molecular genetic evidence for a multipurpose genome

Case in point:PB:
"I didn't forget about this reference. I read it last weekend and the content of the article simply doesn't rebut my observation that the ZFX gene is completely stable during '20 million' years. That there are genetic elements jumping around in the genome and accumulate on the X chromosome in this region is in accord with the vision of a multipurpose genome where variation is induced by such elements, not by accumulation of SNPs or other mutations. These jumping elements affect gene expression and thus induce phenotypic variations."As mam has pointed out, THE GENE is NOT stable over that period.You then just ramble on and on about how there are no mutations at neutral sites blah blah blah....Ignoring evidence doesnot mean that it is not there.No wonder professionals tend not to respond to your hysterical diatribes...[This message has been edited by SLPx, 10-30-2002]

dear Dr Page,And these observations are all in accord with a multipurpose genome and not in accord with evolutionism. You are, of course, free to deny that.best wishes,
Peter

dear Quetzal,Before I respond to your comments (next week), I recommend you to reread my hypothesis in letter #1, since I have the feeling that either you didn't read it, or you didn't understand it. Either way, a better understanding of what I wrote in this letter would improve the discussion. Also, I recommend you to read dr J. Davison's essays in Syamsu's mailing #7. Maybe, you get a better feeling what is wrong with evolutionism, since you are still under the impression that it can explain all biological phenomena. But it can't, as once more demonstrated in his papers. They have been published in peer reviewed journals, so it must be science, isn't it? Finally I recommend you to read on somatic mutations, how the are expected to disperse in copicing plants and to read a book on molecular mechanism of evolutionism, including neutral evolution. I have the feeling that you can use a course. In the meantime I will read recent books on population-genetics and have a look whether they are up to date with molecular biology. My guess at this moment: they aren't.best wishes,
Peter

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Originally posted by peter borger:
dear Quetzal,

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Before I respond to your comments (next week), I recommend you to reread my hypothesis in letter #1, since I have the feeling that either you didn't read it, or you didn't understand it. Either way, a better understanding of what I wrote in this letter would improve the discussion. Also, I recommend you to read dr J. Davison's essays in Syamsu's mailing #7. Maybe, you get a better feeling what is wrong with evolutionism, since you are still under the impression that it can explain all biological phenomena. But it can't, as once more demonstrated in his papers. They have been published in peer reviewed journals, so it must be science, isn't it? Finally I recommend you to read on somatic mutations, how the are expected to disperse in copicing plants and to read a book on molecular mechanism of evolutionism, including neutral evolution. I have the feeling that you can use a course. In the meantime I will read recent books on population-genetics and have a look whether they are up to date with molecular biology. My guess at this moment: they aren't.

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best wishes,
Peter

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You mean there's actually something in that ill-connected diatribe that I (or Mammuthus) haven't already refuted? Will wonders never cease...As far a somatic mutations go - I'm sure since you're obviously so knowledgeable on the subject you can recommend a few articles, books or research that I should look at. Unfortunately, I'm limited to peer-reviewed journals for my information. For example, I'm forced to rely on articles such as Reproductive systems and evolution in vascular plants, which includes a fascinating look at the expected differences in sexual vs asexual plant populations. It discusses somatic mutations in relation to differences in progeny of selfed organisms, for instance. (I'd like to point out once again that neither Peakall nor Hanson checked somatic mutations, only 18s, and rbcl loci, and only a limited number of those.) Perhaps you could educate me on the subject.I'll reread the Davison essays as you suggest - I only skimmed them the first time around. However, that is a substantial red herring which won't get you out of responding substantively to my refutation of your last few posts. If you wish to discuss them specifically, I suggest starting another thread.Essentially, your use of Wollemia as prima facie evidence of the validity of your "theory" in your OP on this thread has been shown to be completely erroneous. I don't have to refute every sentence you wrote in the OP, as the only evidence you've presented has been decisively shown to be bogus.I'll look forward to your discussion of pop gen once you get a chance to read up on the subject. I'll be especially interested in hearing how pop gen and molecular biology are incompatible.

