molecular genetic evidence for a multipurpose genome

This is the magical, mystical organism you've been tantalizing us with for the last several weeks? Wollemi nobilis??!!! You have got to be kidding me!Look at the reality:1. The species is clonal. (I thought you said your magic organism wasn't a clone?) The miniscule population (39 individuals) represents the descendents of a single tree - the ultimate in population bottlenecks, hence refuting your #5 - the very point you thought it proved.2. The species propagates by coppicing - roots grow out from the main tree, then send up shoots. IOW, it isn't a sexually reproducing organism in the wild. Interestingly enough, it was discovered during planning for conservation of this unique species that it DOES produce viable seeds like other conifers. Why it clones itself in the wild is unknown at this time.3. The entire family Araucariaceae, of which W. nobilis is a member, shows low genetic variability.This is bizarre, Peter - your own lengthy book quote completely refutes your hypothesis because the bloody plant is a clone of itself that's been isolated from all other populations for thousands of years! All you seem to be doing is rehashing yet another creationist coelocanth-is-a-living-fossil "argument from journalistic sensationlism".

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Q: 1. The species is clonal. (I thought you said your magic organism wasn't a clone?) The miniscule population (39 individuals) represents the descendents of a single tree - the ultimate in population bottlenecks, hence refuting your #5 - the very point you thought it proved.

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PB: If you know so much about this tree why don't you write a letter to Dr Peakall (University of Canberra), and explain to him how it all works. I think he will be pretty pleased, so he can publish his work --at last-- in a peer reviewed scientific journal.

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Actually, I did. Dr. Peakall was quite kind enough to forward to me two of his articles:Hogbin PM, Peakall R, Sydes MA, 2000. Achieving practical outcomes from genetic studies of rare Australian plants, Aust. J. Bot. 48, 375—382Peakall R. 1998. Exceptionally low genetic diversity in an ancient relic, the Wollemi pine: implications for conservation theory and practice. 45th Annual meeting of the Genetics Society of Australia. Abstracts 86.From the latter:

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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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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.A point of correction: Dr. Peakall is with the Australian National University in Canberra, not the "university of Canberra".

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Actually there are two populations of the tree, both were analysed and demonstrated exactly the same DNA (as mentioned in letter #1). Surviving populations with invariable DNA points in the direction of a stable multipurpose genome, not in the direction of evolution.

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Actually, there are THREE populations of the tree - which of course Woodford didn't know at the time he published his book. 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..."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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Q: The species propagates by coppicing - roots grow out from the main tree, then send up shoots. IOW, it isn't a sexually reproducing organism in the wild. Interestingly enough, it was discovered during planning for conservation of this unique species that it DOES produce viable seeds like other conifers. Why it clones itself in the wild is unknown at this time.

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PB: If you have your information from New Scientist december 1997 than I have to dissapoint you. Coppicing was the initial thought of Peakall but according to Woodford's book (2000) it does not coppice, but sexually reproduces (see mailing #1).

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Sorry to disappoint you, but I have my info from the person who actually studied the plant. You need to reread your book, as well as my post. The plant propagates by coppicing IN THE WILD. It was found during conservation planning, however, that it quite readily reproduces sexually ex situ - making it much easier to replicate the plant in collections in multiple facilities, and giving hope to the long-term conservation of the species. IOW, the species DOES produce viable seeds and pollen. The investigation into the reasons for this is on-going - and makes for quite fascinating research in its own right.Where you are correct is that there is no evidence yet that the three populations were connected by subterranean roots (digging up the ground between the stands could be hazardous to the trees). Given the physical separation between stands, Dr. Peakall considers it unlikely. That's why there's on-going study - to answer that question.

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Q: The entire family Araucariaceae, of which W. nobilis is a member, shows low genetic variability.

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PB: That is true. Araucariacaea demonstrate very low variability and that is in accord with the hypothesis of a multiporpose genome. Low variablity due to extremely stable DNA guarded by hundreds of DNA repair enzymes. Observed variation is due to regulatory, rather than mutational phenomena. All in accord with the multipurpose genome.

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Nope, wrong again. The data indicates there are evolutionary constraints in action, not some mythical multipurpose genome. See, for example, Setoguchi, H., Osawa, T.A., Pintaud, J.C., Jaffre, T. & Veillon, J.-M. 1998. Phylogenetic relationships within Araucariaceae based on rbcL gene sequences. Amer. J. Bot. 85: 1507-1516, or Hanson, L. 2001. Chromosome number, karyotype and DNA C-value of the Wollemi Pine (Wollemia nobilis, Araucariaceae). Bot. J. Linn. Soc. 135: 271-274.In addition, the tree isn't all that similar to the Cretaceous Araucariaceae. See, for example: Chambers, T.C., Drinnan, A.N., McLoughlin, S. 1998. Some morphological features of Wollemi Pine (Wollemia nobilis, Araucariaceae) and their comparison to Cretaceous plant fossils. Internat. J. Plant Sci. 159: 160-171.

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PB: What do you mean by 'argument of journalistic sensationalism'? As far as I know nothing has been published on this tree for sensationalism. Please be specific in your statements.

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Lol, almost everything published in the popular press on this tree, beginning with the first accounts of its discovery, have been sensational journalism in action. "Dinosaur tree", "living fossil", "green dinosaur", etc are all splashy, flashy journalistic bombast. Even the full title of Woodford's book which you like so much, "The Wollemi Pine. The Incredible Discovery of a Living Fossil from the Age of the Dinosaurs" lends proof to my contention. Nice try.As to the horseshoe crab and coelocanth, please start a new thread if you want to drag out these old creationist chestnuts - more examples of "argument from journalistic sensationalism".

