molecular genetic evidence for a multipurpose genome

PB:
As demonstrated on this site evolutionism can readily be falsified on the level of the genome and thus cannot be the right hypothesis to explain life on earth in all its variation.M: You start with an unwarranted conclusion as you have yet to refute anything.PB:
Why? Evolutionism supposed to have its foundations in molecular biology and genetics, and when the theory can be falsified at this level it lacks a proper foundation and thus cannot be a good theory.M: Evolution has its foundation in the study of morphology...Darwin and his predecessors had no knowledge of either molecular biology or genetics. You would do better to know the basis of evolution before you presume to refute it.PB:
Therefore, I introduced the concept of the multipurpose genome.
The concept of a multi purpose genome is not entirely new since a similar concept has been introduced by P. Scheele in his book ‘Degeneration’ and by L. Spetner in his book ‘Not by Chance’.
In my opinion their hypotheses cannot explain all biological observations --like sequence similarities within related species-- and so it cannot be complete.
Therefore I also introduced and provided scientific evidence for non-random mutations. The non-random mutations should be conceived as non-random with respect to nucleotide and position. At present they should not be conceived as deliberately introduced as a response to environmental change, since that cannot be scientifically proven. In genetics non-random mutations are generally referred to as hot-spots. This type of mutations may have important implications for common descent (see my mailing # 184 in ‘molecular genetic evidence against random mutation’ and is still open for discussion). In conjunction with non-random mutation the idea of a multipurpose genome are able to explain all biological phenomena, including genetic redundancies and phylogenetics.M: Your inability to understand what random means is the only astonishing content of this entire post Peter. When you have been called on your "non-random" mutation fallacy you invariably make minor protests and then cease to continue addressing the subject and then bring it up later in another context. Repeating this fallacy will not make it correct.Where in my HV1 or HV2 region exactly will I sustain the next mutation of my mtDNA? If you cannot tell me exactly then it is still a random process regardless of hotspots or not. C-T transitions are more likely to occur because of chemical constraints. But that does not mean you know which C-T will occur in any given lineage. Your non-randomness is falsified as mutations occur outside of hotspots as well. Here is a test for you. Get a bacterial clone and subject it to some kind of pressure for 1000 generations. You should be able to perfectly predict every single mutation in the genome before you start...see if it matches your prediction.PB:
The concept 'multipurpose genome' holds that: 1) DNA sequences —although plastic-- are stable throughout time,M: This is absolute nonsense. How can the DNA sequences be plastic yet not change throughout time? This is falsified as some organisms show extreme genetic diversity and others do not. DNA variation is itself variable among groups.PB:
2) organisms demonstrate genetic redundancies that reside in the genome without selective constraint,M: This is not substantiated. Endogenous retroviruses are "selfish genes" not vital to the organism itself yet are selectively maintained as they themselves struggle to propagate within the host genome. Thus, they show selective constraint. Eye color genes are redundant and selectively constrained. rDNA genes i.e. 18S are highly repeated and show tremendous selective constraint. Point 2 is thus also falsified.PB:
3) adaptive phenotypes are due to duplication and/or shuffling of preexisting DNA elements —either genes or other non-coding elements-- that affect gene expression, or due to loss of (redundant) genes [=degeneration theory], andM: This hardly seems to support a multipurpose genome. Actually a phenotype can only be adaptive if it provides some reproductive advantage to the organism. Most duplications or shuffling of genes cause severe disease or lethal mutations i.e Alu elements integrating in factor 8 gene etc. Also, minor changes in the timing and location of hox gene expression by point mutations in the promoters lead to the most phenotypic novelty. By making phenotypic change exclusively dependent on gene duplication and exon shuffling you have falsified point 3.PB:
4) the function of natural selection is to remove degenerate organisms.,Nope, Wordswordsman is still around
Define degenerate. A single point mutation can result in spontaneous abortion...the entire organism was not degenerate. Natural selection sorts organisms by relative fitness not because of degeneracy. i.e.
a species that better utilizes an environment better than another will replace the less adapted species. Niether species is degenerate.PB:
5) there is/has been creation (=creaton interactions with matter in a morphogenetic field giving rise to genes and genetic programs in preexisting genetic programs).M: What evidence is there for a morphogenetic field? This is a non-falsifiable hypothesis as it states that an unobservable (god/morphogenetic field) created all living things i.e. plane old creationism. And to top it off, it is an argument by you against abiogenesis as opposed to evolution i.e. you seem to not know what the difference is between the two.PB:
Predictions:
1) predicts that within species we do not see abundant variation with respect to genes, and usually such genetic alterations are neutral or degenerate (although distinct alleles can be expected through the principle of degeneration, which is in effect the action of entropy).
It also predicts that all organism --even the simplest-- have an elaborate and accurate mechanism to counteract mutations.M: This absolutely does not follow from your statement that DNA is plastic and stable (polar opposites). Acutally nothing follows from premise 1. However, this is also falsified as some species do have abundant variation in some genes and others not. If your prediction is that all organisms have elaborate and accurate mechanisms to counteract mutation it does not fit with the observations that even related species have tremendous variation in genetic variability i.e. Homo sapiens and Pan troglodytes for example.PB:
2) predicts that a considerable part of the genes of any organism can be knocked out without being lethal.M: Knock out a hox gene and see what happens. As to lethality, that is immediate selection against the organism. But say you knock out a gene involved in sperm production. That specific organism has been just as effectively knocked out of the gene pool. Prediciton 2 is both wrong and overly simplistic.PB:
3) predicts that adaptive phenotypes of organism do never demonstrate new genes.M: This sentence makes little sense but if I get your meaning the synsyctin gene (a captured endogenous retroviral envelope gene) which is critical for placental devleopment only in Old World Monkeys and hominids falsifies this prediction.PB:
4) predicts that organism lacking vital DNA elements are selected against.M: This actually falsifies your premise of a multipurpose genome as all organisms should have redundancies to compensate for the lack of a vital element in your argument.PB:
5) predicts that there should be organisms that have not undergone genetic changes (yet).M: This is not clear from your multipurpose idea either. Obviously to pre-compensate for the predicted envirnomental changes that the genome knows are coming it should be shuffling and duplicating all the time to have the proper genes for the predicted environment (Lamark thought this way to). Genetic homogeneity argues against your idea. And your lovely tree clone example is different from other species of pine thus it has undergone genetic change.PB:
Falsification:
The concept will be falsified by the observation of the evolution of new genes unrelated to preexisting genes.M: Actually, molecular biology and genetics and inconsistencies of your own falsify your idea. The morphogenetic field business is a non testable hypothesis and is a substitution for the words intelligent design or god.As to your truly funny tree example, please address Quetzal's comments regarding that subject.PB from the top...
...when the theory can be falsified at this level it lacks a proper foundation and thus cannot be a good theory.M: Hence, the mutlipurpose genome/morphogenetic field/creaton idea cannot be a good theorycheers,
M