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I have the feeling that you can use a course.

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arrogant fool

PB to Quetzal:Finally I recommend you to read on somatic mutations, how the are expected to disperse in copicing plants and to read a book on molecular mechanism of evolutionism, including neutral evolution.M: I have repeatedly seen you expose your own ignorance of evolution and population genetics on this board. It is highly hypocritical of you to claim Quetzal needs further education on the subject when you steadfastly refuse to inform yourself. Quetzal has repeatedly rebutted your posts at a much higher level of scientific discourse than you have provided so I do not see that HE has to bone up on his molecular biology but rather you do. I find the tactic you are using of avoiding his (and several of my) posts by claiming he does not have the requisite background for this debate lame...it suggests you cannot counter Quetzal's posts so would rather attack him personally.PB:
I have the feeling that you can use a course. In the meantime I will read recent books on population-genetics and have a look whether they are up to date with molecular biology. My guess at this moment: they aren't.M: I have repeatedly recommended Hartl and Clark as a starting point for you. I am glad you at least are stating here that you intend to do some reading. Happy reading cheers
M

Dear Dr Page,You say:
As mam has pointed out, THE GENE is NOT stable over that period.I say:
The gene is regulated differently in different organisms and may be affected by the insertion of the DNA elements Mammuthus described.
It doesn't rebut the observation of Dr Kim et al that the presented sequence of the ZFX gene is stable over 20 million years. This sequence simply stands as a falsification of evolutionism.You then just ramble on and on about how there are no mutations at neutral sites blah blah blah....I say:
Please Dr Page grow up and face the facts. I haven't had a rebuttal from you, neither from Mammuthus on this specific topic. Mammuthus tried to feed me a red herring with his jumping DNA elements in ZFX region, but it was about Dr Kims article, remember. I can see right through these fallacies.You say:
Ignoring evidence doesnot mean that it is not there.I say:
Ignoring evidence is exactly what you do now for about three months. Better respond to the LCR16a gene, the IL-1beta incongruence. They are still unsolved and you 'promissed' to solve the problems for evolutionism.You say:
No wonder professionals tend not to respond to your hysterical diatribes...My response:
1) the letter I wrote was a very neat letter, I was disappointed that I didn't get a response,
2) now you are here you have an excellent opportunity to help me out with the alpha-actinin genes. Notably, you are the evolutionary biologist of this site.
3) apparently you are not a professional, since you keep responding to my 'hysterical diatribes'.Thanks in advance, and best wishes,
Peter

PB:
Please Dr Page grow up and face the facts. I haven't had a rebuttal from you, neither from Mammuthus on this specific topic. Mammuthus tried to feed me a red herring with his jumping DNA elements in ZFX region, but it was about Dr Kims article, remember. I can see right through these fallacies.M: And your fallacy is to ignore that the Erlandsson Wilson and Paabo study which compared the relative amounts of SUBSTITUTIONS not just transposition events in the ZFX and ZFY regions....so it is hardly a red herring but rather your selectively ignoring the evidence that refutes your hypothesis.

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Mammuthus: They [cheetahs] have niether poor genetic content nor have they lost genetic information. They have reduced allelic variation in the population i.e. cheetah's almost monomorphic.

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LOL! This is utter nonsense. Your two sentences are a contradiction. Maybe a citation you used earlier the same day will help:An empirical genetic assessment of the severity of the northern elephant seal population bottleneck.
Weber DS, Stewart BS, Garza JC, Lehman N.
Department of Biological Sciences, University at Albany, State University of New York, 12222, USA.A bottleneck in population size of a species is often correlated with a sharp reduction in genetic variation.Do you believe no genetic information is lost after a bottleneck occurs? Why in the world would there be less genetic variation? Perhaps you deny the cheetah is the result of a bottleneck? If so, why are they almost monomorphic?I really hope you admit your silly observation was flat wrong and move on.