Mammuthus: I hadn't thought about that. I wonder how Peter's morphogenetic field "hypothesis" explains continuous gradations in populations of the same species over the full geographic extent of its range. One sterling example is the red-backed salamander of the eastern US (Plethodon cinereus). There is significant phenotypical variation in a gradual blending of characteristics from the southern to the northern end of the range, as well as east-west, northeast-northwest, etc. Taxonomists only divide the species into subspecies using a suite of average traits at the extreme ends of the range (and because taxonomists always want to pigeonhole organisms into neat categories). However, the geographic divisions are not only arbitrary but pretty near meaningless.How about it Peter? Want to try and answer M's question?

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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.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).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.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.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.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).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.Try again, Peter.

Actually, there was another bit that I forgot to address in your post, Peter.

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(By the way, Dawkins is a zoologist trying to get a bit of understanding of genes. I could educate him in this topic, and I wouldn't let you get away with qouting him, that's for sure).

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And yet, Dawkins IS a zoologist and actually knows something about morphology, anatomy, and evolution. Nonetheless, I would never quote one of his popular books in a scientific discussion. Your ENTIRE argument rests on one popular press book written by a JOURNALIST! Can you say, "double standard"?Tell you what, Peter, I won't use Dawkins if you don't use Woodford. Fair deal?

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Originally posted by Tranquility Base:
I recently read a population genetics article where the researcher pointed out that, without exception, their field of study related to microevolution. Yes, just as Erwin did (I feel like Brad dropping names wihtout refs like that) this researcher used the dirty micro word.

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I am happy to call it evolution but I can understand creationists who don't want to call it that. In any case it has almost nothing to do with macroevolution.

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Citing allelic frequency changes, and allelic mutations, as evidence for macroevolution is extremely misleading.

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Hi TB:I'm not sure I agree with you here. Although I've always cringed at the "artificial" distinction between micro- and macroevolution (primarily because it's been so badly misused), the terms ARE becoming fairly widespread in the lexicon. Although I really dislike "argument from quotation", these two passages underscore the reality of what is being discussed:1. "Evolutionary processes that occur at rates fast enough to be manifested as change within a single species lineage (*within-species* patterns) are included within the domain of *microevolution*. By contrast, processes that occur at slower rates, so that their effects are manifested in *among-species* patterns, are consigned to the realm of *macroevolution*. Microevolution and macroevolution are thus considered to be parts of a more inclusive whole represented by the hierarchical nature of biological systems."Brooks D & McLennan D. 1991. "Phylogeny, Ecology, and Behavior: A Research Program in Comparative Biology" University of Chicago Press, p. 16.2. "Nearly all the factors that have been used to distinguish the origin of higher categories can be attributed to the same processes of speciation, behavioral adaptation and the gradual accumulation of morphological differences that characterize evolution at the levels of populations, species, and genera. There are no fundamental differences between the early stages in the radiation of placental mammals in the earliest Cenozoic and what is known to have occurred in the origin of the species flocks in the East African Great Lakes...Although formulation of a distinct theory of macroevolution does not appear to be justified, it may be convenient to retain the terms microevolution and macroevolution to describe the different patterns of evolution that are observed at the level of populations and species versus higher taxonomic levels and time spans exceeding 5-10 million years."Carroll R. (1997) "Patterns and Processes of Vertebrate Evolution". Cambridge University Press, pg. 392 (emphasis in original).I especially like the Carroll quote because he talks about the paleontological "pattern" observed in the fossil record, and brings in a modern example for illustration. This is the same issue - pattern, i.e. mode and tempo - that led Gould and Eldredge to formulate punk eek. Basically, both authors are saying, "yes, we can make a differentiation for different purposes", but both are saying that there is no fundamental difference in the processes between the two.To close, you might find this article interesting - from the late SJ Gould himself: Tempo and mode in the macroevolutionary reconstruction of Darwinism.[This message has been edited by Quetzal, 10-29-2002]

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).

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Originally posted by peter borger:
dear Quetzal,

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

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best wishes,
Peter

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

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I never said genes were lost.

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Are you sure you never implied this? I invite your attention to this bit:

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Do you believe no genetic information is lost after a bottleneck occurs? Why in the world would there be less genetic variation?

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Perhaps the problem is you haven't defined your terms. What is, in your definition, "genetic information"? How do you detect/quantify its "loss" (or gain, for that matter)? How is it lost without loss of genes? Is there some other way of losing information? If so, what?Mammuthus, however, never said genes were lost - he asked if you believe so, since your entire point rests on "loss of information" whatever that is.

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I truly hope you do not have a PhD, because there is simply no excuse for anyone, even an evolutionist, to claim that a bottlenecked animal such as the cheetah has not lost genetic information due to the isolation event and subsequent genetic drift. According to the dream world of Mammuthus, if we isolate the poodle completely, and let it breed only with other poodles, we can eventually get a St Bernard.

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Now this is an amazing departure. Please show specifically where Mammuthus even mentioned dogs. Let alone discussed the derivation of a St. Bernard from a poodle. Are you capable of rational discussion, or just killing strawmen? It's actually quite easy to "claim" that a genetic bottleneck doesn't cause "loss of information" since no one has defined what that means... And I'd be willing to bet Mammuthus has a WHOLE lot more understanding of pop gen than you do - at least going by what you've shown so far.Spare us the infantile ad hominems. Evcforum isn't whatever childish creationist board you apparently usually frequent.

