molecular genetic evidence for a multipurpose genome

Some further papers on genetic bottlenecks...though I still say you need to go to a population genetics reference in order to understand this basic concept.cheers,
MScience 1985 Mar 22;227(4693):1428-34 Related Articles, LinksGenetic basis for species vulnerability in the cheetah.O'Brien SJ, Roelke ME, Marker L, Newman A, Winkler CA, Meltzer D, Colly L, Evermann JF, Bush M, Wildt DE.A population genetic survey of over 200 structural loci previously revealed that the South African cheetah (Acinonyx jubatus jubatus) has an extreme paucity of genetic variability, probably as a consequence of a severe population bottleneck in its recent past. The genetic monomorphism of the species is here extended to the major histocompatibility complex, since 14 reciprocal skin grafts between unrelated cheetahs were accepted. The apparent consequences of such genetic uniformity to the species include (i) great difficulty in captive breeding, (ii) a high degree of juvenile mortality in captivity and in the wild, and (iii) a high frequency of spermatozoal abnormalities in ejaculates. The species vulnerability of the cheetah was demonstrated by an epizootic of coronavirus-associated feline infectious peritonitis in an Oregon breeding colony in 1983. Exposure and spread of the coronavirus, which has a very low morbidity in domestic cats (approximately 1 percent), has decimated a heretofore productive and healthy captive population. The extreme genetic monomorphism, especially at the major histocompatibility complex, and the apparent hypersensitivity of the cheetah to a viral pathogen may be related, and provide a biological basis for understanding the adaptive significance of abundant genetic variation in outbred mammalian species.J Virol 1993 Jan;67(1):222-8 Related Articles, LinksGenetic bottlenecks and population passages cause profound fitness differences in RNA viruses.Clarke DK, Duarte EA, Moya A, Elena SF, Domingo E, Holland J.Department of Biology, University of California, San Diego, La Jolla 92093-0116.Repeated clone-to-clone (genetic bottleneck) passages of an RNA phage and vesicular stomatitis virus have been shown previously to result in loss of fitness due to Muller's ratchet. We now demonstrate that Muller's ratchet also operates when genetic bottleneck passages are carried out at 37 rather than 32 degrees C. Thus, these fitness losses do not depend on growth of temperature-sensitive (ts) mutants at lowered temperatures. We also demonstrate that during repeated genetic bottleneck passages, accumulation of deleterious mutations does occur in a stepwise (ratchet-like) manner as originally proposed by Muller. One selected clone which had undergone significant loss of fitness after only 20 genetic bottleneck passages was passaged again in clone-to-clone series. Additional large losses of fitness were observed in five of nine independent bottleneck series; the relative fitnesses of the other four series remained close to the starting fitness. In sharp contrast, when the same selected clone was transferred 20 more times as large populations (10(5) to 10(6) PFU transferred at each passage), significant increases in fitness were observed in all eight passage series. Finally, we selected several clones which had undergone extreme losses of fitness during 20 bottleneck passages. When these low-fitness clones were passaged many times as large virus populations, they always regained very high relative fitness. We conclude that transfer of large populations of RNA viruses regularly selects those genomes within the quasispecies population which have the highest relative fitness, whereas bottleneck transfers have a high probability of leading to loss of fitness by random isolation of genomes carrying debilitating mutations. Both phenomena arise from, and underscore, the extreme mutability and variability of RNA viruses.Curr Biol 2000 Oct 19;10(20):1287-90 Related Articles, LinksAn 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. The northern elephant seal (Mirounga angustirostris) has undergone at least one extreme bottleneck, having rebounded from 20-100 individuals a century ago to over 175,000 individuals today. The relative lack of molecular-genetic variation in contemporary populations has been documented, but the extent of variation before the late 19th century remains unknown. We have determined the nucleotide sequence of a 179 base-pair segment of the mitochondrial DNA (mtDNA) control region from seals that lived before, during and after a bottleneck low in 1892. A 'primerless' PCR was used to improve the recovery of information from older samples. Only two mtDNA genotypes were present in all 150+ seals from the 1892 bottleneck on, but we discovered four genotypes in five pre-bottleneck seals. This suggests a much greater amount of mtDNA genotypic variation before this bottleneck, and that the persistence of two genotypes today is a consequence of random lineage sampling. We cannot correlate the loss of mtDNA genotypes with a lowered mean fitness of individuals in the species today. However, we show that the species historically possessed additional genotypes to those present now, and that sampling of ancient DNA could elucidate the genetic consequences of severe reductions in population size.

