molecular genetic evidence for a multipurpose genome

I am not sure what he is saying anymore either. I have posted the Erlandsson, Wilson and Paabo reference where they sequenced most of the region and compared all the transposition events and POINT MUTATIONS twice now...so this invariant ZFX makes no sense.

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Originally posted by Quetzal:

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Quoted from Peakall 1998: So far, within the Wollemi Pine no allozyme variability has been found at 13 allozyme loci. Furthermore, no variability has been detected at more than 800 loci, visualised by the AFLP method. While the absence of allozyme variability is know for other rare species, the lack of AFLP variation is unexpected, since this method normally reveals polymorphic loci, even when allozyme variation is absent. This suggests exceptionally low genetic diversity in the Wollemi Pine. Long term isolation, small population size and clonality may have contributed to this pattern.

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PB: And if you paid attention to what you read you would have noticed that the title is a misrepresentaion of the content. They didn't find LOW varibility, they found NO variablity at all. In my opinion that is something completely different, and if it would have been LOW --instead of NO-- variability I wouldn't have shown it as an example!! You may think I am, but I'm not stupid!!

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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. Talk about nitpicking — if you’d like, you can always email Dr. Peakall yourself and ask for a clarification. I’m going by what the man wrote — not what I want it to be.

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Q: Ya see, Peter, I don't get my info from popular science books written by journalists. You ought to try it some time. BTW: Dr. Peakall also told me that a detailed genetics paper is now in preparation, and promised to forward a copy when it is submitted.

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PB: To judge from your intonation I hit a raw nerve. Well, at last you met somebody who checks all evo-claims and it may hurt a bit that I already overturned several claims. So, I can imagine that it not so funny. Sorry for that.
And apparently, you --like Dr Page-- seem to find it pleasing to be condescending. As soon as you are able to nitpick your so eager, it shows. I really feel sorry for that and if it demonstrates something: defence of your beliefs.

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Nitpicking? I certainly don’t consider it nitpicking to contrast a popular press book written by a journalist with the scientific, peer-reviewed papers published by the researchers who are actually studying the organism. Not my fault you can’t find more reliable data to back up your claims. Also, feel free to point out specifically where you think I was condescending so I’ll know what to avoid in the future. Although, to be honest, I feel flattered to be compared favorably to Dr. Page.

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If you can send me a copy of the Peakall's articles as soon as you have them in, I would be very grateful.

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Feel free to get them the same way I did — or use a university lending library. I provided the references, you’re quite capable of digging them out. 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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Furthermore, as stated the tree doesn't demonstrate variation in the expected regions, so where exactly do my claims fail. I simply give it another interpretation. By the way, if I recall properly, it was you who claimed in a previous letter (on mtDNA) not to be a molecular biologist so you were not able to interpret the data on this topic. And now suddenly you are able to interpret these molecular data? Very confusing.

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Your claims fail because there are alternate, mainstream explanations for the preliminary data. 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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Thanks for that, I knew he was in Canberra, but as usual I recalled by head (almost photographic memory, I presume). Nitpicking again. You just earned yourself 100 points.

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If you’ll reread the sentence you were responding to, you’ll note I prefaced it with the phrase a point of correction. That doesn’t equate to nitpicking. Now if I’d said, Peter’s ignorant because he doesn’t know that; now THAT would be nitpicking in some ridiculous attempt to score points as you seem to suggest was my intent.

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Actually there are already SEVERAL populations of the tree. I've seen them in the Botanic Gardens in Sydney, the Botanic Gardens of St Thomas, the Zoo, etcetera.

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Okay, allow me to clarify: there are three populations IN THE WILD. Your statement is, as you’ve accused me, nitpicking.

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Q: You really should look into some of the original sources rather than relying on a popular press book - no matter how good it might be. Would you let me get away with quoting Dawkins in a scientific argument? At least he's a scientist...

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PB: O yes since I am not in evolutionisms I am not a scientist. I almost laugh my pants off.

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The statement was a contrast between Dawkins and Woodford. Getting a little shrill, here, Peter. You appear to be LOOKING for some kind of personal attack. Good luck.