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Originally posted by peter borger:
dear Dr Page,

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And these observations are all in accord with a multipurpose genome and not in accord with evolutionism. You are, of course, free to deny that.

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best wishes,
Peter

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And so you keep repeating.You never did explain why there must be mutations in that one exon under NDT.You never did comment on the alignment that I took the time to make for you.I doubt you even looked at it.I think I know why, of course, but I would like to give you the opportunity to explain this spate of blinder-wearing.

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Originally posted by Fred Williams:

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Mammuthus: They [cheetahs] have niether poor genetic content nor have they lost genetic information. They have reduced allelic variation in the population i.e. cheetah's almost monomorphic.

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LOL! This is utter nonsense. Your two sentences are a contradiction. Maybe a citation you used earlier the same day will help:

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An empirical genetic assessment of the severity of the northern elephant seal population bottleneck.
Weber DS, Stewart BS, Garza JC, Lehman N.
Department of Biological Sciences, University at Albany, State University of New York, 12222, USA.

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A bottleneck in population size of a species is often correlated with a sharp reduction in genetic variation.

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Do you believe no genetic information is lost after a bottleneck occurs? Why in the world would there be less genetic variation? Perhaps you deny the cheetah is the result of a bottleneck? If so, why are they almost monomorphic?

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I really hope you admit your silly observation was flat wrong and move on.

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Ahh - the semantics queen strikes!Here's a poser for an information theory expert.What impact on 'information' occurs in the following scenarios:1) An insertion (mutation) ina gene results in an increase in gene exppression. The product is not altered, there is just more of it. This increase in product confers pesticide resistence.2) A gene duplication results in a modified phenotype.Is the 'information' in the above situations increased, decreased, or the same?If the information remains the same or decreases, how does one explain the acquired phenotypic changes?In any event, what is the relationship between "information" and phenotype?A precise definition of information will be necessary to address these issues. The definiiton will need to be legitimate, applicable to biological systems (genomes), and accepted by those in the field.Lacking such a definition of 'information' will be indicative that the presenter is simply engaging in just-so story telling.

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Originally posted by peter borger:
Dear Dr Page,

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You say:
As mam has pointed out, THE GENE is NOT stable over that period.

​

I say:
The gene is regulated differently in different organisms and may be affected by the insertion of the DNA elements Mammuthus described.
It doesn't rebut the observation of Dr Kim et al that the presented sequence of the ZFX gene is stable over 20 million years. This sequence simply stands as a falsification of evolutionism.

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I did not realize that Kim's group had sequenced the entire gene. Perhapos it is in a different publication - other than the one you cited - and one for which the DNA sequences are not yet available?Because, you see, the Kim et al. paper you cite refers only to one exon, and the nucleotide links from the paper only produce DNA sequence data for the region for which I made an alignment (and you deigned not to even look at).
Please supply the citation or the GENBANK numbers for the DNA sequences for the entire ZFX gene. I would most like to see them and analyze them for myself.

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You then just ramble on and on about how there are no mutations at neutral sites blah blah blah....

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I say:
Please Dr Page grow up and face the facts. I haven't had a rebuttal from you, neither from Mammuthus on this specific topic. Mammuthus tried to feed me a red herring with his jumping DNA elements in ZFX region, but it was about Dr Kims article, remember. I can see right through these fallacies.

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I'm sure you can, being a creatonist and all.However, I most certainly did face the facts, and unlike you, Peter, I seem to be able to understand them. The only fallacy I see is the continued reference to the ZFX "GENE" being stable for 20 million years. I already presented you with 'my math' demonstating why chance alone can account for why there are no substitutions in the referred to 300+ bp locus. You simply ignored it and continued on with your mantra.Mantra spewing is a common creationist characteristic. Sad.