Quetzal dealt with your assertions very comprehensively but I have a few things to add.PB:
CONSERVATION BIOLOGIST’S CONCERN ABOUT DWINDLING POPULATIONS IS BASED ON INBREEDING AND A DECLINE OF THE GENEPOOL. THIS HAS BEEN OBSERVED ON THE CHEETAH, THE FLORIDA COOGAR, ALLOCASUARINA, ETCETERA. IN MY OPINION, THE CURRENTLY LIVING ORGANISMS HAVE POOR GENOMIC CONTENT DUE TO LOSS OF GENETIC INFORMATION FROM THE MULTIPURPOSE GENOME.M: Then your assertion is falsified. They 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. Since they are not extinct their genetic content is not poor. If you become extinct you sucked If the genome is so multipurpose how can it have poor genetic content? Or are you saying that all individuals carry every bit of genetic variation within the population? If so this is easily falsified as well.PB:
THESE ORGANISMS ARE AN ENDSTATION OF CHANGE (‘EVOLUTION’ IF YOU LIKE). BREEDING PROGRAMS CAN NEVER ADD NEW GENES TO THE GENEPOOL OF THESE ORGANISMS, IT CAN ONLY MIX THE PREEXISTING GENES ALREADY PRESENT IN THE UNIVERSE OF GENES OF KINDS (FOR INSTANCE THE FLORIDA COOGER HAS A KINK IN ITS TAIL. THE ONLY WAY TO BREED IT OUT IS BY ADDING A COMPENSATORY GENE TO THE POOL. THAT IS NOT SO HARD TO ACHIEVE, SINCE THE GENE CAN BE FOUND IN ALL SUBSPECIES OF COOGER). ALL THIS HAS NOTHING IN COMMON WITH EVOLUTIONISM. SUBSPECIATION THROUGH LOSS OF GENOMIC CONTENT/INFORMATION IS PERFECTLY CONCEIVABLE THROUGH THE MULTIPURPOSE GENOME.PB: Not surprisingly you seem to not know the difference between a gene and an allelic variant. You are claiming here that new allelic variants cannot arise which is falsified by a great deal of experimental results and observations in the wild. You are also inconsistent in saying there are no genetic relationships among organisms yet you claim there are subsepcies of cougars's. Which is it? You claim speciation requires genetic loss? Also not observed. False. Breeding programs (where possible) introduce genetic variation into the population with some of the primary benefits being that deleterious mutations remain heterozygous and the immune system contains enough variation to respond to infections so the population does not crash.PB:
HOW DOES THIS RELATE TO THE WOLLEMIA NOBILIS? THE MULTIPURPOSE GENOME (OR ‘ALL-PURPOSE GENOME’ AS IT HAS BEEN CALLED BY DR PEAKALL) ALLOWS LOSS OF GENES BUT IT IS NOT COMPULSARY. THE STABILITY OF DNA IS GUARDED BY A TREMENDOUS AMOUNT OF REPAIR ENZYMES, SO IT PREDICTS NOT TO FIND A LOT OF VARIATION BETWEEN SEPARATED / ISOLATED POPULATIONS.M: Funny that these enzymes are shared by most multicellular organsisms yet the mutation rate is highly variable even among related groups and mutations do happen with a probability that can be estimated. Your prediciton is also falsified in that some isolated populations show tremendous variability i.e. Pan troglodytes, Gorilla gorilla etc etc etc.Also please define the multiple purposes of the genome. As far as I can see its only "purpose" is to make sure it continues into the next generation.PB:
THAT’S WHAT WE SEE IN WOLLEMIA. THAT’S WHY I AM ALSO INTERESTED IN THE GENOMES OF HORSESHOECRAB. SEPERATION FOR EONS ON DIFFERENT CONTINENTS WOULD LEAD —ACCORDING TO EVOLUTIONSISM-- TO A LOT VARIATION IN THE DNA ON NEUTRAL POSITIONS.M: W.nobilis has not been separated for eons on different continents and Quetzal debunked your myth of horseshoe crab genetic uniformity.PB:
THE MULTIPURPOSE GENOME DOESN’T NEED VARIATIONS (ALSO IT IS ALLOWED ON NEUTRAL POSITIONS) OVER TIME. IN CONTRAST, IT HOLDS THAT RANDOM VARIATION IS BAD, SO IT PREVENTS THE SENSE-SEQUENCES FROM CHANGE THROUGH SPECIFICATION OF REPAIR MECHANISM. INDEED, THE MULTIPURPOSE GENOME REQUIRES STABILITY OF SENSIBLE-SEQUENCES. IF WE DON’T FIND VARIABILITY OF SEQUENCES THAN EVOLUTIONISM CANNOT BE CORRECT AND WE NEED ANOTHER THEORY THAT IS MORE EXPLANATORY. THE MAJOR PART OF ANY GENOME ISN’T HETEROZYGOTHIC SO I SEE MORE MAJOR PROBLEMS FOR EVOLUTIONS.M: Let's follow this sentence...your hypothesis does not predict variaton, but it happens anyway, but variation is bad, but undefined sense sequence thingy's don't vary therefore all bases are not heterozygous and therefore evolution has problems? You back in the Netherlands smoking at a pot cafe???
In your confusion you forget that a lot of sequence does not vary due to selection and genetic drift..but I am sure you were getting to that PB:
EVOLUTIONISMS EXPLANATION WOULD BE THAT THE TREES USED TO BE OMNIPRESENT, THAN DUE TO CLIMATIC CHANGE THE POPULATION DWINDLED, ALMOST DISAPPEARED BUT ONE. THAN THIS ONE STARTED TO COPICE AND TO DIPERSE AGAIN, WITHOUT ANY VARIABILITY IN THE DNA. EVEN IF THIS WAS THE RIGHT VISION, THE INVARIABILITY OF THE TWO (OR THREE) SITES CANNOT BE EXPLAINED. THAT WAS MY POINT, AND STILL IS MY POINT.M: Where would it be mandated by evolutionary theory that the trees used to be omnipresent? Population genetics and evolutionary biology both take into account effective population size variation...you do know what the difference is between population size and effective population are don't you??? Why would evolutionary theory predict that climate caused the population to dwindle? There are other mechanism that can cause population crashes other than climate.

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

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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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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+++++++++++++++++++++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.

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Originally posted by peter borger:
dear Dr Page,

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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.

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Best wishes,
Peter

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++++++++++++++++Evolution is still standing, you have not addressed SLPx's criticisms of your skewed and misdefined ZFX reference, you have not supported your own hypothesis, you are not even answering posts regarding your own hypothesis! So please don't pull the Wordswordsman tactic of claiming that it is a "sin" to argue with people who disagree with you as a way of dodging substantive questions that arise no matter how hostile you and SLPx are to each other. Quetzal and I have had most of our posts left unanswered by you recently....if I used your standard as you have just applied it to SLPx I could say.."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 ALTERNATIVE TO EVOLUTION and there has never been A VIABLE ALTERNATIVE. Get used to this OLD worldview, it will help you survive. "Oh wait, I can already say this

All you can do is answer with a strawman? I never said genes were lost. Ever. It never ceases to amaze me the desperation of PhD evolutionists to avoid admitting a blatant mistake to preserve their pride (I think I read some time ago you have a PhD, I apologize if I’m wrong). I know full well the difference between a gene and an allele. Try to be less puffed up on yourself. I’m truly sorry a layman such as myself has to point out such an obvious fact to you.M: LOL!!! I am puffed up? Considering you complete ignorance about the subject you are debating it is you who should deflate your ego. Your personal attacks and claims that all questios to you are strawmen demonstrate the paucity of you knowledge and your inability to support your stupid claims.FW:
I truly hope you do not have a PhD, because there is simply no excuse for anyone, even an evolutionist, to claim that a bottlenecked animal such as the cheetah has not lost genetic information due to the isolation event and subsequent genetic drift.M: Oh so you "Dr." Williams are in a position to evaluate Ph.D's in genetics although you are completely ignorant of the subject...perhaps you could use a spell back in kindergarten.FW:
According to the dream world of Mammuthus, if we isolate the poodle completely, and let it breed only with other poodles, we can eventually get a St Bernard. But anyone with half a brain knows we can’t. We even get to cheat and use truncation selection, something that does not occur in nature, and we *still* will not be able to produce a St. Bernard. Now if you object to this analogy, explain why the poodle has suffered loss of genetic information and the cheetah hasn’t.M: Poor Freddy Fred boy Since you cannot answer my questions you have to make up statements that I never made. LOL!!!
Since you would rather trade insults with me as opposed to anwering the question posed to you I am not surprised that you pulled the last paragraph out of your fantasy world. Do you think that cheetah's have more or less genes than before the bottleneck? Define allelic variation. If you cannot you should keep your mouth shut regarding the accuracy of my statements.FW:
Learn to think outside your fantasy box and stop posting pure nonsense. Are you prepared to defend this ludicrous position, even if I find a PhD evolutionist to refute your nonsense? Hey Scott, I’m curious. Do you buy this nonsense? Tough spot you are in, eh? Do you reluctantly agree with your idol, or defend your colleague. Do you think the cheetah has not lost ANY genetic information from its pre-bottleneck parent population? This really ought to be fun to watch your reaction.M: Learn to think Fred. You obviously cannot get beyond your religios zealotry to actually form logical thought in your brain. Scott if free to agree or disagree with me.....my guess is he will also get a laugh out of your silly posts.Have a nice day and stay off the drugs..or at least lower the dosage

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Originally posted by peter borger:
Et tu, mammuthus?

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You say:

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Conclusion, there is no ALTERNATIVE TO EVOLUTION and there has never been A VIABLE ALTERNATIVE. Get used to this OLD worldview, it will help you survive.

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I say:
You are wrong, there is an alternative, but you don't want this alternative since it doesn't correspond with your personal worldview. Therefore, nobody else outside the field of evolutionism is allowed to say something about evolutionism and that is how it is kept alive and propagated. It is nothing but a meme. But you know that it has fallen, Mammuthus, I've shown you how to falsify it. Of course, you can always claim that space-aliens are involved (as Dr Page likes it).