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Q: "Surviving populations with invariable DNA" is a serious misstatement. Lack of genetic variability due to long-term isolation and/or severe genetic bottleneck is a relatively well-understood phenomenon. There are numerous examples, from cheetahs to elephant seals. It doesn't, however, imply that the DNA can't vary - simply that it hasn't for the reasons noted. Throw in clonality, and you'd almost expect it...

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PB: I notice that you are perfectly able to copy opinions of evolutionary biologists. I am not impressed by their opinions and you should know that by now. Did you ever ponder these evolutionary riddles youself? Do you have a personal opinion/explanation on these observations? I would really like to know about it.
Furthermore, if it is so well understood explain it to me.
And, it doesn't explain the invariable DNA between the two (or three, or more) stands in the wild.
Please explain to me why it is a misstatement. The trees survive wonderfully, and their DNA is unvariable. I don't see a misstatement here. How can their DNA be so stable? No somatic mutations? Ever thought about that?

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Uhh, that was my opinion. Unlike you, I HAVE studied wild populations with a eye towards developing conservation strategies — that used to be my profession, and is still my avocation. Although not a genetics researcher, I do understand the use of genetics studies in this context. One of the reasons I got (vaguely) interested in Wollemia in the first place — it presented an interesting conservation management challenge. So yeah, in answer to your further condescension, because I’ve personally seen the results in the wild I agree with the findings of the ecologists that small, isolated in-bred populations which have undergone severe population bottlenecks tend to homogenize their genotypes — in the case of cheetahs, for example, to the point where they can accept skin grafts from each other. The specifics of Wollemia, and particularly why it seems to be an extreme case of this, haven’t yet been published. I’m content to wait for an explanation — from the people actually doing the studies. However, I’m willing to bet that in a few generations those specimens that have been transplanted in the various institutes and botanical gardens around Australia WILL begin to significantly diverge unless very stringent controls are put in place.

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As far as your misstatement goes — you state the DNA is unvariable. I call into question your assertion. Show from ANY available data that the DNA of Wollemia is incapable of variation. In fact, from the available published information there is no way you can even infer that the stands are 100% identical genetically. The full study hasn’t been published yet. Can you show me there are NO mutations at all anywhere in the genome of Wollemia? Also, can you show that there was NO variation in the modern organism compared with the fossils (hint — look up the Chambers 1998 article I referenced)? If you can’t your assertion stands as falsified: the DNA of Wollemia nobilis is not incapable of variation.

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So it is able to copice and also to reproduce sexually. Sounds pretty redundant to me. Multipurpose genome?

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Nope. Sounds like we need more information.

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1. I was not only correct in this statement, all my claims on the tree's DNA are correct and you didn't show otherwise. 2. Do you really think that I am presenting this site with disinformation? 3. Of course not, I show all examples that violate evolutionism, including the Wollemia nobilis. I know the answer to their questions: multipurpose genome, no explanation in the evolutionary paradigm. 4. And Peakall knows, since he talked about an ALL-PURPOSE genome regarding the W. nobilis. (Numbers added to make response clear)

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1. NONE of your claims about the tree’s DNA are correct, as I have shown, using the papers referenced. Look ‘em up.
2. Disinformation? Not really. Deliberate, skewed interpretation coupled with misunderstanding and a weak argument from personal incredulity, usually.
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.
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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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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Now THAT’S condescending. Meaningless words? Are you denying that organisms are constrained by their natural history (genetics, ecology, ancestry)? I gave you several reasons why your favorite organism may have been constrained — clonality in the wild, miniscule in-bred population (bottleneck), etc. You’re waaaayyy out there on this one, Peter. Nothing in the concept states that evolution ceased or any of the other strawmen you’re arguing here. What is an endstation of evolution? Can you even conceive of any possible way of falsifying or providing evidence for the existence of any single species of any organism of any kind anywhere on the planet outside of a strictly controlled lab lineage has ceased to evolve? It’s certain as taxes that Wollemia hasn’t stopped (or somehow is no longer capable of) evolving — one of the key issues dealt with by the conservation biology people is how to prevent hybridization. If you don’t think this is a problem, I suggest you look up the stringent efforts being used with the Catalina mahogany (Cercocarpus traskiae) conservation efforts.