dear mammuthus,Thanks for your lenghty response.M: Hi Peter..I aim to please ...I'll see if I can make this shorter but no promises..PB:
Even if you found a new organism in your garden tomorrow and found out in your lab that the DNA is completely invariable it wouldn't refute anything, would it? Your a faithful believer. (Nothing inherently wrong with that, although not very scientific)M: If I found an unusual finding I would actually confirm it rigorously before running around pronouncing I had discovered something spectacular. It is not faith but the wish to do proper reproducible scienc. If I found a new organism that showed no or little genetic variation I would test for a genetic bottleneck or whether the organism is clonal and not claim woo hoo! genetics is dead. (that you do that is both inherently wrong and non scientific.)PB:
And that demonstrates that evolutionism is an outdated theory based on morphology. I think --and this will not be completely novel to you-- morphology is subject to DNA sequences and regulation of these sequences.M: I was correcting your mistatement as to the origins of the theory not desputing regulation of morphology. By the way, environment can have a tremendous impact on morphology regardless of sequence i.e. phenocopies or if you have ever seen a victim of thalidomide with limb reduction.PB:
It should be clear now that I do not require deterministic mutations for this hypothesis. As demonstrated in this thread a major part of mutations are non-randomly introduced, i.e non-random with respect to nucleotide and position (see the 1G5 genes in Drosophila subpopulations, mtDNA in hominoids/human subpopulations).M: It should be clear that unless the system is deterministic your entire hypothesis falls apart. You claim that similarity between organisms is solely due to non-random mechansim making them seemingly similar not because of common ancestry. I have asked without getting an answer before, do you believe you are related to your parents or was your DNA spontanously created and non-random giving the seeming appearance that you are related to them? In any case, as soon as you discover a mutation that occurs outside your "non-random" site your hypothesis is falsified and this has been observed in almost all instances.PB:
I concur that deterministic mutations have not (yet) been detected. I already predicted where your mutations most likely will be introduced in your mtDNA in a previous mail. And if you currently have a C on those positions they will likely be a T when it mutates. Thus, the non-randomness I speak off is with respect to nucleotide and position (not when), but may have important implications for molecular phylogenetics.M: This is not really a valid argument Peter. Sometimes you get C to G or C to A. Sometimes C to T. That C to T is more common is a purely chemical constraint. Which C to T mutates is random in a given generation. The only implication that it has for molecular phylogenetics is that the transition transversion ratio is taken into account as a variable.PB:
By plastic I mean that preexisting sequences can be duplicated and/or shuffled.M: So you don't believe there are point mutations, single base deletions, or complete changes in chromosomal content? You have some reading to do
The ZFX/ZFY paper also shows how point mutations accumulate in the ALU's...acutally when a HERV integrates the 5 and 3' LTRs diverge by point mutations and deletions etc etc etc.MY RESPONSE:
All according to the evolutionary paradigm. Actually the ribosomal RNAs are a nice example of stability that is maintained by the hypothetical idea of 'concerted evolution'. You should be aware that is but a hypothesis. In fact, evolutionism requires this hypothesis otherwise it cannot explain the high level of stability within the rRNA genes. However, I wonder whether this hypothesis is still tenable and probably it has to be replaced by purifying selction soon (as observed for the histon H3 and H4 genes. The one story is replaced by the other story. You are free to believe them, I don't). The hypothesis of multipurpose simply holds that these rRNA genes are guarded by highly specific DNA repair mechanism.
(By the way, did you mean the "selfish meme" )M: Ever hear of gene conversion? There are a lot of basic (and observed) methods of DNA sequence homogenization of which you seem to be completely unaware. Selection on 18S is not on one copy and by the way, there can be very different 18S copies within a single genome. There can also be rDNA pseudogenes.PB:
If all mechanisms that induce variations --due to shuffling of preexisting DNA elements-- are already present than it advocates a multipurpose genome and not evolutionism. Nothing evolved, only the order of the DNA elemenst is different.M: To bad that novelty and novel regulation does appear to refute this as the exclusive mechanism. Even for shuffled genes, the globin cluster of humans is exceptionally different from elephants....plenty of evolution occurring...PB:
If a single point muations leads to a big enough degeneration (for instance members of the Src-family), it will be lethal and selected against.M: You sure about that one? Sickle cell anemia and cystic fibrosis are both extremely fitness reducing diseases yet both persist in the population...heterozygotes get an advantage from carrying the "bad copy" thus a big degeneration is maintained. You remove the mitochondira in its entirety from yeast and they survive by switching to fermentation i.e. the petite mutant lines. If what you said were true we would not have such a large genetic load.PB:
The (sub)species that is not utilising an environment optimally is degenerate compared to the (sub)species that does. It will be selected against.M: Hey, welcome our new evolutionary biologist Peter Borger
Actually, that is not necessarily correct either. Both may diverge so that they do not overlap.PB:The creatons and the morphogenetic field can be inferred from the fossil record. You infer evolution from the fossil record and fill in the gaps between the phyla with hypothetical transition forms, also a non-falsifibale hypothesis. So, what is the difference?M: If you find an animal fossil like say a mastodon that has many shared features with elephants but also pronounced differences, how is this evidence for creatons in a morphological field? Why would there be gaps in a morphogenetic field? How do you quantifiy a creaton? All untestable and non falsifiable.Find me a mastodon fossil that is older than a T.rex and evolution is in trouble.previous post M: This absolutely does not follow from your statement that DNA is plastic and stable (polar opposites). Acutally nothing follows from premise 1. However, this is also falsified as some species do have abundant variation in some genes and others not. If your prediction is that all organisms have elaborate and accurate mechanisms to counteract mutation it does not fit with the observations that even related species have tremendous variation in genetic variability i.e. Homo sapiens and Pan troglodytes for example.MY RESPONSE:
Expand on the example please. If you mean shuffling I don't see a problem. If you mean SNPs I also don't see a problem.M: So you have no problem with data that falisifies your premise that there is only variation due to shuffling of genes and not point mutations etc?I SAY:
I don't see a problem here. The organism that doesn't produce sperm will not produce offspring and is therefore degenerate. Its DNA will disappear from the genepool.M: But if it is a multipurpose genome obviously there should be a compensatory path for such mutation for such an important pathway. You are arguing from a strict selectionist point of view yet proposing a strictly Lamarkian pre-adaptation hypothesis...they are polar opposites.PB:
How do you know that it is a captured retrovirus gene? It can be the other way around. The retrovirus captured the protein and used it for its envelope. It happend a lot in the virus world that they capture genes from their hosts. I thought you used this method to explain the IL-1beta incongruence?M: Where did I say that about IL-1 beta? Syncytin is an envelope protein common to all retroviruses both exogenous and endogenous. The direction of capture is clear from the lack of such a viral gene outside of old world monkeys and hominids.PB:
No, it doesn't falsify anything (sounds familiar, in't it ). The multipurpose genome hypothesis hold that part of the genes is redundant, not all. In fact it holds that the part that is responsible for variations is redundant, and that are usually genes involved in regulation of gene expression. Hey, that is exactly what we see in biology: Redundant regulatory networks! In addition, there are also essential non-redundant genes.M: This is totally inconsistent. You are constantly changing your terms and hypothesis around from selectionist to adaptationist and from here to partial redundant and multipurpose from only multipurpose. This is falsified by single copy genes involved in variation. If something is lacking in the genome your creatons should create it so that the organism can persist.PB:
If an organism was created recently and doesn't yet have major defects (due to entropy acting on the genome) in DNA repair mechanisms, it is expected that the DNA does not change. That is what we see for the W. nobilis.M: To bad that is not what we see for muskoxen and bears where we see past diversity is much greater than that of today (i.e. ancient DNA). Quetzal also gave examples of organisms that have suffered genetic bottlenecks and were not created recently. Quetzal already pointed out your complete and total error regarding W. nobilis.
.PB:
Actually, molecular biology does not falsify this hypothesis. For instance, you showed me the '10.000 generations of bacteria reference' and it was demonstrated that SNPs were NOT abundant. Thus the sequences are stable and the phenotype-changes were merely due to shuffling/deletion/duplication of preexisting elements. All in accord with my hypothesis.M: Actually, they only measured gene rearrangments as it was easier...this was not a test of the increase in SNPs. There are plenty of examples of phenotypic change due to point mutations or have you missed 50 years of genetics?PB:
See my reponse to Quetzal. However, in a previous letter you concurred that such organism would overturn evolutionism. Can you please expand a bit on this contradiction.M: The contradiction is as Quetzal pointed out, that you have not provided such an organism but have rather again shown a profound lack of population genetics knowledge. As a suggestion you may want to get a copy of Danial Hartl and Andrew Clark's Population Genetics. It is a bit too mathematical at times but it is a fairly comprehensive book on the genetics of populations. That is not meant as an insult Peter but if you don't have a foundation in the subject matter then you will be far less prepared to object to it.I look forward to your response to this post and to that of Quetzal's regarding W. nobilis.cheers,
M