Thanks for your reply.

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Since evolutionists generally reject a thorough definition of information (since it refutes their theory), for the sake of discussion we can limit the definition to the following: An algorithm that programs something that is useful for the organism’s gene pool. We’ll assume the sender is nature (as opposed to the obvious choice of intelligence). That is, we’ll already assume that nature (via blind selection and chance mutation) created the algorithms (aka genes) in the parent population. I’m already giving you a huge (realistically unbridgeable) head start.

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Okay, you have a few problems here. First of all, you're mixing three (at least) definitions of information: teleo-semantic, Shannon-Weaver and Kolmogorov-Chaitin Algorithmic Information Theory (AIT). Although all three can be used in biology, they are incompatible since they measure three different things. Semantic, because you are discussing "usefulness"; Shannon because you're babbling about "senders"; and KC because you're talking about string length. This is fairly typical of creationist misuse of information theory. Pity; from your reputation I was hoping you'd have some new approach.However, you have an even larger flaw in your argument here. To be able to identify a trait (code string or algorithm, if you wish) as "useful" to the organism, you must take into consideration all the environmental factors impacting on the particular trait. Therefore, to be able to analyze the information content reflected in a particular trait, especially in terms of "loss" or "gain" of information, you have to assign a value to the information contained in the environment that effects it. Since you've already cited him, I'm surprised you didn't know this - Tom Schneider talks about this quite thoroughly in Sequence Logos, Machine/Channel Capacity, Maxwell’s Demon, and Molecular Computers.Before we even begin to discuss the complex system dynamics of population bottlenecks in relation to information theory, you need to refine what type of info you're talking about. Try this (we'll start simply):A man is walking down the street on a windy day. A tile, blown off a roof falls directly toward his head.1. Assume the man notices the tile. What is the information content of this situation? What factors must be taken into consideration when analyzing the amount of information in this scenario (i.e., how is the man "informed")? Which information theory applies?2. Assume the man doesn't notice the tile. What is the information content of this situation? Again, what factors should be taken into consideration that would effect the amount of information?If you can't answer this simple example, I find it difficult to comprehend how you can even begin to approach the bottleneck/information discussion.Awaiting your reply.

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I've had a good look at figures of Dilwynite- and Wollemia pollen and it is easy to discriminate between the two. So, this argument fails. Show me the figures where they demonstrate that the pollens of dylwinites and wollemia pollen are indistinguishable.

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I gave you the reference, look it up for goodness sake!

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Probably so, or probably not? Of course this the evolutionary vision and I am aware of it. It does however NOT explain the invariability in the region that are usually highly variable regions. That was my point and still is my point. It tells me that DNA sequences are stable throughout time and that difference between individual trees is not likely to be due to pointmutations, but rather through differential gene regulation. Differential regulation probably involves the histon code.

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So, anything written by an evolutionary biologist, botanist, geneticist, etc is by definition incorrect according to your view? Continue to believe whatever you wish. You’ve been shown to be wrong — repeatedly. I have cited multiple references, and every single article ever published on Wollemia nobilis. If you wish to continue arguing that the authors of these studies are completely wrong, there’s not much I can do to convince you otherwise.

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Demonstrate where the data are erroneous and incomplete, back it up with refernces.

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Suggest you actually go back and read all the references I’ve provided. Your interpretations have been shown to be erroneous. The data is incomplete because Peakall hasn’t completed the study — the initial sequencing was done on only 18s (by Peakall), and rcbl by (Setaguchi et al), references for which you have already been provided. This means that your assertion that this flipping tree somehow proves multipurpose genomes are absolutely stable and evolutionary theory completely overthrown is based at best on limited data from an initial study.

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Of course I am not being taken seriously by evolutionists. When I registered to this site it was one of the first things that came into my mind as a possible evolutionist's fallacy: O this guy doesn't understand anything about biology, so we don't have to take him seriously. I am used to that fallacy already.

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If I didn’t think you were serious, I’d have ignored you completely. However, you have shown your ignorance or willful misunderstanding of even basic biology every time you type a new response.

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Furthermore, I don't know exactly how you make up your mind but I have the feeling that as long as an evolutionary vision hasn't been put forward, you simply do not know what to say about the data. For the rest you adapt to any evolutionary explanation that comes by, without objectively looking at the plausibility of the explanation. In contrast, I can immediately recognise whether molecular data are in accord with evolutionism or not. And I don't buy far-fetched evolutionary explanations anymore, since I can make up stories myself.

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Yet another personal attack. Nope, wrong again. Since I’m not the one actually performing the original research, I tend to listen to the folks that are. When what they are saying contradicts other things — either my own personal observations or some other scientist — I dig into the subject in more depth and make up my own mind. On the other hand, I tend to only reference articles in these discussions which I agree with — otherwise I wouldn’t post them. Not my fault if the articles contradict your little fantasies. And I agree — you’re great at making up far-fetched stories.

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Finally, the case of Wollemia is extreme AND unusual. Even Dr. Peakall acknowledged that. If it is so common, give me the references please that show NO variability in subpopulations of organisms.

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I did — I referenced several plants, a couple of mammals, etc. Pay attention. If you can’t keep up, take notes.

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All your answers are biased by the axioma "evolution is true". You are unable to think beyond this axioma. Probably --most likely-- the axioma you live with is wrong, and I provided a different explanation, that may be wrong but --most likely-- it may as well be right.