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I've had a close-up look at all families of the Araucariacaea --the can all be found in Australia-- and I agree with you that I do not understand that Wollemia, Agathis and Araucaria are classified as Araucariacaea. They don't even resemble each other and are also highly distinct from fossilised Araucaria. (Never understood classifications beyond (sub)species anyway).

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Really? This is fascinating. Please reference the articles you published on the phylogeny of the Araucariacea. (Hint: Agathis and Wollemia are sister clades based on both 18s and rbcL data — of course, you knew that).

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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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Dear Quetzal you really don't understand what I am trying to convey, is it? For your understanding: Between two isolated populations (like two or three isolated stands of trees) of 'living fossils' molecular evolutionism expects to find loads of variablity with respect to neutral positions, redundant genes, 'junk' DNA etcetera. If we don't find it, than I rest my case: multipurpose genome. We didn't observe it for the first organism analysed in this way, the W. nobilis. The other studies have not yet been carried out. I wait for them and I have a close eye on it, since I am almost certain that it will provide more falsification of evolutionism.

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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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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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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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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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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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Try again, Peter.

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Originally posted by Mammuthus:
PB:
5) there is/has been creation (=creaton interactions with matter in a morphogenetic field giving rise to genes and genetic programs in preexisting genetic programs).

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M:
According to this premise, all organisms in close proximity to one another should be genetically identical. Thus, when you were concieved Peter, you should have been most genetically similar to your mother, father, and any bacteria, viruses, and fungi that would have been present. If anyone else was in close proximity, they would be equally closely related to you as their matter would also be in the morphogenetic field. Ultimately, there should be no genetic differences among any humans and there should also be no more than one sex since this is also a genetic difference.

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At the species level, all organisms that are in the same environment should be almost genetically identical not just to one another but to ALL organisms as they all reside and reproduce within the same morphogenetic field. Thus, South American monkey should in no way genetically resemble Old World monkey as they are not in the same field. If you posit that the field is world wide, then there should be absolutley no genetic differences between a tomato, person, bacteria.

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bumpity bump

My understanding is that the "morphogenetic field" as some Ho etc embryology may suggest IS NOT the same thing as Sheldrake's "morphic resonance" which rather appears to make a monkey out of Mammuthus's word program use etc but this as far as have been able to ascetain if anything would have to have been an insectivore and not a primate but what do i know?

Dear guys (Quetzal and Mammuthus),You will have your reply. Don't worry about that.Best wishes,
Peter

dear Mammuthus,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.best wishes,
Peter