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You say:
Ignoring evidence doesnot mean that it is not there.

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I say:
Ignoring evidence is exactly what you do now for about three months. Better respond to the LCR16a gene, the IL-1beta incongruence. They are still unsolved and you 'promissed' to solve the problems for evolutionism.

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There is no gene in an LCR as you have already 'admitted'. I have been unable to find your reference to such a paper describing a gene in an LCR. Searching Medline for "LCR16a" produced only the paper I already cited, and it mentioned nothing of genes.
I have also been unable to find your specific reference for the paper you believe props up your claims re: IL-beta 1. One would thnk that since these are such linchpiuns for your falsification of NDT that you would gleefully cite them at every request.

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You say:
No wonder professionals tend not to respond to your hysterical diatribes...

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My response:
1) the letter I wrote was a very neat letter, I was disappointed that I didn't get a response,

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The recipient probably saw through the facade...

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2) now you are here you have an excellent opportunity to help me out with the alpha-actinin genes. Notably, you are the evolutionary biologist of this site.

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What about them?

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3) apparently you are not a professional, since you keep responding to my 'hysterical diatribes'.

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This is a discussionboard. Were you to write an 'official' email or letter to me prattling on about these 'unanswered questions' and 'anomolies' and such I probably would not respond, either.
While it is true that research for me is on a back burner these days, I do still consider myself a 'professional' in that I have the requisite background education, experience, and pertinent publications. I would not even consider proclaiming some other field of science 'unscientific' or to have 'falsified' something that I am clearly unable to comprehend sufficiently.

dear Dr Page,Everyone can see now that discussions with you do not lead anywhere, since you are unable to answer, or you distort my words and answer to that. Why, I wonder? To keep the hype alive? Of course! However, I know --and I demonstrated it several times and I can do it over and over again-- that the hype has fallen en will never stand again. Molecular biology is not in accord with the hype. Conclusion, there is no evolution and there has never been evolution. Get used to this new worldview, it will help you survive.Best wishes,
Peter

Dear Dr Page:Your definition of a gene:"Eukaryotic gene: a sequence of DNA that encodes one (or more) protein produts. consists of intronic (non-protein encoding) and exonic (protein encoding) portions. exons and introns are of variable lengths and number."My comments:
No regulatory sequences included for expression? What is a gene that cannot be expressed? A junk gene?Sounds to me as a very oldfashioned definition.Best Wishes
Peter

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Originally posted by Fred Williams:

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Mammuthus: They [cheetahs] have niether poor genetic content nor have they lost genetic information. They have reduced allelic variation in the population i.e. cheetah's almost monomorphic.

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LOL! This is utter nonsense. Your two sentences are a contradiction. Maybe a citation you used earlier the same day will help:

​

An empirical genetic assessment of the severity of the northern elephant seal population bottleneck.
Weber DS, Stewart BS, Garza JC, Lehman N.
Department of Biological Sciences, University at Albany, State University of New York, 12222, USA.

​

A bottleneck in population size of a species is often correlated with a sharp reduction in genetic variation.

​

Do you believe no genetic information is lost after a bottleneck occurs? Why in the world would there be less genetic variation? Perhaps you deny the cheetah is the result of a bottleneck? If so, why are they almost monomorphic?

​

I really hope you admit your silly observation was flat wrong and move on.

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+++++++++++++++++++++I will gladly admit that you have absolutely no idea about you are talking about. Do you believe genes are lost from a species after a bottleneck or alleles? You clearly do not know the difference. Cheetah's today have the same genes as cheetahs from thousands of years ago. What they have is a reduction in variants of the genes (hint they are diploid organisms) thus they do not have poor genetic content and they maintained the genes that make them cheetahs...they are monomorphic i.e. the gene copies are identical due the death of the individuals carrying the other variants and the population growing from the extremely small remaining (bottleneck) population.
Learn some population genetics and stop wasting my time with your posts based on your incredible ignorance.