PB:
5) there is/has been creation (=creaton interactions with matter in a morphogenetic field giving rise to genes and genetic programs in preexisting genetic programs).M:
According to this premise, all organisms in close proximity to one another should be genetically identical. Thus, when you were concieved Peter, you should have been most genetically similar to your mother, father, and any bacteria, viruses, and fungi that would have been present. If anyone else was in close proximity, they would be equally closely related to you as their matter would also be in the morphogenetic field. Ultimately, there should be no genetic differences among any humans and there should also be no more than one sex since this is also a genetic difference.At the species level, all organisms that are in the same environment should be almost genetically identical not just to one another but to ALL organisms as they all reside and reproduce within the same morphogenetic field. Thus, South American monkey should in no way genetically resemble Old World monkey as they are not in the same field. If you posit that the field is world wide, then there should be absolutley no genetic differences between a tomato, person, bacteria.

Here is another one If genomes are multipurpose and pre-adaptive, why are most species that ever lived extinct? Mammoths and elephants are extremely similar genetically yet mammoths are extinct...surely their multipurpose genome would have rearranged to adapt to new environment? Actually, mammoths went extinct in multiple different environments so in multiple morphogenetic fields, the same result occurred...why did creatons and the morphogenetic field stop functioning worldwide at the end Pleistocene for some animals but not others in exactly the same regions i.e. mammoths, American horses, camels, giant ground sloths, cave bears, several species of birds etc. etc., but not bison, deer, wolves, etc.? Same problem for neanderthals...besides having been in the same morphogenetic field as humans they had very distinct mtDNA genomes...but why did their multipurpose redundant genomes fail to "create" more individuals or adapt to whatever the change was that caused them to become extinct?

deleted by Mammuthus due to duplication of message[This message has been edited by Mammuthus, 10-24-2002]