DEAR QUETZAL,THANKS FOR YOUR EXTENSIVE REPLY,YOU WROTE:quote:
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Quoted from Peakall 1998: So far, within the Wollemi Pine no allozyme variability has been found at 13 allozyme loci. Furthermore, no variability has been detected at more than 800 loci, visualised by the AFLP method. While the absence of allozyme variability is know for other rare species, the lack of AFLP variation is unexpected, since this method normally reveals polymorphic loci, even when allozyme variation is absent. This suggests exceptionally low genetic diversity in the Wollemi Pine. Long term isolation, small population size and clonality may have contributed to this pattern.
PB: And if you paid attention to what you read you would have noticed that the title is a misrepresentaion of the content. They didn't find LOW varibility, they found NO variablity at all. In my opinion that is something completely different, and if it would have been LOW --instead of NO-- variability I wouldn't have shown it as an example!! You may think I am, but I'm not stupid!!--------------------------------------------------------------------------------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. Talk about nitpicking — if you’d like, you can always email Dr. Peakall yourself and ask for a clarification. I’m going by what the man wrote — not what I want it to be.MY RESPONSE:
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.
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. 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.quote:
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Q: Ya see, Peter, I don't get my info from popular science books written by journalists. You ought to try it some time. BTW: Dr. Peakall also told me that a detailed genetics paper is now in preparation, and promised to forward a copy when it is submitted.PB: To judge from your intonation I hit a raw nerve. Well, at last you met somebody who checks all evo-claims and it may hurt a bit that I already overturned several claims. So, I can imagine that it not so funny. Sorry for that.
And apparently, you --like Dr Page-- seem to find it pleasing to be condescending. As soon as you are able to nitpick your so eager, it shows. I really feel sorry for that and if it demonstrates something: defence of your beliefs.--------------------------------------------------------------------------------Nitpicking? I certainly don’t consider it nitpicking to contrast a popular press book written by a journalist with the scientific, peer-reviewed papers published by the researchers who are actually studying the organism. Not my fault you can’t find more reliable data to back up your claims. Also, feel free to point out specifically where you think I was condescending so I’ll know what to avoid in the future. Although, to be honest, I feel flattered to be compared favorably to Dr. Page.MY RESPONSE:
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.quote:
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If you can send me a copy of the Peakall's articles as soon as you have them in, I would be very grateful.
--------------------------------------------------------------------------------Feel free to get them the same way I did — or use a university lending library. I provided the references, you’re quite capable of digging them out. 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.MY RESPONSE:
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.quote:
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Furthermore, as stated the tree doesn't demonstrate variation in the expected regions, so where exactly do my claims fail. I simply give it another interpretation. By the way, if I recall properly, it was you who claimed in a previous letter (on mtDNA) not to be a molecular biologist so you were not able to interpret the data on this topic. And now suddenly you are able to interpret these molecular data? Very confusing.
--------------------------------------------------------------------------------Your claims fail because there are alternate, mainstream explanations for the preliminary data.MY RESPONSE:
NO, THERE ARE NO EXPLANATIONS FOR THE INVARIABILITY OF DNA BETWEEN THE TWO (NOW THREE) POPULATIONS IF THEY WERE NOT DERIVED BY CLONING.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.quote:
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Thanks for that, I knew he was in Canberra, but as usual I recalled by head (almost photographic memory, I presume). Nitpicking again. You just earned yourself 100 points.
--------------------------------------------------------------------------------If you’ll reread the sentence you were responding to, you’ll note I prefaced it with the phrase a point of correction. That doesn’t equate to nitpicking. Now if I’d said, Peter’s ignorant because he doesn’t know that; now THAT would be nitpicking in some ridiculous attempt to score points as you seem to suggest was my intent.MY RESPONSE:
OKAY, SORRY FOR THAT. I THOUGHT YOU WERE NITPICKING.quote:
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Actually there are already SEVERAL populations of the tree. I've seen them in the Botanic Gardens in Sydney, the Botanic Gardens of St Thomas, the Zoo, etcetera.
--------------------------------------------------------------------------------Okay, allow me to clarify: there are three populations IN THE WILD. Your statement is, as you’ve accused me, nitpicking.MY RESPONSE:quote:
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Q: You really should look into some of the original sources rather than relying on a popular press book - no matter how good it might be. Would you let me get away with quoting Dawkins in a scientific argument? At least he's a scientist...
PB: O yes since I am not in evolutionisms I am not a scientist. I almost laugh my pants off.--------------------------------------------------------------------------------The statement was a contrast between Dawkins and Woodford. Getting a little shrill, here, Peter. You appear to be LOOKING for some kind of personal attack. Good luck.MY RESPONSE:
SORRY, TO HAVE MISUNDERSTOOD YOU. I THOUGHT YOU REFERRED TO SCIENTISTS IN GENERAL. IT WASN’T MEANT AS A PERSONAL ATTACK. 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).quote:
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Q: "Surviving populations with invariable DNA" is a serious misstatement. Lack of genetic variability due to long-term isolation and/or severe genetic bottleneck is a relatively well-understood phenomenon. There are numerous examples, from cheetahs to elephant seals. It doesn't, however, imply that the DNA can't vary - simply that it hasn't for the reasons noted. Throw in clonality, and you'd almost expect it...
PB: I notice that you are perfectly able to copy opinions of evolutionary biologists. I am not impressed by their opinions and you should know that by now. Did you ever ponder these evolutionary riddles youself? Do you have a personal opinion/explanation on these observations? I would really like to know about it.
Furthermore, if it is so well understood explain it to me.
And, it doesn't explain the invariable DNA between the two (or three, or more) stands in the wild.
