11-21-2002 9:16 PM Fred Williams has not replied

  
Itzpapalotl
Inactive Member


Message 270 of 317 (23109)
11-18-2002 1:41 PM
Reply to: Message 269 by Fred Williams
11-18-2002 12:43 PM


Hi Fred
I am sorry if i misrepresented your position, i though you denied just gene duplication was a gain of information (two copies of the same book) so therefore if there was positive selection for a particular function after duplication that would represent a gain in information as the duplicated gene would no longer be the same as the original. Would it be a gain of information if the duplicated gene had a different role from the original gene?. For example supposing the antifreeze gene was formed from a duplicated trypsinogen gene as the evidence suggests would that fit your definition of an increase in information?.
The examples are not just speculation but based on clear evidence, what conclusions would you draw from the evidence and how are the conclusion of the authors of the papers wrong?.

This message is a reply to:
 Message 269 by Fred Williams, posted 11-18-2002 12:43 PM Fred Williams has replied

Replies to this message:
 Message 271 by Fred Williams, posted 11-18-2002 7:10 PM Itzpapalotl has not replied

  
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