PB:
What I understand from Quetzals mailing is that genetic variability hasn't been found between the trees in two (or three, now) seperated stands. That has been scientifically demonstrated in Peakall's lab. So, my claims on this tree are still standing. And, also my assertion that it violates molecular evolution still stands. Even the assertion that 'neither geneticist, paleontologist, dendrologist nor C14 expert would be able to disproof that the organism had been created a century ago' still stands.M: First off, you can sequence the mtDNA of 3 cheetahs and find no genetic variation to. It is historically known that they went through a bottleneck (perhaps down to a single breeding pair) and they are still today extremely genetically uniform. All as predicted by population genetics much less evolution. Same goes for the musk oxen. The entire population of musk oxen in Greenland were a transplant of a few from Alaska...thus, they are identical in the sequences thus far studied. Of 37 modern muskoxen only 8 very similar haplotypes were found...though I have some upcoming surprises about 15 thousand year old muskoxen
Very few W. nobilis exist so it would have been a much greater surprise if the 3 stands demonstrated genetic variability as that would be inconsistent with a bottleneck. Bottlencks can be observed expreimentally and in the wild. Your concept of morphogenetic fields cannot so is thus unsupported.As to your arguement that no one could "prove" that W. nobilis was not created 100 years ago...(you don't prove in science which you obviously do not know)...Find the closest relative of W. nobilis and you can determine how long ago it separated from that relative..thus much evolution has occurred and had to occur before the trees present as the genome does not spontaneously change after the organism is present, except for a few loci M: I was correcting your mistatement as to the origins of the theory not desputing regulation of morphology. By the way, environment can have a tremendous impact on morphology regardless of sequence i.e. phenocopies or if you have ever seen a victim of thalidomide with limb reduction.PB:
Indeed, and how do you think this works?M: Are you being serious or joking? Are you really unaware of why thalidomide is a mutagen? Before I go into this I need to know if you have any knowledge of developmental biology.PB:
I not only claimed that, but also provided scientific evidence for that. I already mentioned that there are two types of mutations: random and non-random. The latter is non-random with respect to nucleotide and position, and will give the illusion of common descent if one compares between species. I expect to find more evidence if we look within subpopulations instead of looking between distinct species.M: And again, you have not provided any evidence for non-random mutation except for your poor tactic of redefining random to suit your purpose though it is not correct. There are lots of papers on subpopulation variation and they don't show non-random mutation. You still cannot tell me for the hottest of hotspots if a mutation will occur there in the next generation or not.PB:
That is what YOU expect. And I also expected to find this, untill I discovered that mutations can be non-random. As mentioned in the mtDNA example where subspecies are compared several observations can be made that are not in accord with molecular evolutionism. I already pointed it out in another thread and we could continue there if you like. (Observations: fast evolutionary clock, no common descent, non-random nucleotide substitutions)M: We can continue as you like. Your repeating non-random mutation is not making it any more valid....so please continue but actually supply something substantive.PB:
Of course, I acknowledge all these forms of mutations. They all have their place in the hypothesis of the multipurpose genome. Usually they are neutral or degenerate. Changes in chromosomal content I am not yet sure off. How? deletions? rearrangements? additions from other sources? However, I guess, they all fit the multipurpose genome. Will think about it if you elaborate on it.M: Actually, you have previously denied other forms of mutation contribute to variation. However, you stated multipurpose genome was all about shuffling of existing sequences only with no acknowledgement of point mutations etc...do you wish to revise your premise?As to your questions, I think we may be talking past each other. I am not sure what you are asking me. I can give you examples of close species with different chromsomal content but I am not sure if that is what you are asking for.PB:
Did the sequence divergence start after integration or did they already diverge before integration? How do you assess this?M: That is an easy one. Novel integration events have been observed including with HIV when the virus integrates into the genome of its host. The LTRs are identical..the divergence is post integration.MY RESPONSE:
No, I know of these mechanisms. I only wondered where the other copies go? They seem to disappear from the genome without a trace since otherwise we would observe them as junk DNA and we would be able to track them back in time. In fact such mechanisms predict that a considerable amount of pseudogenes must exist that vary in sequence from 0-100 %. For histon H4 we don't find them. Why, I wonder?M: Please read any basic chapter on recombination and you should be able in 2 seconds to see why the reciprocal recombinant is lost.PB:
And who says that they derived through evolution? You see novelty and novel regulation and you say that evolution did it. It is but a plain statement. I do not negate that mutations occur. I negate that elephants and human have a common ancestor linked by a Darwinian mechanism.M: actually you deny that you are linked to your parents by common ancestry as well. It is not a plain statement but one supported by paleontology, morphology, biochemistry, and genetics....what have you got?PB:
Apparently, the diploid genome allows this bit of degeneracy. However, it is loss of a diploid redundancy. So, I see no problem.Talking about anemia. Did you know that the hemoglobin gene is an apparent "hot gene". I propose there is some kind of mechanism that prefers this gene above --say-- the ZFX gene. Over 250 mutations in the hemoglobin gene are known, while the ZFX gene is completely stable for 20.000.000 years [as discussed]. Directed mutations? Yes, I keep trying it!).M: Ah, so now the mutlipurpose is now only semi-multipurpose on certain occasions? As to ZFX..you are not helping your case by posting this fallacy again (as discussed)M:
You remove the mitochondira in its entirety from yeast and they survive by switching to fermentation i.e. the petite mutant lines. If what you said were true we would not have such a large genetic load.PB:
Nice example of redundancy. I see no problems here.M: Except that in almost all other organisms such a loss is lethal? Selective redundancy? Redundancies on Tuesdays but not Thursdays? I see big problems for your hypothesis with the redundancy argument.PB:
There is a big difference between selection against, and natural selection as driving force of evolutionism. You need the genes first and than you can select on these genes. So, the genes have to be derived from some other gene (duplication is the favourite, I guess) and than they have to evolve into another gene without selective constraint (the duplictated genes demonstrate redundancy after duplication) that gives selective advantage. Prediction: we should oberve redundancy correlated to duplication in any genome. Fact: we don't see it. Clear case.M: Clear to you but that is not a prediction of any evolutionary biologist. Some cases do operate as you have said. In other cases a gene involved in one function takes on a new function i.e. homoglobins in bacteria versus multicellular organisms. And you the need organism to be selected on by its environment at the phenotypic level, not the gene to be selected for to pre adapt the organism to something..get it?PB:
It isn't. However, if you find a manatee and an elephant and you claim (as evolutionism does) that the are linked by Darwinian principles, than I like to have evidence for that.
Otherwise, I claim that the genomes have been created through creaton-matter-interactions.M: There is a lot of evidence for a manatee-elephant association..you up for reading it?PB:
Maybe there ar gaps in the creatons. Maybe we pass through an interstellar creaton wave every 26.000.000 years or so. This vision would also nicely fit extinctions (anti-creatons?) and sudden appearance of species.M: Except that it is a non-testable hypothesis just like plain old biblical creationism.M: Find me a mastodon fossil that is older than a T.rex and evolution is in trouble.PB:
There have been books published on this topic. If I recall properly by Michael Cremo. Never read it though.M: LOL!!!!!!!!!!!!!!!!!!!!PB:
I do not have objections to observations like point mutations. They have their place in the hypothesis of the multipurpose genome. Point mutations due to inefficient repair of DNA and this may be due to a degenerate loss of repair genes. Shared point mutations in related genomes may be due to non-random mechanism as previously explained.M: Glad you don't object to point mutations as that would make for some very strange demonstrations in front of the White House
You have falsified your own hypothesis. Two humans have the same repair mechanism (as do chimps and humans)yet any two individuals have different amounts and locations of mutations so it cannot be due to loss of repair genes.PB:
As mentioned before the multipurpose genome also includes essential genes. Not only redundancies. The Lamarkian adaptation hypothesis coud be revisited, but has to be adapted to current understanding of (epi)genetics.M: Go ahead an revisit Lamark and tell me what our current understanding is of epigenetics and how it relates to evolution and then how it relates to your hypothesis.PB:
In a previous letter. I was going to check out viral sequences in this region of chromoseme 2. Didn't find them yet. Where did the virus get his protein?M: 8% of the human genome is composed of HERVs so there are plenty of options...you have a lot of work cut out to support your assumption PB:
Do you think it a simple task to set up a new hypothesis that covers all biological phenomena? It takes a lot of effort, but luckily you and other biologists already provided some good comments.
Creatons are not omnipresent, so the phenomena we observe in the genome are usually the result of entropy, or preexisting mechanisms (shuffling, duplications, etc).M: You have claimed multiple times that it was easy to support your hypothesis and very easy to refute evolution based on your hypothesis. Suddenly it is hard? How do you know if creatons are omnipresent or not since you have never measured one or observed one? How will you go about identifying such a particle?PB:
Apparently, these muskusoxes and bears have lost a lot of redundant gentic information that used to be present in their multipurpose genome. That happens a lot. It is predicted by the hypothesis.M: Then the hypothesis is falsified as the ancient and modern muskoxen and bears have the same genetic content as modern representatives.PB:
Sometimes a point mutation in a PREEXISTING gene occurs and leads to phenotypic change. Either through inactivation of the gene (=degeneracy of the genome) or through a slight decrease of specificity. Spetner wrote a book on this topic. According to him none of the examples added information to the genome. Maybe you have such examples. I would be pleased to know about it.M: Syncytin for one.PB:
First of all, you are unable to insult me even if you wanted to. I'm always open for critique and completely stoic to insults.M: You often seem rather prickly these days. However, you did not deny your lack of knowledge of the fields you are criticizing and have not indicated a willingness to inform yourself. If you did so you might bolster your credibility and not make so many errors.PB:
However, I have provided such an organism. The three seperated populations of W. nobilis did not derive from cloning, still they were not able to demonstrate genetic differences. That's what I promissed and that is what you get. Maybe population genetics has something to do with it, since it says that low genetic variablity may be expected in small population (due to losses ). However, this example violates molecular evolution. You know that and I know that. Although the Wollemia nobilis may be an evolutionary riddle, it is not a riddle to me.M: On the one hand you say that population genetics predicts this and thus it falsifies evolution...evolution is population genetics...again Daniel Hartl and Andrew Clark Principles of Population Genetics..there is even a "Cliffs Notes" version with less of the mathematical derivations for some of the equations they present.PB:
Gleichfalls.Tschuss,
Mammuthus

PB
Will respond in more detail on your comments, but I can already reveal that the concept of a multipurpose genome --although it is a fact-- is not easy to understand. M: Interesting. In your next post you claim the concept of a mutlipurpose genome is a hypothesis not a fact....do you know the difference?