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Whether it’s true or not is what we’re discussing, isn’t it? So far, you’ve shown a grand total of zip, zilch, nada that indicates you’ve falsified evolution as you’ve claimed. You haven’t even raised a decent question yet. The only thing you’ve done is make unsupported assertions and refused to answer direct questions.Tell you what: here’s my axiom (and so you’ll stop claiming I don’t know anything). For me, to understand biodiversity and the birth and death of populations and species — and how to preserve them - requires an understanding of the natural history and ecology of individual species, and the biology of the individual organisms that make up the species. Survival of populations in the wild is dependent on effective population size, distribution, and density. The number of birds crammed into a small forest fragment or the number of algae cells on a wet rock effects food supply, how heavily predators and pathogens strike, to what degree reproduction is delayed or effective, how long individuals live, which new competitors can force themselves into the community, etc. To understand life, you must specify the context — the parameters of which are a function of a particular time and place. To understand biodiversity, you have to understand the processes of speciation and extinction - the birth rate of new species and the longevity of the clades they in turn spawn. You have to understand the first order effects of any environmental change, and the second-order ripples they cause, the third-order changes caused by the second, etc. And you need to understand the natural history underpinnings of the creation of ecosystems — because no organism on the planet lives in isolation. That is where my axiom comes from. Creaton waves, magical multipurpose genomes, spurious non-random mutations do absolutely NOTHING to advance my understanding of the processes that are critical to my work. Every single plant, animal, insect or fungus that I’ve ever encountered; every single interaction in the wild I’ve ever studied, merely confirms what science tells me about evolution. Hope that answers your question Dr. Borger.

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I could tell Dr Peakall about my vision, but I guess that I will have similar responses as I get from you, mammuthus, Dr Page. So, why bother. His assertion of an all-purpose genome was in response to the invariability between the two stands. Now there are even three stands. This is the context of his 'all-purpose genome': "Whatever crash-tackled the tree, one of the most conservative organisms that life has ever thrown up, must have been bordering on apocalypse. So seriously", Peakall told me, "the best genetic constitution hasn't been able to get it out of the canyon. But the flipside is, once it settled down in there its all-purpose genome has allowed it to do as well as it can. I think there's a lot of luck in this story." (The wollemi pine, J. Woodford in discussion with Dr Paekall. Page 171) So, Dr Peakall acknowledges --actually invents-- an ALL-PURPOSE genome.

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I’m still waiting for you to contact him for an explanation. If you think he’s so dead certain about the reality of your assertion, you should be jumping at the chance.

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You didn't provide an explanation. Even Dr Paekall didn't have an explanantion. Why? Because there is NO evolutionary explanation. You are free to think that you have provided an explanation, but I know better from a molecular stance.

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{Begin Borger mode}You’re just so wrapped up in your dogmatic assertion of creatons and multipurpose genomes that you can’t accept any other explanation.{/Borger mode} I’ve given you several explanations from pop gen and ecology that could account for the limited variation in this species. Try actually developing a logical argument against them — like tell me WHY clonality, or extreme bottleneck, or any of the other explanations don’t make sense. All you’re doing is handwaving — in fact, if you hand wave much more you’re going to achieve liftoff.

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All mainstreams explanation you provided end in a dead alley. I wouldn't have had a problem with the Wollemia nobilis if there was only one stand with identical DNA. Now there are two (or three) identical populations that cannot have been cloned from each other, I --and with me Dr Peakall-- have a severe molecular evolutionary problem with the tree. I pointed this out in my previous letter, but you just don't seem to get my --and Dr Peakall's-- point.

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Okay, so I stand corrected: you HAVE received a response from Dr. Peakall. Please post it so we can all see how much he supports your position.

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Your idea is that small populations are highly susceptible to diseases since they are gentcally uniform. Maybe your idea is wrong. Judging the Wollemia the are perfectly able to survive under several different conditions. Even in the city of Sydney I've encountered them. So, that is the multipurpose genome in action. Furthermore, I wonder whether you can provide evidence for your assumption that genetically uniform populations are more prone to diseases or that this observation merely reflects loss of genetic information that leads to extinction upon unusual stimuli from the environment (diseases). I guess this is a chicken-egg problem, so my vision against yours.

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Even in the city of Sidney you’ve encountered them? Amazing — and here I’d thought everyone was saying they were rare. Oh, you mean you encountered them in the controlled environment of a botanical garden or institute? Bit of a different story, that.There’s quite a bit in the literature on disease and bottlenecks — my suggestion would be to read some conservation biology. Look up feline infectious peritonitis and check out the FIP outbreak in African cheetahs in East Africa during the 1980’s. There was also a mini-epidemic at the Los Angeles Zoo. In every other species that can be infected by this virus, the mortality rate is about 1%. The 1980’s outbreak in cheetahs was 60% fatal. Do some actual research for a change before you claim that the scientists studying an issue are wrong.

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(I read somewhere that the current population of the oryx was bred from 2 individuals and the alleged extinct cape lion has been found in a Russian zoo and all descended from a couple left there by a circus in the previous century. The concept of inbreeding and enhanced susceptibility to diseases doesn't seem to account for these organisms, including Wollemia. It is a questionable concept.)