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Best wishes,
peter

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Hi Peter
actually I was being both ironic with that post and trying to get you back into the debate. There are a lot of questions you have left hanging regarding your hypothesis. You are starting to adopt the useless style of arguement of Fred Williams where you make big claims, don't support them, and then refuse to answer any questions and you have not done this up until this point. I would like for at least you, me, and Quetzal to return to the debate we were having before things degenerated.You and SLPx obviously personally hate each other just like anybody with a brain on this board hates debating with Fred Williams
But I have always enjoyed arguing with you and Tranquility Base in particular and bear no personal animosity towards either of you. I have not seen any particular venom from you or TB towards myself either. But I would like the debate to return to one that is more productive.

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Originally posted by peter borger:
Dear dr Page,

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You never responded to my comments on the ZFY region. The only response I've had was Percipient's and it was meaningless. So, if you wanna discuss this topic in detail, I have no problems with that. For me it is just another little exercise in contemporary biology. And that's my job, I can do it on the side.

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Talking about unskilled. It was you who told me that you were an anatomist by education, so give me a good reason why you are allowed to write on evolutionary topics. At least I am a biologist by educations and so I am allowed to write on evolutionary topics. It was also you who wasn't up to date with contemporary biology (remember the histon code?). And your current actions......speak for themselves.

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Best wishes,
Peter

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[This message has been edited by peter borger, 11-02-2002]

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********Just to point out Peter, I also brought up the Erlandson study of the entire region comparing insertions, deletions, and point mutations and you have not addressed those issues and claiming that the region remains invariant. Sorry, but that is patently false.

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Originally posted by Mammuthus:
Quetzal dealt with your assertions very comprehensively but I have a few things to add.

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PB:
CONSERVATION BIOLOGIST’S CONCERN ABOUT DWINDLING POPULATIONS IS BASED ON INBREEDING AND A DECLINE OF THE GENEPOOL. THIS HAS BEEN OBSERVED ON THE CHEETAH, THE FLORIDA COOGAR, ALLOCASUARINA, ETCETERA. IN MY OPINION, THE CURRENTLY LIVING ORGANISMS HAVE POOR GENOMIC CONTENT DUE TO LOSS OF GENETIC INFORMATION FROM THE MULTIPURPOSE GENOME.

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M: Then your assertion is falsified. They 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. Since they are not extinct their genetic content is not poor. If you become extinct you sucked If the genome is so multipurpose how can it have poor genetic content? Or are you saying that all individuals carry every bit of genetic variation within the population? If so this is easily falsified as well.

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PB:
THESE ORGANISMS ARE AN ENDSTATION OF CHANGE (‘EVOLUTION’ IF YOU LIKE). BREEDING PROGRAMS CAN NEVER ADD NEW GENES TO THE GENEPOOL OF THESE ORGANISMS, IT CAN ONLY MIX THE PREEXISTING GENES ALREADY PRESENT IN THE UNIVERSE OF GENES OF KINDS (FOR INSTANCE THE FLORIDA COOGER HAS A KINK IN ITS TAIL. THE ONLY WAY TO BREED IT OUT IS BY ADDING A COMPENSATORY GENE TO THE POOL. THAT IS NOT SO HARD TO ACHIEVE, SINCE THE GENE CAN BE FOUND IN ALL SUBSPECIES OF COOGER). ALL THIS HAS NOTHING IN COMMON WITH EVOLUTIONISM. SUBSPECIATION THROUGH LOSS OF GENOMIC CONTENT/INFORMATION IS PERFECTLY CONCEIVABLE THROUGH THE MULTIPURPOSE GENOME.

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PB: Not surprisingly you seem to not know the difference between a gene and an allelic variant. You are claiming here that new allelic variants cannot arise which is falsified by a great deal of experimental results and observations in the wild. You are also inconsistent in saying there are no genetic relationships among organisms yet you claim there are subsepcies of cougars's. Which is it? You claim speciation requires genetic loss? Also not observed. False. Breeding programs (where possible) introduce genetic variation into the population with some of the primary benefits being that deleterious mutations remain heterozygous and the immune system contains enough variation to respond to infections so the population does not crash.

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PB:
HOW DOES THIS RELATE TO THE WOLLEMIA NOBILIS? THE MULTIPURPOSE GENOME (OR ‘ALL-PURPOSE GENOME’ AS IT HAS BEEN CALLED BY DR PEAKALL) ALLOWS LOSS OF GENES BUT IT IS NOT COMPULSARY. THE STABILITY OF DNA IS GUARDED BY A TREMENDOUS AMOUNT OF REPAIR ENZYMES, SO IT PREDICTS NOT TO FIND A LOT OF VARIATION BETWEEN SEPARATED / ISOLATED POPULATIONS.

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M: Funny that these enzymes are shared by most multicellular organsisms yet the mutation rate is highly variable even among related groups and mutations do happen with a probability that can be estimated. Your prediciton is also falsified in that some isolated populations show tremendous variability i.e. Pan troglodytes, Gorilla gorilla etc etc etc.

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Also please define the multiple purposes of the genome. As far as I can see its only "purpose" is to make sure it continues into the next generation.

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PB:
THAT’S WHAT WE SEE IN WOLLEMIA. THAT’S WHY I AM ALSO INTERESTED IN THE GENOMES OF HORSESHOECRAB. SEPERATION FOR EONS ON DIFFERENT CONTINENTS WOULD LEAD —ACCORDING TO EVOLUTIONSISM-- TO A LOT VARIATION IN THE DNA ON NEUTRAL POSITIONS.

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M: W.nobilis has not been separated for eons on different continents and Quetzal debunked your myth of horseshoe crab genetic uniformity.

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PB:
THE MULTIPURPOSE GENOME DOESN’T NEED VARIATIONS (ALSO IT IS ALLOWED ON NEUTRAL POSITIONS) OVER TIME. IN CONTRAST, IT HOLDS THAT RANDOM VARIATION IS BAD, SO IT PREVENTS THE SENSE-SEQUENCES FROM CHANGE THROUGH SPECIFICATION OF REPAIR MECHANISM. INDEED, THE MULTIPURPOSE GENOME REQUIRES STABILITY OF SENSIBLE-SEQUENCES. IF WE DON’T FIND VARIABILITY OF SEQUENCES THAN EVOLUTIONISM CANNOT BE CORRECT AND WE NEED ANOTHER THEORY THAT IS MORE EXPLANATORY. THE MAJOR PART OF ANY GENOME ISN’T HETEROZYGOTHIC SO I SEE MORE MAJOR PROBLEMS FOR EVOLUTIONS.

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M: Let's follow this sentence...your hypothesis does not predict variaton, but it happens anyway, but variation is bad, but undefined sense sequence thingy's don't vary therefore all bases are not heterozygous and therefore evolution has problems? You back in the Netherlands smoking at a pot cafe???
In your confusion you forget that a lot of sequence does not vary due to selection and genetic drift..but I am sure you were getting to that

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PB:
EVOLUTIONISMS EXPLANATION WOULD BE THAT THE TREES USED TO BE OMNIPRESENT, THAN DUE TO CLIMATIC CHANGE THE POPULATION DWINDLED, ALMOST DISAPPEARED BUT ONE. THAN THIS ONE STARTED TO COPICE AND TO DIPERSE AGAIN, WITHOUT ANY VARIABILITY IN THE DNA. EVEN IF THIS WAS THE RIGHT VISION, THE INVARIABILITY OF THE TWO (OR THREE) SITES CANNOT BE EXPLAINED. THAT WAS MY POINT, AND STILL IS MY POINT.