Hi Peter,
Hope you had a nice weekend...my replies follow below.PB:
Population genetics is the field of multipurpose genome and allele frequency variation, not the field of evolution. Nothing evolved here, just variation with respect to preexisting alleles in the gene pool.M: Do you even know what evolution is? That you made this statement demonstrates profoundly that you do not. Variation of allele frequencies over..what? Over time! That is evolution. And it really has nothing to do with multipurpose. Multipupose should mean Lamarkian evolution which has not been observed.PB:I am curious. Same genepool as contemporary muskoxen? It would fit 'multipurposism'.M: Nope, so it does not fit mulitpurposism.PB:
The closest relative of the pine is one of the Araucaria family. It is known that they have very low variablity. Maybe Quetzal can repond to this in more detail, since he has got the papers on the DNA work done on this topic.M: Fair enough. I will let Quetzal answer this since the two of you were debating the topic specifically.PB:
How does the environment have impact on gene regulation, I mean. Not the effect of thalidomide. I know how it works. It is a vascular growth inhibitor and now in use to treat certain solid tumors.M: I am sorry Peter but I find it almost impossible to believe that you do not know this. Have you ever heard of maternal environment effects in Drosophila? Do you not get how thalidomide is a non-genetic morphological mutation? Do you know what penetrance is? Phenocopy? This is all first year or even high school biology!PB:
Remember the 1G5 gene and ancient mtDNA? I also like to have a look on the paper that do not show this in subpopulations. Could you please provide me with the references.M: Pick up anything by Cann R and Wilson AC ...or Stoneking M. or Sajantilli A and Paabo, S. (search terms for medline). Luca Cavalli Sforza or Jim Neel's various books on the subject would not be bad sources either.PB:
What evidence do you need to accept non-random mutations? I showed you the 1G5 gene and the ancient mtDNA already, what else do you need?M: I have already told you what evidence multiple times Peter. In order for non-random mutation to abide by the rules you have proscribed you would have to be able to tell me with absolute certainty which sites would mutate in the next generation of any organism. If you just say probably this position or that one then it fits the evolutionary random mutation defintion and not yours.PB:
Denial of mutations would be stupid. I probably refered to point mutations as not being relevant in generating novelties, and usually neutral or degenerate.M: Read up on hox gene mutations. Not all are major changes as your hypothesis demands.MY RESPONSE:
Sounds reasonable if the LTRs diverged. Can you refer to the paper.M: I'll get them to you a little later. I am a bit under time pressure today. Alternatively, punch in LTR divergence into medline and you should get a lot of references on the subject.
PB:
I wasn't referring to reciprocal recombinations. Is not how genes duplicated at the first place. I should be done by unequal crossing over. By any means, the identical copies of histon genes and the hundreds of copies of identical tRNA genes are by definition REDUNDANT. How can they be stable in the genome? Concerted evolution? I wanna see the evolutionary relics in the genome, diverging from 0-100% over time.M: There was just a paper on rDNA psuedogenes. They are relics. There are also tRNA psuedogenes in the genome. If you want to watch them diverge to 100% you will be out of luck. How do you identify a 100% divergent sequence? Everything you are asking for is present.PB:
For histons the mechanism of concerted evolutionism has been abandoned recently for obvious reasons. It is now purifying selection.
PB:
Inappropriate analogy. It has been observed that my parents are my ancestors. It is a biological observation.M: Oh really? Is your conception a biological observation? You and your parents never actually observed the fertilization event that lead to your conception. Paternity studies have shown an average of about 8% non-paternity in most populations...thus it looks like most ancestry is unknown. The analogy stands.PB:
You are wrong in your statement that it is supported by all these disciplines. It is inferred from the fossil record, although nobody ever demonstrated it beyond doubt (transitionforms). Morphology doesn’t say anything about evolution, and phylogenetics observations violate the rules wherever you look (IL-1beta, LDH, alpha-globin, maybe even cytochrome c) so you’re not on solid ground with your assertion.M: That you say morphology has nothing to do with evolution especially as fields such as evo devo are showing a tight link demonstrates your lack of knowledge not lack of support for my assertion. That you don't know how envirnonment impacts gene regulation also does your credibility harm. Your phylogenetics background is equally shabby as you constantly misquoted Page and Holmes as claiming species trees must correlate with gene trees even though all evolutionary biology texts explicitly state that this is not the case. If you misrepresent my assertions you can build a strawman and defeat it. However, you have not put a dent in the actual assertions I have made thus far.PB:
I do the same observations as you but I can explain them by inferring (anti)creaton-matter-interactions (for the appearance of new genera, extinctions, morphology). For the rest there is the multipurpose genome and non-random mutations (this is NOT deterministic mutations).M: However, non of what you state in this paragraph is observable or consistent with the data. In addtion, non-randomness is not observed so it is thus falsified. anti creaton matter etc is a non-testable or falsifiable hypothesis i.e. not science.PB:
As mentioned the new theory is still in preparation/under construction. It took the neo-Darwinians almost a century to set up their non-falsifiable theory (untill I got involved ).
Fallacy? The ZFX gene doesn't change for 20 million years as demonstrated by biomolecular scientists and you call that a fallacy?M: Too bad that the ZFX region has changed as you have consistenly ignored. Evolution is falsifiable. Your dillusions of scientific grandeur are also not particularly helping your cause. I am personally gratified when people attack scientific theories as that is when the really interesting discoveries are made. But you spouting nonsense is hardly an attack on the theory and you have already claimed your agenda with respect to evolution is your personal loathing of atheists. You have fallen back to making claims repeatedly that have been shown to be incorrect yet you persist in repeating these fallacies. Either bring substantive or correct data to the table or admit your lack of such data. It does not mean a hypothesis is wrong but you cannot claim you have support for your hypothesis that does not exist.M: Except that in almost all other organisms such a loss is lethal? Selective redundancy? Redundancies on Tuesdays but not Thursdays? I see big problems for your hypothesis with the redundancy argument.MY RESPONSE:
No, all organisms have a tremendous amount of genetic redundancies. Why would al redundancies be the same? I don't see a reason for that. I already demonstrated redundancies for several organism including Arabidopsis and E coli. Leave out 10% of the genome and no problem for the organism. Apparently these genes --that do not demonstrate more change than essential genes-- are in the genome without selective constraints. It is a Darwinian paradox. Insoluble. Here, the multipurpose genome is far superior to Darwinism. You know that, but you are free to deny it.M: Depends. The bacteria placed back in the wild would probably not survive in competition against the bacteria with the 10% not deleted. Selection is not limited to immediate lethality. It is a Borger unable to understand paradox. Not a paradox for those who actually study the subject. Redundancies by your theory should be identical as they are all caused by the same particles interacting in the same field using the same mechanism. This result is not consistent with you hypothesis.PB:
All according to the FACT of evolutionism, isn’t it. I was objecting to evolutionism, since it is NOT a fact. As demonstrated --and denied-- over and over. Moreover, evolutionism also has to explain the origin of these novel genes.M: Evolutionary theory also covers evolution of new genes. There is even a field of reconstructing ancient genes and testing their enzymatic properties. You can deny facts as much as you want..it does not decrease their veracity.M: There is a lot of evidence for a manatee-elephant association. you up for reading it?MY RESPONSE:
There may be a lot of manatee-elephant associations. There is also a lot of bacterium-elephant association. Next thing you are going to say is since there is an association they have a common ancestor through a Darwinian mechanism. Well a red car and a red bike have also significant associations. Both consist of metal, have wheels, and even have the same colour. Am I to conclude that they are made in the same factory?M: Poor analogy. A red car and red bike are not subject to heritable mutation and thus cannot evolve by natural means. Manatees and elephants can and do. Elephants and manatees have more in common by orders of magnitude than either does to bacteria so your argument is simply foolish. But from your answer I can assume you are not interested in reading up on the associations.PB
MY RESPONSE:
Actually extinctions are associated with an interval of roughly 26 million years. Case proven
How do you explain extinctions?M: Case falsified. 10,000 years ago there was a mass extinction. The peridicity of mass extinctions is not supported either. There are extinctions happening currently.Extinctions are a wonderful source of novelty. If you knock out top predators, grazers etc. it opens up all the occupied niches to exploitation by groups that were prevented previously. Mammals fill most of the niches previouly occupied by dinosaurs.PB:
Your assumption is that these organisms have the same repair mechanism. However, the expression and interaction is differently regulated per individual. As mentioned several times now, there are 2 types of mutations non-random and random. The random mutations is all evolutionism requires, according to evolutionism. However, the non-random mutations line up if you compare (sub)species and give an illusion of common descent. In addition, they are alternated by random mutations. The latter are interpreted as being generated after the species split off from a common ancestor. In my opinion the two types of mutations work simultaneously. So, I don’t see a problem here.M: The problem is that now you have fallen back to admitting random mutation whereas before mutation was non random. Before all organisms were using the same repair mechanism and now each individual is unique. Your hypothesis is falling apart.PB:
It is clear from my own field that some ‘adaptations’ occur that cannot have resulted from mutations in DNA alone, since the adaptations occurs suddenly and everywhere at the same moment. For instance, asthma. It is a desease affecting ‘solely’ Western societies, and its prevalence increased from around 1% 40 years ago to 10% now. That is within 1-2 generations. It suggests an effect of the environment/lifestyle on the development of the disease. It is my personal opinion that the disease is largely due to epigenetic modifications of chromatin and/or DNA structure that results in an alternative development of immune system and lungs (sometimes aggravated by genetic predisposition).
Similar observation have been done on rapid adaptations of human populations on high altitude. It is as if the info of adaptation is pre-existing.M: How is anything about either condition work against genetics or evolution?PB:
If the IL-1beta was carried by a virus and integrated adjacent to IL-1 alpha then I expect to find the remnants of the virus there too isn’t it?M: It really would depend. If it is a retroviral insertion you would expect to find LTR's on both sides of the gene (though they can and do get removed by recombination). If the integration was reasonably recent the LTRs should still be recognizable as such. If the integration was extremely ancient, you will have the 100% divergence you asked for previously.PB:
Not refute, I provide an alternative. And that will take a bit of time. Falsifications of evolutionism can readily be found by scrutiny of current literature on the topic. As demonstrated.M: You claimed that your hypothesis was very easy to establish. Yet now you still persist in falling back on "it is not done yet" when there are holes in it. You might have thought of that before announcing your replacement of evolution You have not demonstrated falsification of evolution to date..but please keep trying. Especially the over reliance of many on neutrality...I am not a big fan of neutral evolution explaining everything either.PB:
No, it is not. Apparently they didn’t loose their genetic content. It is not obligatory to loose genetic content, it is a possibility to get variation.M: Previously you stated they must have lost information due to degeneracy and here you say the opposite. Which is it?PB:
Where does syncytin come from? I mean if it is a viral protein, the virus got it somewhere and integrated it into another genome. Where did the virus get it?
And you said in the previous letter: "Syncytin is an envelope protein common to all retroviruses both exogenous and endogenous. The direction of capture is clear from the lack of such a viral gene outside of old world monkeys and hominids." Clear for the theory of evolutionism you mean. It can be envisagd that it was a unique old world monkey gene caputered by an endogenous retrovirus and later escaped from the genome. Where do you think viruses have their origin? In the genome of course.M: Chicken and egg question. In some ways we are like complicated viruses so maybe viruses were the first life forms on the planet. They are certainly profoundly successful organisms. But anyway, all envelope proteins were old world monkey derived it does not explain the presence of this retroviral component in organisms from bacteria to humans.PB:
Yes, I have a cold. It affects the temper I guess. However, all I do is giving a different interpretation on scientific observations. Nothing wrong with that in my opinion. I learned a lot from this discussion and if a thesis is not tenable I give in. That’s the scientific way. It would be rather unscientific to claim that a hypothesis is a fact while it still can be falsified. But, I am working on that.M: Hope you are feeling better. Like I said, I am also up for this type of arguing and I have learned a lot to because the discussion forces me to keep going back to my literature collections and read and re read papers. I find it productive no matter how it goes..with the exception of my debate with Wordswordsman which was a colossal waste of time.PB:
Since when is change in allele frequencies evolutionism? It is easy to explain by a multipurpose genome. If population genetics is evolutionism than I AM an evolutionist too. But, it is NO evolutionism, since it doesn't say anything about the generation of new organisms, novel genes, etc. You know --and every educated biologist should know-- that you cannot present population genetics as evolutionism.M: Population genetics is inextricable from evolution. Evolution deals with species which are composed of populations that are ultimately determined by their genetics. educated biologists know this You have "created" and artificial distinction between the fields as the principles of evolution are based on the principles of population dynamics.Best wishes and hope you are feeling better,
Mammuthus[This message has been edited by peter borger, 10-26-2002][/B][/QUOTE]