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Of course you have references for your oryx assertion, right? I mean which species are you talking about: O. gazella, O. tao, O. beisa, O. leucoryx? Your extremely sloppy scholarship is showing again - you are once more making utterly spurious assertions about what scientists are doing with absolutely no effort on your part to either learn about or understand what it is you’re attacking.As to the cape lion — what’s your point? Two cubs were imported to South Africa from Siberia — but they’re a related subspecies. There are, however, 11 reported specimens of what may be descendants of the cape lion in Ethiopia. Even if they are — and aren’t hybrids with another lion subspecies - as far as I know no genetic tests have been performed (except to show the Siberian cubs were a separate subspecies). So asserting that they are or are not genetically homogenous is pretty speculative, even for you.Of course you’re correct that there’s no risk of pathogens with Wollemia either. That’s undoubtedly why they’ve instituted a complete contamination barrier — including forcing the scientists studying the trees to wash their boots in antiseptic before working with the wild populations — because they’re unconcerned about the introduction of new pathogens.

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My response: endstations can indeed go extinct. Either endstations stay unchanged for eons or they go extinct. Could & Eldredge wrote extensively on this observation.

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No, you misunderstood — endstation as I used it IS extinction. Otherwise the population continues to evolve. When it can’t, it goes extinct. Gould and Eldredge wrote extensively on the mode and tempo of evolution, they didn’t talk at all about endstations or whatever. Now Vrba wrote quite a bit about extinction and selection sweep. Maybe you’re confused.

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Q: 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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PB: I presume that the individuals of these organism demonstrate genetic differences? So, there is no threat to evolutionism. Why bother about hybrids, it merely demonstrates that they are of the same kind. If these organism are able to form hybrids with other organisms what is the problem? Does the hybrid have more or less distinctive genes? Does the genepool increase by cutting the hybrid down?

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Loss of information has nothing to do with speciation? Get familiar with contemporary biology is my advise.

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Read what I wrote! It’s quite straight forward conservation biology. 700 specimens, all genetically related to only three individual genotypes in a single population. And yes, there are genetic differences — don’t tell me you don’t know what a karyotype is I’ll leave you to guess why your questions on the debate over the Catalina mahogany hybrid show you don’t have the first clue what you’re talking about.

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Please provide the reference for the lizard. I will check it on DNA analysis. I expect not to find the change at the nucleotide level (as for the bacteria), but rather on the level of gene expression. This has also been demonstrated in mice. For instance, the agouti-colour is non-mendelian inherited. It depends on a jumping DNA element (usually referred to as a retroviral element) that affect the expression of the agouti-gene.

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I did give you the complete reference. (Hint: look at the original post. See the little line under the title? Click on it and you have access to the original article in the original journal). What the hell does color inheritance in mice have to do with population bottlenecks or even conservation of isolated populations? Nice attempt to baffle with bs by dragging in a complete irrelevancy in an apparent attempt to show off how much you know

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Q: Evolution predicts both variation and stasis, depending on the particular organism and the environmental factors that effect it.
PB: Of course. I could have expected this. In other words evolutionism doesn't predict anything. Pretty bad for a theory.

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Now you’re back to denying organisms have a natural history. Oh yeah, I forgot — magical creaton waves poofed them into existence de novo.

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Yes, and evolutionism doesn't predict anything. I will work on the inconsistencies if they are present. However, the rule on this planet is that species suddenly appear, do not change over time and then become extinct. Pretty much in accord with my hypothesis and not in accord with the gradual changes required by evolutionism.

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I assume this is the Peter Borger Rule of Biodiversity? Again, depends on the organism in question, the environmental factors impinging on it, etc. Some lineages change — speciate — quite readily, others don’t. There’s a lot of interesting debate over the causal factors of this difference.

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Sensible-regions are regions that have a function and do therefore not change. These regions make sense, therefor sensible region. They can be protein coding regions, but also regions that code RNAs involved in regulatory mechanism, regions involved in lining up chromosomes during cell divisions, etcetera. More and more RNA consensus sequences are discovered that are required for gene expression. It will be a major part of the 'junk-DNA'.

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So sensible regions are exons? What happens when one of the various mutations occurs in these sensible regions?

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No, Dr Borger agrees with Dr Peakall that evolution is not sitting well here. He says: 'Wollemia is likely the exception that disproves the rule. The assumption has been made that genetic variability is good because it is the basis of natural selection. The Wollemi pine might actually proof that in some systems it is possible to have exceptionally low variability and stay reasonable happy' (page 170). In my opinion, the Wollemi pine is not an exception but the tree is the extreme of the multipurpose genome. It is proof for a multipurpose genome.

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I’d like you to post the response from Dr. Peakall where he says evolution isn’t sitting well — not the Woodford quotation — the response to your email that you’ve apparently received from him. I’ve never said — nor has any biologist that I’ve ever read — that low variability is a guarantee of extinction, although it's usually a good sign the population is in serious trouble. I also agree that Wollemi Pine isn’t an exception — just an extreme example of a normal distribution. As far as variability is good, although a gross oversimplification, in essence this is true. It’s the key to your question above concerning disease susceptibility. I’m surprised I have to explain this basic concept. The more genetically homogenous a population, the less likely it will contain adaptive variants able to survive or take advantage of new selection pressures. IOW, introduce a new pathogen into a population with lots of variation, there’s much more likelihood that there will be some individuals in the population with at least partial resistance to the pathogen. In a homogenous population, the odds of having an individual or group with resistance is much less, and hence if a pathogen effects one individual, it will effect ALL the individuals in the population.

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Q: No, youre changing your statement. You said that the DNA was incapable of variation.

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PB: No, I didn't say that. Reread my first mail, where I roughly outlined the concept of the multipurpose genome.