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M: Where would it be mandated by evolutionary theory that the trees used to be omnipresent? Population genetics and evolutionary biology both take into account effective population size variation...you do know what the difference is between population size and effective population are don't you??? Why would evolutionary theory predict that climate caused the population to dwindle? There are other mechanism that can cause population crashes other than climate.

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Bump

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Originally posted by Quetzal:

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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...

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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.

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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.

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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.

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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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BUMP

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Originally posted by Mammuthus:

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Originally posted by peter borger:
dear Mammuthus,

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I know these papers and I know the evolutionary vision of the authors. Still this vision is not explanatory. Maybe you could respond on the specific questions to Dr Wagner. That would clear things up and you will --on the side-- prevent evolutionism from falling.

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best wishes,
Peter

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Hi Peter,
You will have to tell me then why they are not explanatory. You have shown on several occassions profound misunderstandings of the papers,particularly studies of the ZFX/ZFY region so the burden is on you to demonstrate that your arguements are based on a real flaw in the data or arguments of the authors and not on your lack of understanding of population genetics, biochem, and randomness.

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1) Do these data mean that approximately 450 bp changes occurred on neutral positions?

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SORRY PETER BUT NOTHING IN YOUR LETTER INDICATES TO ME WHERE THIS QUESTION COMES FROM. ARE YOU REFERREING TO SOMETHING IN THE ARTICLE?

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2) Do these data mean that it would take about 10(exp)6 years for 3 random mutation to occur in the duplicated gene? Thus 150 million years for 450 neutral mutations?

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ONLY IF YOU BELEIVE THAT DNA EVOLVES IN A CLOCKLIKE MANNER. I DON'T SO THE ESTIMATE OF TIME WOULD HAVE A TREMENDOUS VARIANCE ATTACHED TO IT. PURELY NEUTRAL LOCI MIGHT EVOLVE IN A CLOCKLIKE MANNER HOWEVER BUT IT IS DEPENDENT ON A LOT OF OTHER FACTORS I.E. EFFECTIVE POPULATION SIZE; MUTATION RATE ETC.

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3) Do these data mean that after each point-mutation there was neutral purifying selection? And, what exactly is it? I mean, what exactly is selection on neutral genes?

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I HAVE NO IDEA WHAT NEUTRAL PURIFYING SELECTION IS SUPPOSED TO MEAN. SELECTION OCCURS ON GENES THAT PROVIDE AN ADVANTAGE OR DISADVANTAGE TO THE ORGANISM. NEUTRAL GENES CAN BECOME HOMOGENIZED BY GENE CONVERSION BUT IT IS NOT BECAUSE OF SELECTIVE CONSTRAINT.

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3a) Is it independent from nearby genes? Independent from the rest of the genome?

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IT DEPENDS. SOME GENES EVOLVE BY CONCERTED EVOLUTION USING VARYING HOMOGENIZATION PROCESSES SUCH AS GENE CONVERSION. BUT THIS IS NOT THE CASE FOR ALL GENES.

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: Mol Biol Evol 2002 May;19(5):689-97 Related Articles, Links

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Purifying selection and birth-and-death evolution in the histone H4 gene family.

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Piontkivska H, Rooney AP, Nei M.

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Institute of Molecular Evolutionary Genetics, Pennsylvania State University, 328 Mueller Lab, University Park, PA 16802, USA. oxp108@psu.edu

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Histones are small basic proteins encoded by a multigene family and are responsible for the nucleosomal organization of chromatin in eukaryotes. Because of the high degree of protein sequence conservation, it is generally believed that histone genes are subject to concerted evolution. However, purifying selection can also generate a high degree of sequence homogeneity. In this study, we examined the long-term evolution of histone H4 genes to determine whether concerted evolution or purifying selection was the major factor for maintaining sequence homogeneity. We analyzed the proportion (p(S)) of synonymous nucleotide differences between the H4 genes from 59 species of fungi, plants, animals, and protists and found that p(S) is generally very high and often close to the saturation level (p(S) ranging from 0.3 to 0.6) even though protein sequences are virtually identical for all H4 genes. A small proportion of genes showed a low level of p(S) values, but this appeared to be caused by recent gene duplication. Our findings suggest that the members of this gene family evolve according to the birth-and-death model of evolution under strong purifying selection. Using histone-like genes in archaebacteria as outgroups, we also showed that H1, H2A, H2B, H3, and H4 histone genes in eukaryotes form separate clusters and that these classes of genes diverged nearly at the same time, before the eukaryotic kingdoms diverged.

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: Proc Natl Acad Sci U S A 2000 Sep 26;97(20):10866-71 Related Articles, Links

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Purifying selection and birth-and-death evolution in the ubiquitin gene family.

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Nei M, Rogozin IB, Piontkivska H.

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Institute of Molecular Evolutionary Genetics and Department of Biology, Pennsylvania State University, 328 Mueller Laboratory, University Park, PA 16802, USA. nxm2@psu.edu

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Ubiquitin is a highly conserved protein that is encoded by a multigene family. It is generally believed that this gene family is subject to concerted evolution, which homogenizes the member genes of the family. However, protein homogeneity can be attained also by strong purifying selection. We therefore studied the proportion (p(S)) of synonymous nucleotide differences between members of the ubiquitin gene family from 28 species of fungi, plants, and animals. The results have shown that p(S) is generally very high and is often close to the saturation level, although the protein sequence is virtually identical for all ubiquitins from fungi, plants, and animals. A small proportion of species showed a low level of p(S) values, but these values appeared to be caused by recent gene duplication. It was also found that the number of repeat copies of the gene family varies considerably with species, and some species harbor pseudogenes. These observations suggest that the members of this gene family evolve almost independently by silent nucleotide substitution and are subjected to birth-and-death evolution at the DNA level.

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3b) Does this type of selection take place on the level of the organism? How?

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AGAIN; YOU REALLY NEED TO LEARN SOME POPULATION GENETICS OR AT LEAST GET A GRASP OF WHAT RELATIVE FITNESS MEANS. EVEN IF A MUTATION IS NOT IMMEDIATELY LETHAL; IF IT PUTS THE ORGANISM AT A DISADVANTAGE IT WILL BE SELECTED AGAINST. YES; IT IS AT THE LEVEL OF THE ORGANISM

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4) Are there identical (=very recently duplicated) genes in known genomes?

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Annu Rev Cell Dev Biol 2002;18:53-80 Related Articles, Links

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Gene co-option in physiological and morphological evolution.

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True JR, Carroll SB.

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Department of Ecology and Evolution, State University of New York at Stony Brook, Stony Brook, New York 11794-5245, e-mail: jrtrue@life.bio.sunysb.edu

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Co-option occurs when natural selection finds new uses for existing traits, including genes, organs, and other body structures. Genes can be co-opted to generate developmental and physiological novelties by changing their patterns of regulation, by changing the functions of the proteins they encode, or both. This often involves gene duplication followed by specialization of the resulting paralogous genes into particular functions. A major role for gene co-option in the evolution of development has long been assumed, and many recent comparative developmental and genomic studies have lent support to this idea. Although there is relatively less known about the molecular basis of co-option events involving developmental pathways, much can be drawn from well-studied examples of the co-option of structural proteins. Here, we summarize several case studies of both structural gene and developmental genetic circuit co-option and discuss how co-option may underlie major episodes of adaptive change in multicellular organisms. We also examine the phenomenon of intraspecific variability in gene expression patterns, which we propose to be one form of material for the co-option process. We integrate this information with recent models of gene family evolution to provide a framework for understanding the origin of co-optive evolution and the mechanisms by which natural selection promotes evolutionary novelty by inventing new uses for the genetic toolkit.