It is almost all at a click of the mouse Hopefully you will address some of my questions but more importantly, you have not addressed Quetzal's rebuttal of your W. nobilis example of a "created" organism....looking forward.cheers,
MHum Mol Genet 2001 Jun 15;10(13):1335-46 Related Articles, LinksDifferential expression of the actin-binding proteins, alpha-actinin-2 and -3, in different species: implications for the evolution of functional redundancy.Mills M, Yang N, Weinberger R, Vander Woude DL, Beggs AH, Easteal S, North K.Neurogenetics Research Unit, Children's Hospital at Westmead, Westmead, Sydney, NSW 2145, Australia.The alpha-actinins are a multigene family of four actin-binding proteins related to dystrophin. The two skeletal muscle isoforms of alpha-actinin (ACTN2 and ACTN3) are major structural components of the Z-line involved in anchoring the actin-containing thin filaments. In humans, ACTN2 is expressed in all muscle fibres, while ACTN3 expression is restricted to a subset of type 2 fibres. We have recently demonstrated that alpha-actinin-3 is absent in approximately 18% of individuals in a range of human populations, and that homozygosity for a premature stop codon (577X) accounts for most cases of true alpha-actinin-3 deficiency. Absence of alpha-actinin-3 is not associated with an obvious disease phenotype, raising the possibility that ACTN3 is functionally redundant in humans, and that alpha-actinin-2 is able to compensate for alpha-actinin-3 deficiency. We now present data concerning the expression of ACTN3 in other species. Genotyping of non-human primates indicates that the 577X null mutation has likely arisen in humans. The mouse genome contains four orthologues which all map to evolutionarily conserved syntenic regions for the four human genes. Murine Actn2 and Actn3 are differentially expressed, spatially and temporally, during embryonic development and, in contrast to humans, alpha-actinin-2 expression does not completely overlap alpha-actinin-3 in postnatal skeletal muscle, suggesting independent function. Furthermore, sequence comparison of human, mouse and chicken alpha-actinin genes demonstrates that ACTN3 has been conserved over a long period of evolutionary time, implying a constraint on evolutionary rate imposed by continued function of the gene. These observations provide a real framework in which to test theoretical models of genetic redundancy as they apply to human populations. In addition we highlight the need for caution in making conclusions about gene function from the phenotypic consequences of loss-of-function mutations in animal knockout models.J Mol Evol 1996 Feb;42(2):247-56 Related Articles, LinksEvolution of the src-related protein tyrosine kinases.Hughes AL.Department of Biology, Pennsylvania State University, University Park 16802, USA.A phylogenetic analysis of src-related protein tyrosine kinases (PTKs) showed that one group of these genes is quite ancient in the animals, its divergence predating the divergence of the diploblast and triploblast phyla. Three other major groupings of genes were found to predate the divergence of protostome and deuterostome phyla. Most known src-related PTKs of mammals were found to belong to five well-differentiated families: srcA, srcB, abl, csk, and tec. One srcA gene (fyn) has an alternatively spliced seventh exon which shows a different pattern of relationship from the remainder of the gene; this suggests that this exon may have been derived by a recombinational event with another gene, perhaps one related to fgr. The recently published claim that mammalian members of this family expressed in the nervous system evolve more slowly at nonsynonymous nucleotide sites than do those expressed in the immune system was not supported by an analysis of 13 pairs of human and mouse orthologues. Rather, T-cell-specific src-related PTKs were found to have higher rates of nonsynonymous substitution than were those having broader expression. This effect was particularly marked in the peptide binding site of the SH2 domain. While the SH2 binding site was highly conserved among paralogous mammalian members of the srcA and srcB subfamilies, no such effect was seen in the comparison of paralogous members of the csk and tec subfamilies. This suggests that, while the peptide binding function of SH2 is conserved within both srcA and srcB subfamilies, paralogous members of the csk and tec subfamilies have diverged functionally with respect to peptide recognition by SH2.: Proc Natl Acad Sci U S A 1991 Jun 15;88(12):5232-6 Related Articles, LinksInterleukin 1 receptor antagonist is a member of the interleukin 1 gene family: evolution of a cytokine control mechanism.Eisenberg SP, Brewer MT, Verderber E, Heimdal P, Brandhuber BJ, Thompson RC.Synergen, Boulder, CO 80301.Interleukin 1 receptor antagonist (IL-1ra) is a protein that binds to the IL-1 receptor and blocks the binding of both IL-1 alpha and -beta without inducing a signal of its own. Human IL-1ra has some sequence identity to human IL-1 beta, but the evolutionary relationship between these proteins has been unclear. We show that the genes for human, mouse, and rat IL-1ra are similar to the genes for IL-1 alpha and IL-1 beta in intron-exon organization, indicating that gene duplication events were important in the creation of this gene family. Furthermore, an analysis of sequence comparisons and mutation rates for IL-1 alpha, IL-1 beta, and IL-1ra suggests that the duplication giving rise to the IL-1ra gene was an early event in the evolution of the gene family. Comparisons between the mature sequences for IL-1ra, IL-1 alpha, and IL-1 beta suggest that IL-1ra has a beta-stranded structure like to IL-1 alpha and IL-1 beta, consistent with the three proteins being related. The N-terminal sequences of IL-1ra appear to be derived from a region of the genome different than those of IL-1 alpha and IL-1 beta, thus explaining their different modes of biosynthesis and suggesting an explanation for their different biological activities.: J Mol Evol 1994 Jul;39(1):6-12 Related Articles, LinksEvolution of the interleukin-1 gene family in mammals.Hughes AL.Department of Biology, Mueller Laboratory, Pennsylvania State University, University Park 16802.The phylogeny of interleukin-1 family genes shows that human interleukin-1 alpha (IL-1 alpha) is more closely related to IL-1 alpha of the bovine than to IL-1 alpha of the mouse, whereas human interleukin-1 beta (IL-1 beta) is more closely related to IL-1 beta of the mouse than to IL-1 beta of the bovine. The IL-1 receptor antagonist (IL-1ra) shows homology to the C-terminal region of both IL-1 alpha and IL-1 beta. In the C-terminal region, the IL-1 alpha genes of human and mouse have diverged more from each other at nonsynonymous sites than have either IL-1 beta or IL-1ra; because the same pattern is not seen at synonymous sites, it must be due not to a difference in mutation rate but rather to a greater degree of functional constraint on this region in the IL-1 beta and IL-1ra proteins than in the IL-1 alpha protein. But synonymous sites in IL-1 beta of mouse have evolved more rapidly than in IL-1 beta of human, indicating a higher rate of mutation in the former gene. In the N-terminal region of the protein, nonsynonymous sites have evolved at similar rates in IL-1 alpha and IL-1 beta. The first exon of the IL-1ra gene, which encodes the leader peptide, shows evidence of homology with the first exon of IL-1 beta, which is not translated. Thus, it seems likely that IL-1ra evolved by duplication of an IL-1 beta gene and loss of expression of exons 2-4.Mol Biol Evol 2000 May;17(5):804-12 Related Articles, LinksSex chromosomal transposable element accumulation and male-driven substitutional evolution in humans.Erlandsson R, Wilson JF, Paabo S.Max-Planck-Institute for Evolutionary Anthropology, Leipzig, Germany. riker1@biochem.kth.seWe sequenced the genomic region containing the human Y-linked zinc finger gene (ZFY). Comparison of ZFY to the related region on the X chromosome (ZFX) and to autosomal sequences reveals a significant accumulation of transposable elements on the sex chromosomes. In addition, five times as many retroviruslike elements (RLEs) are present in the ZFY region as in the ZFX region. Thus, transposable elements accumulate more rapidly on the sex chromosomes, and the insertion of RLEs may occur more frequently in the male than in the female germ line. When the accumulation of substitutions in Alu elements was analyzed, it was found that the Alu elements at the Y-chromosomal locus diverged significantly faster than those at the X-chromosomal locus, whereas the divergence of autosomal Alu elements was intermediate. The male-to-female mutation rate ratio was estimated to be 2.5.