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Q: 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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PB: Of course I do not have to prove an absence. The authors already showed that where variability was expected it wasn't found. In addition, I didn't say that DNA is incapable of change, but the mechanisms my be different than assumed. Change at the single nucleotide level is not a major change inducing mechanism. Rather, shuffling of DNA elements that affect gene expression will do the trick. All evidence currently present points in this direction. You may call that evolution, I know it isn't. It is variation induction through preexisting genetic elements. Probably the genome of Wollemia --and other members of the Araucariacaea-- still specifies the most optimal array of DNA repair enzymes.

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Sorry Peter, your message 16 on this thread specifically states the DNA is unvariable, i.e., not capable of variation. You have been challenged to show the mechanism by which DNA is prevented from variation. Your assertion = your evidentiary support required. Try again.

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As demonstrated above, I will. Present the literature if you are so sure.

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I have. You have not produced ONE SINGLE PIECE OF EVIDENCE outside Woodford’s book. I have presented you with numerous articles from peer reviewed journals written by the scientists actually studying the issue. Your entire argument thus far rests on your continual restatement that they don’t know what they’re talking about.

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Sometimes I wonder why do I still discuss with evolutionism-believers. They are so stuck in their own paradigm that they are unable to think otherwise. Even if it has been falsified over and over.

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Free your mind and I will show you the world how it really is.

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Thanks, I’ll decline. I get enough of a rush out of the real world — I don’t need to accept your fantasy.

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Dr Peakall was the first scientist I heard talking about an All-Purpose genome and he further opened my eyes. I think that Dr Peakall tries to get his data in accord with evolutionism since he has to 'publish or perish'. So he introduces things like the exception that proves a rule. With believers of evolutionism as the only peers for scientific journals he will have a pretty hard time to get it in if he didnt do that, dont you think so? The hypothesis of the multipurpose genome holds that stability ensuring DNA repair mechanisms (plus the redundant genetic code) keep the DNA sense-sequences from changing. The variation observed (since not all the tree are the same) is due to jumping/shuffling DNA elements that affect gene regulation.

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Besides, you demonstrate that you don't understand my hypothesis. The hypothesis of MP is an alternative for evolutionism and often it is superior in explanations.

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Please quote the response you received from Dr. Peakall. You’re spending a lot of words explaining to us ignorants here on this board what he really means. I challenged your interpretation using what Dr. Peakall actually wrote. Unless you can bring me Dr. Peakall’s exact response, then you are engaging in yet more baseless assertion.Wait a sec, I just caught this — from the above, it now appears you are stating that there IS variation in the trees — which is what I’ve been saying for 9 pages. Have you retracted your assertion, and I missed it?As for not understanding your hypothesis — on the contrary, I at least understand what you’ve presented so far. I also understand that it’s completely spurious, based on utter lack of evidence and gross misunderstanding of basic conservation biology, genetics, ecology, etc. Misunderstandings which you repeatedly and effectively demonstrate all on your own every time you post. Keep it up — you’re making my argument better than I ever could.

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What I mean is that all DNA elements required to phenotypic adaptations are already present in the multipurpose genome. For instance, the multipurpose genome has a program for sexual reproduction as well as a program for copicing. The environment simply demands which one (or both) is operative. If sexual reproduction hasn't been sensed for a while, this information is transmitted to the roots and the copicing program is initiated. Both programs can only be kept in the genome through preservation of the programs and that demand for an array of stability ensuring DNA replication mechanisms. It is an example of genetic redundancy and redundancies demand elaborate repair systems, otherwise they will be lost through entropy.

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I think Mammuthus already hit you on this one. However, so I understand you, are you saying that all organisms possess a multipurpose computer system that allows them to switch genetic programs at will? If every organism had a multipurpose genome — which is what you assert — every organism should be able to fill every niche on the planet at will. Great! I want to have a gill system that allows me to forego SCUBA gear. How do I turn on the ability to breathe water?

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Q: 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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PB: If you can unequivocally proof that this completely novel gene came about without the interference of creatons, it would be bad for the hypothesis. For instance, the TcR gene in mammals seem to drop out of the sky (O I see, the current story is 'birth-and-death-evolution and purifying selection'). What's wrong with the idea of creatons?. Nobody ever saw birth and death evolution, and nobody ever saw a creaton. So, there is no difference (except that evolutionism is scientifically accepted).

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Great! Your hypothesis is falsified:Nurminsky DI, Nurminskaya MV, De Aguiar D, Hartl DL (1998), Selective sweep of a newly evolved sperm-specific gene in Drosophila, Nature 396:572-575

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The pattern of genetic variation across the genome of Drosophila melanogaster is consistent with the occurrence of frequent 'selective sweeps', in which new favourable mutations become incorporated into the species so quickly that linked alleles can 'hitchhike' and also become fixed. Because of the hitchhiking of linked genes, it is generally difficult to identify the target of any putative selective sweep. Here, however, we identify a new gene in D. melanogaster that codes for a sperm-specific axonemal dynein subunit. The gene has a new testes-specific promoter derived from a protein-coding region in a gene encoding the cell-adhesion protein annexin X (AnnX), and it contains a new protein-coding exon derived from an intron in a gene encoding a cytoplasmic dynein intermediate chain (Cdic). The new transcription unit, designated Sdic (for sperm-specific dynein intermediate chain), has been duplicated about tenfold in a tandem array. Consistent with the selective sweep of this gene, the level of genetic polymorphism near Sdic is unusually low. The discovery of this gene supports other results that point to the rapid molecular evolution of male reproductive functions. (emphasis added)