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5) Is evolution a phenomenon driven by random mutation?
YES

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I am going to let Quetzal have first crack at a response to your post to him but I found several deep flaws in your statements that I will address if he does not.

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Best wishes and thanks for responding to the posts
M

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BUMP

quote:

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Originally posted by Quetzal:
Peter: do me a favor - don't respond in all capital letters. It gives me a headache. Thanks.

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quote:

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Q: Actually, the abstract states exceptionally low genetic diversity, not no variability. To be fair, it also states that the loci examined to date don’t show variation where expected (or where found in other organisms) — the key word being to date.

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PB: YOU ARE WRONG. THE PAPER DEMONSTRATE NO VARIATION AT ALL. NO VARIATION IS SOMETHING DIFFERENT THAN LOW VARIATION. EVEN IF IT IS ‘TO DATE’ IT STILL IS NO VARIATION TO DATE. NOT LOW VARIATION TO DATE.

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Peter, the article states explicitly low variability. You can argue semantics all you want, but your wishing something doesn’t make it valid.

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IN ADDITION, IF THE TREES WERE ABUNDANT ONCE WE WOULD EXPECTED THEIR POLLEN IN THE FOSSIL RECORD, THEY ARE NOT PRESENT. THE ONLY POLLEN RESEMBLING WOLLEMIA ARE THE DELWINITES, AND THEY DISAPPEAR 2 MILLION YEARS AGO FROM THE FOSSIL RECORD.

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This is completely inaccurate. From the Chambers article I cited: Pollen of Wollemia is indistinguishable from the fossil pollen form-genus Dilwynite. If we’re going to continue this discussion, I think it behooves you to actually read the literature.

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FURTHERMORE, AND NOT UNIMPORTANT, THE THREE STANDS DO NOT DEMONSTRATE ANY VARIABILITY. ONLY, IF THE TREES WERE DERIVED THROUGH CLONING WE WOULD EXPECT TO FIND THIS. HOWEVER, DR PEAKALL POINTS OUT THAT IT IS HIGHLY UNLIKELY THAT THE TWO (OR THREE) STANDS ARE DERIVED THROUGH CLONING.

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This is also an inaccurate statement. Dr. Peakall points out that it’s unlikely the three different stands were formed by cloning. In other words, it’s unlikely due to physical separation that the three stands were formed by coppicing from a single stand. He does, however, state that each stand individually probably represents a clone from an original seeding.

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AFTER READING WOODFORD'S BOOK I GOT INTERESTED AND SCREENED THE NET FOR MORE OF THE WOLLEMIA NOBILIS. ALL I FOUND WAS THE NEW SCIENTIST PAPER, SO I HAD TO REFER TO WOODFORDS BOOK. YOU DEMONSTRATED IN YOUR RESPONSE THAT WOODFORD'S CLAIMS HAVE NOT BEEN CHALLENGED YET. EVEN STRONGER, ACCORDING TO YOUR INFORMATION, THERE ARE NOW THREE STANDS WITH IDENTICAL TREES. THE BOOK CONTAINS INTERVIEWS WITH PEAKALL AND FIRST HAND INFORMATION ON THE TREE. IT EVEN INCLUDED THE FIGURES OF DNA ANALYSIS, ALTHOUGH THEY ARE A BIT OBSCURE.

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Looking back over your initial post, it appears to me that Woodford didn’t actually make any claims — you did based a on a few quotations from Woodford’s book. Be that as it may, YOUR claims have not been substantiated because you’re basing your assertions on either erroneous or incomplete data. The published information on Wollemia is not yet definitive. You are making assertions that allegedly overthrow the last century and a half of evolutionary theory based on an incomplete data set — published in a popular press book written by a newspaperman. Not very likely anyone’s going to take you very seriously if that’s all you’ve got. Given the fact that there ARE quite prosaic explanations, backed by numerous examples of other organisms — from vertebrates to plants — the case of Wollemia may be extreme but not all that unusual.

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Q: You can even take the opportunity to explain to Dr. Peakall why he’s got it all wrong. I’ll be fascinated to see his response.

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PB: MAYBE HE IS WRONG. THE TREES AS THEY STAND VIOLATE MOLECULAR EVOLUTIONARY PRINCIPLES. I QUOTED DR PEAKALL ON THIS TOPIC AND HE ALSO INTRODUCED THE ALL PURPOSE GENOME TO EXPLAIN THE NON-DEGENERACY OF THE TREES.

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lol. Okay, email him and tell him that he’s wrong. He’s at ANU, and quite prominently listed in the literature. As far as the quote from New Scientist, please tell me how one off-hand comment during an interview provides evidentiary support for overthrowing evolution. I guarantee you that Dr. Peakall hasn’t published anything on all purpose genome anywhere. It would be interesting to see the entire quote in context — I’d be willing to bet that he means something other than what you are asserting.

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Q: Your claims fail because there are alternate, mainstream explanations for the preliminary data.

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PB: NO, THERE ARE NO EXPLANATIONS FOR THE INVARIABILITY OF DNA BETWEEN THE TWO (NOW THREE) POPULATIONS IF THEY WERE NOT DERIVED BY CLONING.

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Where’d you come up with this one? I even provided you several explanations. You also haven’t shown the lack of clonality — which has been observed in Wollemia, btw. Look back at my post, toward the bottom (#1, #3, #4). You also need to read some more — your lack of understanding of population genetics is showing again. Try reading up on inbreeding depression, or topics such as habitat fragmentation and the effects of genetic drift and reduced gene flow on the genetic variability of micropopulations. There is a LOT of literature on the subject. Conservation biology depends on the understanding of these processes.

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Q: It’s YOUR responsibility, as the claimant in this case, to provide testable, replicatable reasons why the mainstream explanations are in error. So far, all you’ve done is hand-wave away anything that contradicts you. As to your little ad hominem aside, it appears I struck a nerve. If you feel I’m unqualified to discuss the issue with you, then you are free to ignore anything I post. That won’t, of course, help your case, but perhaps it will make you feel better. As a clarification — I forbore to challenge your sequence data on that one issue. Doesn’t mean even someone as ignorant as I apparently am can’t see the flaws in your arguments.

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Ooops, missed responding to this one Peter. You have failed to provide a refutation of the mainstream explanations — merely re-asserted your original premise. Try again.

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PB: HOWEVER, WOODFORD IS A POPULAR SCIENCE WRITER AND DAWKINS IS A POPULAR SCIENCE WRITER. I DON’T SEE THE DIFFERENCE. ANYWAY, THE WOODFORD BOOK ALSO CONTAINS PERSONAL STATEMENTS OF PEAKALL AND I REFERRED TO THEM IN MY ORIGINAL MAILING (#1 THIS THREAD).

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You really don’t see the difference between Dawkins — a scientist — and a journalist?