Please explain to me why it is a misstatement. The trees survive wonderfully, and their DNA is unvariable. I don't see a misstatement here. How can their DNA be so stable? No somatic mutations? Ever thought about that?--------------------------------------------------------------------------------Uhh, that was my opinion. Unlike you, I HAVE studied wild populations with a eye towards developing conservation strategies — that used to be my profession, and is still my avocation. Although not a genetics researcher, I do understand the use of genetics studies in this context. One of the reasons I got (vaguely) interested in Wollemia in the first place — it presented an interesting conservation management challenge. So yeah, in answer to your further condescension, because I’ve personally seen the results in the wild I agree with the findings of the ecologists that small, isolated in-bred populations which have undergone severe population bottlenecks tend to homogenize their genotypes — in the case of cheetahs, for example, to the point where they can accept skin grafts from each other. The specifics of Wollemia, and particularly why it seems to be an extreme case of this, haven’t yet been published. I’m content to wait for an explanation — from the people actually doing the studies. However, I’m willing to bet that in a few generations those specimens that have been transplanted in the various institutes and botanical gardens around Australia WILL begin to significantly diverge unless very stringent controls are put in place.MY RESPONSE:
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. 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.
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. 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.YOU SAY:
As far as your misstatement goes — you state the DNA is unvariable. I call into question your assertion. Show from ANY available data that the DNA of Wollemia is incapable of variation. In fact, from the available published information there is no way you can even infer that the stands are 100% identical genetically. The full study hasn’t been published yet. Can you show me there are NO mutations at all anywhere in the genome of Wollemia? Also, can you show that there was NO variation in the modern organism compared with the fossils (hint — look up the Chambers 1998 article I referenced)? If you can’t your assertion stands as falsified: the DNA of Wollemia nobilis is not incapable of variation.MY RESPONSE:
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.YOU WRITE:quote:
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So it is able to copice and also to reproduce sexually. Sounds pretty redundant to me. Multipurpose genome?
--------------------------------------------------------------------------------Nope. Sounds like we need more information.quote:
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1. I was not only correct in this statement, all my claims on the tree's DNA are correct and you didn't show otherwise. 2. Do you really think that I am presenting this site with disinformation? 3. Of course not, I show all examples that violate evolutionism, including the Wollemia nobilis. I know the answer to their questions: multipurpose genome, no explanation in the evolutionary paradigm. 4. And Peakall knows, since he talked about an ALL-PURPOSE genome regarding the W. nobilis. (Numbers added to make response clear)
--------------------------------------------------------------------------------1. NONE of your claims about the tree’s DNA are correct, as I have shown, using the papers referenced. Look ‘em up.MY RESPONSE:
ALL MY CLAIMS ON THE WOLLEMIA’S DNA STILL STAND. WORSE, THERE ARE NOW THREE STAND WITH THE SAME DNA SEQUENCES.YOU WRITW:
2. Disinformation? Not really. Deliberate, skewed interpretation coupled with misunderstanding and a weak argument from personal incredulity, usually.MY RESPONSE:
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.YOU SAY:
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.MY RESPONSE:
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.YOU SAY:
4. Now I insist you email him. Where in ANY his articles does Dr. Peakall talk about an all-purpose genome?MY RESPONSE:
HE IS BEEN QUOTED IN THE WOODFORD’S BOOK IN A PERSONAL INTERVIEW WITH HIM. AS STATED BY WOODFORD (PAGE 169):WE TALKED ABOUT HOW, IN THE CASE OF WOLLEMI PINES, EVOLUTIONARY THEORY DIDN’T SIT COMFORTABLE.AND LATER HE EXPLAINS (PAGE 170):MAYBE WHAT’S HAPPENING HERE, PEAKALL REFLECTED, IS THAT OVER ALONG EVOLUTIONARY HISTORY AND DESPITE LOW DIVERISTY THESE PLANTS HAVE DEVELOPED AN ALL-PURPOSE GENOTYPEYOU SAY:
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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'"
--------------------------------------------------------------------------------Now THAT’S condescending. Meaningless words? Are you denying that organisms are constrained by their natural history (genetics, ecology, ancestry)?MY RESPONSE:
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).YOU WRITE:
I gave you several reasons why your favorite organism may have been constrained — clonality in the wild, miniscule in-bred population (bottleneck), etc. You’re waaaayyy out there on this one, Peter. Nothing in the concept states that evolution ceased or any of the other strawmen you’re arguing here. What is an endstation of evolution? Can you even conceive of any possible way of falsifying or providing evidence for the existence of any single species of any organism of any kind anywhere on the planet outside of a strictly controlled lab lineage has ceased to evolve? It’s certain as taxes that Wollemia hasn’t stopped (or somehow is no longer capable of) evolving — one of the key issues dealt with by the conservation biology people is how to prevent hybridization. If you don’t think this is a problem, I suggest you look up the stringent efforts being used with the Catalina mahogany (Cercocarpus traskiae) conservation efforts.MY RESPONSE:
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.
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.YOU WRITE:
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I've had a close-up look at all families of the Araucariacaea --the can all be found in Australia-- and I agree with you that I do not understand that Wollemia, Agathis and Araucaria are classified as Araucariacaea. They don't even resemble each other and are also highly distinct from fossilised Araucaria. (Never understood classifications beyond (sub)species anyway).
--------------------------------------------------------------------------------Really? This is fascinating. Please reference the articles you published on the phylogeny of the Araucariacea. (Hint: Agathis and Wollemia are sister clades based on both 18s and rbcL data — of course, you knew that).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?MY RESPONSE:
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.quote:
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Dear Quetzal you really don't understand what I am trying to convey, is it? For your understanding: Between two isolated populations (like two or three isolated stands of trees) of 'living fossils' molecular evolutionism expects to find loads of variablity with respect to neutral positions, redundant genes, 'junk' DNA etcetera. If we don't find it, than I rest my case: multipurpose genome. We didn't observe it for the first organism analysed in this way, the W. nobilis. The other studies have not yet been carried out. I wait for them and I have a close eye on it, since I am almost certain that it will provide more falsification of evolutionism.
--------------------------------------------------------------------------------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.MY RESPONSE:
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.YOU SAY:
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.MY REPONSE:
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.YOU SAY:
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.MY RESPONSE:
SOMATIC MUTATIONS MIGHT BE EXPECTED IN COPICING PLANTS.YOU SAY:
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).MY RESPONSE:
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.YOU SAY:
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.MY RESPONSE;
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?BEST WISHES, AND I LOOK FORWARD TO YOU RESPONSE,PETER