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Here’s a brand new gene that was formed from bits and pieces of other genes — not a duplication event.Here’s the follow-up paper: Nurminsky D, Aguiar DD, Bustamante CD, Hartl DL (2001), Chromosomal effects of rapid gene evolution in Drosophila melanogaster, Science 291:128-130

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Rapid adaptive fixation of a new favorable mutation is expected to affect neighboring genes along the chromosome. Evolutionary theory predicts that the chromosomal region would show a reduced level of genetic variation and an excess of rare alleles. We have confirmed these predictions in a region of the X chromosome of Drosophila melanogaster that contains a newly evolved gene for a component of the sperm axoneme. In D. simulans, where the novel gene does not exist, the pattern of genetic variation is consistent with selection against recurrent deleterious mutations. These findings imply that the pattern of genetic variation along a chromosome may be useful for inferring its evolutionary history and for revealing regions in which recent adaptive fixations have taken place.

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Note the comparison with D. simulans, which has a recent —observed — common ancestor with D. melanogaster and DOESN’T have the gene.As to proving it didn’t happen through creatons — lol. You haven’t shown anything even remotely resembling proof that the silly things even exist! Why on Earth would you think I have to prove their absence in this process?

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Q: 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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PB: Please provide the reference you cite from. That these organisms seem to be speciating can be due to loss of DNA compatibility, so I don't see a problem for my hypothesis here. Also Darwin thought he saw speciation on the Galapagos Archipelago in all the different 'species' of finches. However, we now know that they can still interbreed and are thus NO new species. It is in favour of the plasticity of the multipurpose genome (that is due to loss of genes, and differential gene regulation due to shuffling DNA elements).

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In the first place, I did provide the full reference (click on the title). Amazing you can make the assertion that the speciation event is due to loss of DNA compatibility whatever that is. How’d you arrive at that bit of inference when you haven’t, by your own admission, even read the article? From the title? Lol!!!! You didn’t even read THAT correctly. It talks about mating time incompatibility - one of several pre-zygotic barriers (in this case, behavioral, not genetic, originall). Your turn — provide a reference that shows the 13 species of finches on the Galapagos still interbreed.

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The regions that are expected to change over time, and were expected to demonstrate variability, have been analysed and didn't show variability. Why would one analyse regions that are not expected to give a lot of change? Dr Peakall knows what regions to analyse in Araucaria family and he did just that. With the know results. Furthermore, coppicing could explain the invariability within the three stands NOT between the three stands.

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See above — way above.

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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: No, it is the extreme example of the multipurpose genome, characterised by stability of DNA sequences.

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This is now the THIRD time you’ve failed to even address this issue beyond simply re-asserting your original claim. I can only assume that in spite of your vaunted, self-proclaimed expertise, you are unable to do so.

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Inbreeding depression and mutational load counteractions sounds interesting. Could you please provide a reference for this, since I am going to look into the genetics. I mean maybe an alternative genetic program has been switched on in this situation. Next, I will explain my vision on this topic.

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Tell me something Peter: are you simply incapable of looking something up on your own? This is pretty basic stuff. Here’s some articles I happened to have on my hard drive without even bothering to check Pubmed or any of the journals:Bataillon T, Kirkpatrick M (2000) Inbreeding depression due to mildly deleterious mutations in finite populations : size does matter! Genet. Res., 75 : 75-81Willis, JH (1999), Inbreeding Load, Average Dominance and the Mutation Rate for Mildly Deleterious Alleles in Mimulus guttatus Genetics 153: 1885-1898Colas B, Olivieri I, Riba M (1997) Centaurea corymbosa, a cliff-dwelling species tottering on the brink of extinction: A demographic and genetic study, PNAS 94: 3471-3476Reinartz JA, Les DH (1994) Bottleneck-induced dissolution of self-incompatibility and breeding system consequences in Aster furcatus (Asteraceae), Am. J. Bot. 81: 446-455Charlesworth D, Morgan MT, Charlesworth B (1992) The effect of linkage and population size on inbreeding depression due to mutational load Genet. Res., 59: 49-61These should be enough to give you at least some education in the subject. Feel free to ask if you have any questions ONCE YOU’VE ACTUALLY READ THE ARTICLES. I’m getting really, really, REALLY tired of doing your research for you. For someone who throws their academic credentials at me every single chance he gets, you seem to be oddly incapable of looking up the basic concepts of the multiple scientific disciplines you claim to refute.

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A mutation not in the germ line and therefor not inherited by sexual reproduction. However, it can be expected that plants that rely on copicing will demonstrate somatic mutations --even in the 18sRNA or rcb genes. Why, since they tissue derived from rapidly dividing meristemes, and here mutations can be introduced easily. All sister cells grown from the mutated cell will also inherit the mutation. So, somatic mutations are expected. If not, the DNA is extremely stable, and in accord with the prediction done by the multipurpose genome.

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How about we see what the actual data says — WHEN IT’S FINALLY PUBLISHED.

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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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You have once again failed to address this issue in any way whatsoever other than repeating your mantra. Try again.

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Q: 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.

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PB: Show me the DNA analysis and the references. I have the feeling that you still don't understand what I am trying to convey. Speciation can readily be understood from a multipurpose genome, it doesn't need evolutionism.