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PB: CONSERVATION BIOLOGIST’S CONCERN ABOUT DWINDLING POPULATIONS IS BASED ON INBREEDING AND A DECLINE OF THE GENEPOOL. THIS HAS BEEN OBSERVED ON THE CHEETAH, THE FLORIDA COOGAR, ALLOCASUARINA, ETCETERA. IN MY OPINION, THE CURRENTLY LIVING ORGANISMS HAVE POOR GENOMIC CONTENT DUE TO LOSS OF GENETIC INFORMATION FROM THE MULTIPURPOSE GENOME.

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Right, as far as it goes, except for the bit about multipurpose genomes — which as you pointed out is merely your opinion. Conservation biology is concerned with population extinction — causes and prevention. Understanding population genetics is important for this effort. Relict populations, like Wollemia, the Catalina mahogany I mentioned, etc, are highly susceptible to epidemics that can wipe out the entire species precisely because the remaining populations are genetically uniform. There are also a number of other management considerations beyond genetics, which I won’t bother to go into here.

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THESE ORGANISMS ARE AN ENDSTATION OF CHANGE (‘EVOLUTION’ IF YOU LIKE). BREEDING PROGRAMS CAN NEVER ADD NEW GENES TO THE GENEPOOL OF THESE ORGANISMS, IT CAN ONLY MIX THE PREEXISTING GENES ALREADY PRESENT IN THE UNIVERSE OF GENES OF KINDS (FOR INSTANCE THE FLORIDA COOGER HAS A KINK IN ITS TAIL. THE ONLY WAY TO BREED IT OUT IS BY ADDING A COMPENSATORY GENE TO THE POOL. THAT IS NOT SO HARD TO ACHIEVE, SINCE THE GENE CAN BE FOUND IN ALL SUBSPECIES OF COOGER). ALL THIS HAS NOTHING IN COMMON WITH EVOLUTIONISM. SUBSPECIATION THROUGH LOSS OF GENOMIC CONTENT/INFORMATION IS PERFECTLY CONCEIVABLE THROUGH THE MULTIPURPOSE GENOME.

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The only possible endstation of evolution is extinction. What are you talking about the universe of genes of kinds? This statement makes no sense. As to your comment on breeding, you are again in error. In fact, one of the main management concerns with relict populations is finding ways to preserve the existing genome of the organisms. For example, the Catalina mahogany consists of six adult trees in two karyotypes (of which one is a known hybrid). To prevent further hybridization, one recommendation I saw was to cut down the hybrid! Another example is another Australian relict, Haloragodendron lucasii, which consists of a total of 8 populations but only 7 genetic individuals. In fact, one population (of some 700 specimens), contained only 3 different genetically distinct individuals! Isolation, small population size, inbreeding depression, clonality, etc ALL contribute to homogeneity in genomes in once widely variant populations.
Beyond that, speciation has nothing to do with loss of information whatever that means.

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HOW DOES THIS RELATE TO THE WOLLEMIA NOBILIS? THE MULTIPURPOSE GENOME (OR ‘ALL-PURPOSE GENOME’ AS IT HAS BEEN CALLED BY DR PEAKALL) ALLOWS LOSS OF GENES BUT IT IS NOT COMPULSARY. THE STABILITY OF DNA IS GUARDED BY A TREMENDOUS AMOUNT OF REPAIR ENZYMES, SO IT PREDICTS NOT TO FIND A LOT OF VARIATION BETWEEN SEPARATED / ISOLATED POPULATIONS. THAT’S WHAT WE SEE IN WOLLEMIA.

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However, if your multipurpose genome is so stable, how do you explain the vast differences observed between isolated populations of most organisms? You’re trying to argue both directions here and simply getting confused when you meet yourself in the middle. Either populations vary, or they don’t — which is it under your multipurpose genome scenario? Relict populations can be understood in an evolutionary ecology framework, as can their occasionally unusual genetics. Try this article for example: Disrupting evolutionary processes: The effect of habitat fragmentation on collared lizards in the Missouri Ozarks. Do some reading, Peter, you’re destroying your credibility, here.

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THAT’S WHY I AM ALSO INTERESTED IN THE GENOMES OF HORSESHOECRAB. SEPERATION FOR EONS ON DIFFERENT CONTINENTS WOULD LEAD —ACCORDING TO EVOLUTIONSISM-- TO A LOT VARIATION IN THE DNA ON NEUTRAL POSITIONS. THE MULTIPURPOSE GENOME DOESN’T NEED VARIATIONS (ALSO IT IS ALLOWED ON NEUTRAL POSITIONS) OVER TIME. IN CONTRAST, IT HOLDS THAT RANDOM VARIATION IS BAD, SO IT PREVENTS THE SENSE-SEQUENCES FROM CHANGE THROUGH SPECIFICATION OF REPAIR MECHANISM. INDEED, THE MULTIPURPOSE GENOME REQUIRES STABILITY OF SENSIBLE-SEQUENCES. IF WE DON’T FIND VARIABILITY OF SEQUENCES THAN EVOLUTIONISM CANNOT BE CORRECT AND WE NEED ANOTHER THEORY THAT IS MORE EXPLANATORY. THE MAJOR PART OF ANY GENOME ISN’T HETEROZYGOTHIC SO I SEE MORE MAJOR PROBLEMS FOR EVOLUTIONS.

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Evolution predicts both variation and stasis, depending on the particular organism and the environmental factors that effect it. Your theory is both internally inconsistent and in direct opposition to observed populations. To be honest, your paragraph makes very little sense — what are sensible sequences? As for evolution not being correct, you’ve been given reasons why some genomes don’t vary. You’ve been shown populations and species which DO vary when isolated. You have no argument — merely assertion and denial of evidence.

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PB: SO, IF I UNDERSTAND PROPERLY, I HAVE TO PRESENT YOU WITH EVIDENCE FOR SOMETHING THAT ISN’T OBSERVED. THIS IS THE UP-SIDE-DOWN WORLD. I DO NOT HAVE TO PROOF SOMETHING THAT IS ABSENT. IN CONTRAST, YOU HAVE TO PROVE THAT THE WOLLEMIA DNA DEMONSTRATES VARIABILITY OTHERWISE IT VIOLATES MOLECULAR EVOLUTION. AS IT IS NOW, THE WOLLEMIA PINE DOESN’T DEMONSTRATE ANY VARIABILITY IN ALL LOCI TESTED (SEE YOUR PEAKALL REFERENCE). SO, MY ASSERTION STILL STANDS TILL PROVEN OTHERWISE. LET’S AWAIT MORE STUDIES.

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No, you’re changing your statement. You said that the DNA was incapable of variation. Since this is completely counter to all observations and published literature, I am more than justified in asking for evidence of YOUR claim. Show that there is a mechanism, structure, or chemical that prevents Wollemia (because that was the organism we were discussing) from varying.

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Q: 1. NONE of your claims about the tree’s DNA are correct, as I have shown, using the papers referenced. Look ‘em up.

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PB: ALL MY CLAIMS ON THE WOLLEMIA’S DNA STILL STAND. WORSE, THERE ARE NOW THREE STAND WITH THE SAME DNA SEQUENCES.

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Feel free to keep claiming this. The published literature refutes it.

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Q: 2. Disinformation? Not really. Deliberate, skewed interpretation coupled with misunderstanding and a weak argument from personal incredulity, usually.