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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.1) Do these data mean that approximately 450 bp changes occurred on neutral positions?SORRY PETER BUT NOTHING IN YOUR LETTER INDICATES TO ME WHERE THIS QUESTION COMES FROM. ARE YOU REFERREING TO SOMETHING IN THE ARTICLE?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?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.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?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.3a) Is it independent from nearby genes? Independent from the rest of the genome?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.: Mol Biol Evol 2002 May;19(5):689-97 Related Articles, LinksPurifying selection and birth-and-death evolution in the histone H4 gene family.Piontkivska H, Rooney AP, Nei M.Institute of Molecular Evolutionary Genetics, Pennsylvania State University, 328 Mueller Lab, University Park, PA 16802, USA. oxp108@psu.eduHistones 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.: Proc Natl Acad Sci U S A 2000 Sep 26;97(20):10866-71 Related Articles, LinksPurifying selection and birth-and-death evolution in the ubiquitin gene family.Nei M, Rogozin IB, Piontkivska H.Institute of Molecular Evolutionary Genetics and Department of Biology, Pennsylvania State University, 328 Mueller Laboratory, University Park, PA 16802, USA. nxm2@psu.eduUbiquitin 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.3b) Does this type of selection take place on the level of the organism? How?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 ORGANISM4) Are there identical (=very recently duplicated) genes in known genomes?Annu Rev Cell Dev Biol 2002;18:53-80 Related Articles, LinksGene co-option in physiological and morphological evolution.True JR, Carroll SB.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.eduCo-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.5) Is evolution a phenomenon driven by random mutation?
YESI 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.Best wishes and thanks for responding to the posts
M