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No — you made the claim. You show ME the references that indicate the five species of horseshoe crab are genetically identical in accordance with your multipurpose genome. Your MG thingy is incredibly elastic, depending on what you’re responding to:
1. MG is indicated by invariant DNA (Wollemia) which prevents speciation.
2. MG is indicated by the existence of different species which have invariant DNA ()
3. MG can cause speciation, which, according to you, doesn’t exist.
4. Under the MG, genomic plasticity (in invariant DNA?) is due to loss of genes (but I thought it was invariant?).You aren’t even consistent in what you claim for your spurious hypothetical genome.

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Q: That enough variation for you? 'Living fossil'' 'lol' another 'argument from journalistic sensationalism'. Peddle it to someone who doesn't know any better. As to the designation of organism in the case of Wollemia, pending further data, I'd have to say each stand likely represents a single organism (or close enough as no matter).

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PB: Even if they were, the separated populations are expected to demonstrate variability. You keep denying that. Maybe you should talk to Dr Peakall about it, since you don't want to accept it from me.

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The point is, if the stands DO represent only three individuals — rather than three populations — seeded from a single individual, almost no variation would be expected. And you’re right about one thing, I wouldn’t accept uncorroborated ANYTHING from you at this point. Go ahead and contact Dr. Peakall for his input. I might accept what he has to say about the organism he’s studying.

Yep - you're absolutely correct. Decreased population variability != decreased information content. That's the whole point. Creationists have been babbling about "information" for years. I suppose it sounds good to the rubes...

Great reply Fred. You and Peter B seem to be vying for who can give the best non-answer to an honest question.

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Quetzal, methinks you have been reading too much of the gobblygook at T.O. Yours is of the recent evo standard creationists are mixing definitions reply. Why don’t you just deal with the definition I gave you? If you prefer, remove the sender comment. What are you afraid of? I even offered you the simplest level of information, Shannon info. You simply cannot make a case that the cheetah has not lost genetic information from its pre-bottleneck parent population.

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I'm afraid I don't read or post on TO. Actually, the whole point is you haven't given a definition. Hard to work with a definition that is internally inconsistent, idiosyncratic, and fundamentally inapplicable and worse, conflates three completely different information concepts. Tell you what - since the whole information argument was YOUR red herring, you show us (with appropriate equations) how information is lost in a population after a bottleneck.

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MEGAROTFL! Q, I can’t count the times I’ve been down this road. If it isn’t sand patterns on a beach, or pee messages in snow, or rings in a tree, or arrows shot across a battlefield, or tiles heading for one’s dome. Blah blah blah. These are simply diversions and invariably a big waste of time. Stick to the debate.

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So I take it you don't have an answer? Or rather, since you're so conversant with this type of argument, you don't want to pursue it because you're bored with it?Tell you what, since this is old hat for you, repost one of your old arguments with the accompanying math. After all - you're the one that wants to use "information" in a discussion of ecology and population genetics. You define the information content of the system. You derive the necessary equations, and show YOUR assertion is valid.I personally consider the whole "information" argument to be a specious waste of time. So unless you can come up with a compelling reason - or mathematical proof of your contention - I think you're simply blowing smoke. Hence the utterly contentless reply you made.

Hmm, okay. However, I think that still begs the question. Consider:1. At the level of the organism, that means that any mutation, duplication, fusion, recombination etc that results in either an increase in function, a novel function, or greater efficiency internally (in the "environment" of the cell, cascade, or organism's body), OR which generates a beneficial phenotypical change in relation to the particular organism's environment, constitutes "new information". Okay, I can almost buy that. In that case, it's trivially easy to show new information.2. However, considered at the level of the population (which is the level at which we were arguing), and based on the fact that the "new" algorithm must be "useful" to the population, I don't see how anyone can quantify the effect of a single novel function in the genome of a single individual as "useful" - hence Fred's question is impossible to answer. Even assuming this new individually-useful algorithm gets somehow fixed and becomes dominant in the population over X generations, how can it be determined to be "useful" even at this point unless it has a net effect on the marginal fitness of the entire population? OTOH, if all that is required is that some member of some population - even if the population is represented by a billion individuals - "gains" a new algorithm (as in #1), then again it is trivially easy to state that the population's gene pool has gained (albeit incrementally) an increase in information.However, I'd be willing to bet any amount of money you'd care to wager that's not what ol' Fred is trying to get at...

Fred:Quick correction - My response to Moose was intended to imply that there was no correlation between loss of genetic variability in a population and loss of some undefined "information" at the population level. See my post #139 on this thread for why I think the concept is misleading at best - and why your question probably can't be answered, even using your definition. Hope that clarifies what I "think", "imply", "suspect" or any other attribution to me you'd care to make.As far as what I "suspect" Mammuthus meant (and I could be wrong), I think he meant that since the population is still extant - IOW there are still cheetahs living in the wild - they can't be considered (in the context of PB's particular assertion), to be "poor". OTOH, I don't think he is implying that they aren't in trouble. However, ASSUMING no new environmental pressures are brought to bear that further degrade their marginal fitness, and ASSUMING they survive in the wild at all, I think he's saying that there's nothing preventing the cheetahs from evolving (or "improving" if you like) like any other species.IMO, for what it's worth, I think cheetahs may have already passed the point of no return in a conservation sense, and are more than likely doomed. But that's just my opinion based on what I've read on them concerning infertility, infant mortality, disease susceptibility, continuing habitat degradation/restriction, etc, and has nothing to do with whether or not they DO actually survive - or even thrive. There are enough relictual populations of various organisms running around today that by all rights should have been a historical footnote long ago to make these kinds of predictions pretty speculative.