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PB: SCIENCE IS ABOUT INTERPRETATIONS AND I HAVE A DISTINCT INTERPRETATION THAN EVOLUTIONISM. IN MANY ASPECTS MY INTERPRETATIONS IS EQUAL TO EVOLUTIONISM AND IN SOME ASPECT SUPERIOR TO EVOLUTIONISM.

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Lol — publish or perish, Peter. If your explanations are so superior, publish them — I’ll be the first to congratulate you on your Nobel Prize.

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Q: 3. You haven’t shown a single concrete example of anything that falsifies evolution. Every example, argument, quibble, etc, that you’ve produced has been shown to be in error by one person or another here. Mere repeated assertion doesn’t prove your case.

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PB: I HAVE DEMONSTRATED SEVERAL EXAMPLES FROM MOLECULAR BIOLOGY THAT CANNOT BE EXPLAINED BY EVOLUTINISM, YOU SIMPLY DENY THAT. I AM USED TO DENIAL FROM EVOLUTIONIST SO NOTHING NEW HERE.

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Denial? You have been shown not only to be wrong in your interpretations, but woefully ignorant of the sciences and disciplines you are attempting to overthrow. If anyone’s in denial, it’s you.

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Q: 4. Now I insist you email him. Where in ANY his articles does Dr. Peakall talk about an all-purpose genome?

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{PB’s restatement of the OP quote omitted for brevity.}

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I dealt with this argument from quotation above. However, if you’re so absolutely certain that Dr. Peakall supports your multipurpose genome, ask him directly. He’s a pretty nice guy, from our correspondence. I’m sure he’d be delighted to hear 1) how wrong he is on Wollemia and 2) how your miraculous multipurpose genome solves all his problems.

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PB: Evolutionary constraints??? Come on Quetzal, don't fool yourself with these meaningless words. What are evolutinary constraints? That the 'DNA isn't plastic anymore', 'evolution ceased in this tree', 'Evolution slow-down' or other humbug. Actually this all is exactly what the multipurpose genome predicts: "endstations of 'evolutinism'"

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Q: Now THAT’S condescending. Meaningless words? Are you denying that organisms are constrained by their natural history (genetics, ecology, ancestry)?

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PB: AS FAR AS THE MULTIPURPOSE GENOME IS CONCERNED, ORGANISMS ARE CONSTRAINED TO A CERTAIN LEVEL. IT MEANS THAT THE VARIABILITY ACNNOT GO BEYOND A WELL DEFINED BORDER. THIS BORDER IS DEFINED BY THE PREEXISTING REDUNDANCIES IN THE GENOME. NEW GENES ARE NEVER ADDED TO THE GENE POOL, (UNLESS CREATONS ARE INVOLVED).

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Once again, you’re meeting yourself coming two different directions. This isn’t even circular reasoning — your statements here and elsewhere are diametrically opposed to one another. Above you say there are no such things as constraints and the term is meaningless. Immediately afterwards you say that yes, there are constraints. Which is it? Is this one of those things where constraints are visible on Tuesday but not Thursday? As to creatons — I opened a whole new thread just for you to explain how this works.

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ALL ACCORDING TO YOUR AND THE CURRENTLY ACCEPTED HYPOTHESIS OF EVOLUTINISM. I DO NOT ACCEPT THIS THEORY SINCE IT DOESN’T COVER ALL BIOLOGICAL OBSERVATIONS.

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Of course it does. You certainly haven’t come close to showing anything that can’t be explained yet.

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YOU ASKED FOR AN ORGANISM THAT CEASED TO EVOLVE. EASY. ANY ORGANISM THAT IS NOT ABLE TO ADD GENES TO THE GENOME THAT HAVE NOT BEEN PRESENT IN THE UNIVERSE OF GENES OF THAT ORGANISM HAS CEASED TO EVOLVE. IN FACT, MOST ORGANISMS WE SEE TODAY ARE SUBJECT TO THIS CRITERION. THERE ARE NO EVOLVING ORGANISMS; THE MAJOR PART OF VARIABILITY WE SEE IS DUE TO PREEXISTING MECHANISMS OPERATING IN THE MULTIPURPOSE GENOME. I DON’T BLAME ANYBODY THAT THESE MECHANISMS ARE EASILY CONFUSED WITH EVOLUTIONISM. I USED TO DO THAT MYSELF.

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Now we’re getting somewhere. If I understand what you just wrote, any organism that can be shown to have developed any new (i.e., not transposed or whatever), completely novel gene will utterly destroy your theory? Please tell me that’s the case — then we can stop these lengthy responses and all go do something useful.

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Q: Just for fun — how do you personally classify subspecies? How have you gone about identifying specific demes in a wild population? And why do you always put sub in parentheses?

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PB: AS MENTIONED I DO NOT SEE A POINT IN CLASSIFICATION. AS LONG AS ORGANISMS ARE ABLE TO EXCHANGE GENES/INFORMATION AND PRODUCE OFFSPRING —IN WHATEVER MANNERTHEY CAN BE CALLED RELATED, I GUESS.

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I just had to include this section. I’m only going to cite one article out of hundreds that explains how ridiculous this assertion is, and how little you understand of population genetics, speciation, etc: Close genetic similarity between two sympatric species of tephritid fruit fly reproductively isolated by mating time.

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Q: Condescending again, Peter? Actually, the truth of it is the studies haven’t even been carried out on W. nobilis yet. Your statement is trivially true — two populations WOULD be expected to diverge, all other things being equal — not because it’s predicted, but rather because it’s been observed. However, you’re ignoring a few inconvenient facts again.

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PB: YES THEY HAVE BEEN CFARRIED OUT FOR TWO (OR THREE) SEPARATED POPULATIONS AND THE RESULTS WERE SURPRISING (AS DESCRIBED). EVOLUTIONISMS EXPLANATION WOULD BE THAT THE TREES USED TO BE OMNIPRESENT, THAN DUE TO CLIMATIC CHANGE THE POPULATION DWINDLED, ALMOST DISAPPEARED BUT ONE. THAN THIS ONE STARTED TO COPICE AND TO DIPERSE AGAIN, WITHOUT ANY VARIABILITY IN THE DNA. EVEN IF THIS WAS THE RIGHT VISION, THE INVARIABILITY OF THE TWO (OR THREE) SITES CANNOT BE EXPLAINED. THAT WAS MY POINT, AND STILL IS MY POINT.

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There has been nothing remotely resembling a complete analysis (which is what Dr. Peakall is doing even as we speak). The evolutionary explanation you provided, albeit simplistic, is undoubtedly correct. You certainly haven’t shown otherwise. And in fact, the coppicing after seeding from a single original organism certainly DOES explain the lack of variation.

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Q: 1. With your extensive knowledge of population genetics, I’m sure you know that inbreeding depression and mutational load can counteract each other in very small populations. Although possibly an extreme example of this, the observation that Wollemia shows negligible variation at the loci thus far compared between stands could be related to this. In other words, there may not be significant change due to mutation because, if two of the stands were originally seeded from one tree (which hasn’t been shown one way or the other), under even theoretically ideal conditions, the divergence would possibly be minimal over several generations.