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Originally posted by Brad McFall:
My understanding is that the "morphogenetic field" as some Ho etc embryology may suggest IS NOT the same thing as Sheldrake's "morphic resonance" which rather appears to make a monkey out of Mammuthus's word program use etc but this as far as have been able to ascetain if anything would have to have been an insectivore and not a primate but what do i know?

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**********************I get the impression you disagree with something I said Brad. I did not propose a morphogenetic field, Peter did. I also did not attempt to associate insectivores with primates unless you mean the comment I made in one post about Afrotheria. Could you state specifically what your disagreement is and for clarity and brevity sake (I know I am a hypocrite since my posts are often long , do it in few words? Thanks in advance.Mammuthus

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.

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

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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).

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.

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Originally posted by peter borger:
dear SLPx,

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You are purposely obtuse. You know what I mean and you know that I am right.

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No, I know that you do not seem to know the difference between "gene" and "exon." If you did, you would not keep referring to the ZFX/ZFY as the "gene." It is but a small portion of the gene, as I alreeady explained, and, as I already explained, there is no reason to assume that it should have accumulated mutational change. You never did supply your math demonstrating that there should have been change in that particular exon.And, no, PB, I do not know that you are 'right'. About this or anything else, though I have found your repeated claims that Dawkins is out of his league when writing on such things... The irony is just too rich...

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Better try to find an evolutionary explanation for these observations.

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I already provided one, as have others. Your continued ignoring of them and continued insistence that you are right about everything smacks of a neurosis, not a conspiracy of denial.

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In addition, you still owe me an evo-explanation for the incongruence of the IL-1beta genes,

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I have asked repeatedly for a citation. I do not feel like rummaging through your voluminoouis diatribes looking for one passing mention of a concrete document.

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and for the stability of the ZFX region studied by Kim et al.

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Now you are just being obtuse. I already commented on that. You ignored it, apparently.

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Next we can discuss --if you like-- the redundant alpha actinin genes,

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Sure - ref please.

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the redundant src-kinases and where they violate molecular evolution and how you try (?) to save evolutionism from falling.

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Oh - I forgot that Your Grae had disproved evolution already, and that we underlings have simply not realized it yet.But I am still wondering why Your Grace prattled on about LCRs and such....

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And please stop trying to represent me as someone not knowing the difference between genes and exons.

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You are doing that to yourself by continuing ot refer to the study by Kim et al. as one in which a "gene" is used.

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Maybe you can provide this site with a contemporary definition of a gene? That would be great. Thanks in advance.

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best wishes,
Peter

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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.Now maybe PB can provide a contemporary justification for referring to an exon as a gene?

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Originally posted by peter borger:
Dear Dr page,

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And, as demonstrated, I not only claimed it but I also demonstrated how to do it.

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best wishes,
Peter

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What are you blabbering about?

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Originally posted by peter borger:
[Or maybe it is a nice challenge for Dr Page since he is the PhD-ed evolutionary biologist of this site and he knows how it works. I cannot answer these questions, since am only a "asthma research creationist guy".]

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best wishes,
Peter

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Creationist 'challenges' are bogus. All such 'challenges' are of the Kent Hovind type - no matter what is presented, the challenge will never be met. Borger has expressed this type of activity numerous times already - simply ignoring or hand-waving any and all explanations presented to him for his many 'challenges' and 'refutations of darwinism.'But it is true that an asthma resarcher is just another layman when discussing evolutionary biology. Ask Phil Johnson.