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PB: THE RESEARCHERS IN NEW SCIENTIST (NOT A PEER REVIEWED JOURNAL, I KNOW) SAY THAT PROBABLY THE TREES HAVE BEEN IN THE GULLY FOR THOUSAND OF YEARS AND THAT MAY ALSO IMPLICATE THAT THE TREES ARE SEPARATED FOR THOUSANDS OF YEARS. I CANT PROOF THAT AND YOU CANT PROOF THE OPPOSITE. IN MY OPINION, IT POINTS TOWARDS AN EXTREMELY STABLE GENOME, AND THUS ADVOCATES A COMPLETELY STABLE MULTIPURPOSE GENOME (OR RECENT CREATION). IT SIMPLY IS THE EXTREME OF THE NORMAL DISTRIBUTION.

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You’ve managed to both contradict yourself again AND fail to answer my point. In the first place, if you admit Wollemia is at the extreme end of the normal distribution for variability, then I agree with you. However, this completely contradicts your assertion that there’s something special about it. Secondly, explain to me why the combination of inbreeding depression and mutational load in a highly isolated relictual micropopulation as represented by Wollemia doesn’t explain the observation?

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Q: 2. Somatic mutations were NOT tested for — merely 18s and rcbL divergence, which would only be detectable through inheritance of different (i.e., mutated) genes. Somatic mutations are generally not considered during these types of analyses because they are usually limited to a single cell of a single individual in a single generation, and hence are useless for comparative genomics. Somatic mutations are not inherited.

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PB: SOMATIC MUTATIONS MIGHT BE EXPECTED IN COPICING PLANTS.

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You have no clue what a somatic mutation is, do you?

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Q: 3. Wollemia is a very long-lived organism. Several of the oldest trees are tentatively dated to ~1000 years of age. There has been no data published indicating how long ago the three populations separated. If the stands represent first generations, especially if from a single parent plant, there would NO variation between stands — as observed. I think Dr. Peakall contends that each STAND was produced by coppicing from a single original seed — which would mean within the stands all the growth represents the same plant, so again would not show any variation (see also #2 above).

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PB: HOW WERE THE TREES DATED THAN? THEY WERE NOT ALLOWED TO CUT THEM DOWN, I GUESS, SINCE IT IS A HIGHLY PROTECTED SPECIES. FURTHERMORE, PEAKALL DOESN’T SAY ANYWHERE THAT THE TREES ARE DESCENDED FROM ONE TREE, ALTHOUGH I AM SURE THAT THIS WILL BE THE EVOLUTIONARY EXPLANATION. VERY UNLIKELY HOWEVER.

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They were dated based on examination of one dead trunk (~350 years) and extrapolation based on observed growth pattern and comparison with trunk size of living plants. The scientists also made an assumption: the trees may be older even than that (up to 1500 years) based on the observed coppicing pattern — i.e., meaning the original trunk may have long ago rotted away while maintaining a living root system.

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Q: 4. All of your junk DNA, redundancies, etc, would only appear/accumulate in separated populations of multiple organisms over many generations. With Wollemia we are essentially dealing with three organisms only (although that may change with more data), not three populations. That’s the implication of the coppicing growth pattern from an original seeding.

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PB: EVOLUTIONISM EXPECTS TO FIND THIS IN THE GENOME OF THE HORSESHOECRAB. I WAS REFERRING TO THAT.
FOR CURIOSITY, HOW DO YOU DEFINE ORGANISM IN THE SENSE OF WOLLEMI NOBILIS? BY LOOKING AT THE DNA?

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No, we were talking about the tree. However, just to get rid of your horseshoe crab nonsense right from the start — the living members of this group consist of three distinct genera and five species. That enough variation for you? Living fossil — lol — another argument from journalistic sensationalism. Peddle it to someone who doesn’t know any better. As to the designation of organism in the case of Wollemia, pending further data, I’d have to say each stand likely represents a single organism (or close enough as no matter).

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BUMP

FW:
I for one am more than willing to have a rational, civil debate, and have had them with many on this board, including other PhDs (such as Randy and Taz)M: We shall see....but I have serious doubts given your previous postsFW:
who haven’t let their education make them think they know all and are immune to mistakes or ashamed to admit them when they occur. I’m also not afraid to call certain individuals to the carpet when they make cockamamie claims they cannot substantiate. Mammuthus made two cockamamie claims. Let’s see him defend these claims, instead of running off about how I’m incredibly ignorant:M: I see you excluded completely your willingness to admit your mistakes or how about your complete misrepresentations of what I have said in the first place?FW:
Mammuth claims:1) Cheetah has the same amount of genetic information as its pre-bottleneck parent species. He can use the definition at the beginning of my post to make his case. If he cannot make his case with this definition, he can then attempt to use the even more watered-down definition, Shannon information, to make his case.
2) Monkenstick’s graph was somehow a good one, that it has something to say about whether or not non-random mutations exist.M: Let's actually look at what I said in response to Peter Borger post 57 as opposed to whatever Fred Williams wishes to attribute to me.
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PB:
CONSERVATION BIOLOGIST’S CONCERN ABOUT DWINDLING POPULATIONS IS BASED ON INBREEDING AND A DECLINE OF THE GENEPOOL. THIS HAS BEEN OBSERVED ON THE CHEETAH, THE FLORIDA COOGAR, ALLOCASUARINA, ETCETERA. IN MY OPINION, THE CURRENTLY LIVING ORGANISMS HAVE POOR GENOMIC CONTENT DUE TO LOSS OF GENETIC INFORMATION FROM THE MULTIPURPOSE GENOME.M: Then your assertion is falsified. They 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. Since they are not extinct their genetic content is not poor. If you become extinct you sucked If the genome is so multipurpose how can it have poor genetic content? Or are you saying that all individuals carry every bit of genetic variation within the population? If so this is easily falsified as well.
*******************************So I questioned if Peter Borger considers all INDIVIDUAL genomes to host the variation within the population i.e. multipurpose Lamarkian adaptation. Why is it a cheetah (individual)has a "poorer" genetic content now than prior to the bottlneck? They have the SAME genes, they are diploid, the sexually reproduce, etc etc like there ancestors. However, the cheetah population as a whole has less variation. That is the consequence of a genetic bottleneck....if they do not go extinct, they do not have "poor" genetic content. They have lost alleles not genes.That Fred somehow connects the above argument with some fantasy about isolating poodles to produce St. Bernards is his own problem.2) Monkenstick demonstrated random mutation i.e. provided evidence for it. That is more than you have done for non-random mutation. So it is a good one.Unless you will now magically produce the evidence for non-random mutation?[This message has been edited by Mammuthus, 11-04-2002]

Originally posted by Mammuthus:You and SLPx obviously personally hate each other just like anybody with a brain on this board hates debating with Fred Williams SLPx:
Now, now....I don't hate anybody.M: Ok, I stand corrected SLPx
Well, I almost hate Williams, but only because of his personality and his frequent misreporesentation and making of unsuppoorted claims...M: You could add to that his resistance to answering any question put to him....or from my exchanges with him..his very odd interest in the reproduction of poodles SLPx:
What I Do hate is seeing miscreants claim to have 'falsified' thius or 'proved' that and be wholly unable to support such fantastic claims.That gets old fast, and I have no patience at all for such insolence.M: I have little patience for it either but I ultimately would like Peter to re-engage in the debate on his hypothesis. The debate has dropped off the last week or so...I actually wish Tranquiltiy Base would jump in as he usually was good at sticking to topic and made a good effort at responding to all posts that came his way.cheers,
M