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Originally posted by Tranquility Base:
Mammuthus & Peter

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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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[This message has been edited by Tranquility Base, 10-28-2002]

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**********************************************You will then have to explain why this is misleading TB...I mean AQ

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

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Originally posted by Quetzal:

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

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

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Actually, the abstract states exceptionally low genetic diversity, not no variability. To be fair, it also states that the loci examined to date don’t show variation where expected (or where found in other organisms) — the key word being to date. Talk about nitpicking — if you’d like, you can always email Dr. Peakall yourself and ask for a clarification. I’m going by what the man wrote — not what I want it to be.

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

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

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

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

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Feel free to get them the same way I did — or use a university lending library. I provided the references, you’re quite capable of digging them out. You can even take the opportunity to explain to Dr. Peakall why he’s got it all wrong. I’ll be fascinated to see his response.

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Furthermore, as stated the tree doesn't demonstrate variation in the expected regions, so where exactly do my claims fail. I simply give it another interpretation. By the way, if I recall properly, it was you who claimed in a previous letter (on mtDNA) not to be a molecular biologist so you were not able to interpret the data on this topic. And now suddenly you are able to interpret these molecular data? Very confusing.

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

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Thanks for that, I knew he was in Canberra, but as usual I recalled by head (almost photographic memory, I presume). Nitpicking again. You just earned yourself 100 points.

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

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

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

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

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

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

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

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

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

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

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

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Nope. Sounds like we need more information.

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

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1. NONE of your claims about the tree’s DNA are correct, as I have shown, using the papers referenced. Look ‘em up.
2. Disinformation? Not really. Deliberate, skewed interpretation coupled with misunderstanding and a weak argument from personal incredulity, usually.
3. You haven’t shown a single concrete example of anything that falsifies evolution. Every example, argument, quibble, etc, that you’ve produced has been shown to be in error by one person or another here. Mere repeated assertion doesn’t prove your case.
4. Now I insist you email him. Where in ANY his articles does Dr. Peakall talk about an all-purpose genome?

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

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Now THAT’S condescending. Meaningless words? Are you denying that organisms are constrained by their natural history (genetics, ecology, ancestry)? I gave you several reasons why your favorite organism may have been constrained — clonality in the wild, miniscule in-bred population (bottleneck), etc. You’re waaaayyy out there on this one, Peter. Nothing in the concept states that evolution ceased or any of the other strawmen you’re arguing here. What is an endstation of evolution? Can you even conceive of any possible way of falsifying or providing evidence for the existence of any single species of any organism of any kind anywhere on the planet outside of a strictly controlled lab lineage has ceased to evolve? It’s certain as taxes that Wollemia hasn’t stopped (or somehow is no longer capable of) evolving — one of the key issues dealt with by the conservation biology people is how to prevent hybridization. If you don’t think this is a problem, I suggest you look up the stringent efforts being used with the Catalina mahogany (Cercocarpus traskiae) conservation efforts.

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

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

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

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

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

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

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

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

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

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Try again, Peter.

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

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

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

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bumpity bump

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Originally posted by peter borger:
dear Mammuthus,

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

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best wishes,
Peter

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***********************Hi Peter,
You will have to tell me then why they are not explanatory. You have shown on several occassions profound misunderstandings of the papers,particularly studies of the ZFX/ZFY region so the burden is on you to demonstrate that your arguements are based on a real flaw in the data or arguments of the authors and not on your lack of understanding of population genetics, biochem, and randomness.1) Do these data mean that approximately 450 bp changes occurred on neutral positions?SORRY PETER BUT NOTHING IN YOUR LETTER INDICATES TO ME WHERE THIS QUESTION COMES FROM. ARE YOU REFERREING TO SOMETHING IN THE ARTICLE?2) Do these data mean that it would take about 10(exp)6 years for 3 random mutation to occur in the duplicated gene? Thus 150 million years for 450 neutral mutations?ONLY IF YOU BELEIVE THAT DNA EVOLVES IN A CLOCKLIKE MANNER. I DON'T SO THE ESTIMATE OF TIME WOULD HAVE A TREMENDOUS VARIANCE ATTACHED TO IT. PURELY NEUTRAL LOCI MIGHT EVOLVE IN A CLOCKLIKE MANNER HOWEVER BUT IT IS DEPENDENT ON A LOT OF OTHER FACTORS I.E. EFFECTIVE POPULATION SIZE; MUTATION RATE ETC.3) Do these data mean that after each point-mutation there was neutral purifying selection? And, what exactly is it? I mean, what exactly is selection on neutral genes?I HAVE NO IDEA WHAT NEUTRAL PURIFYING SELECTION IS SUPPOSED TO MEAN. SELECTION OCCURS ON GENES THAT PROVIDE AN ADVANTAGE OR DISADVANTAGE TO THE ORGANISM. NEUTRAL GENES CAN BECOME HOMOGENIZED BY GENE CONVERSION BUT IT IS NOT BECAUSE OF SELECTIVE CONSTRAINT.3a) Is it independent from nearby genes? Independent from the rest of the genome?IT DEPENDS. SOME GENES EVOLVE BY CONCERTED EVOLUTION USING VARYING HOMOGENIZATION PROCESSES SUCH AS GENE CONVERSION. BUT THIS IS NOT THE CASE FOR ALL GENES.: Mol Biol Evol 2002 May;19(5):689-97 Related Articles, LinksPurifying selection and birth-and-death evolution in the histone H4 gene family.Piontkivska H, Rooney AP, Nei M.Institute of Molecular Evolutionary Genetics, Pennsylvania State University, 328 Mueller Lab, University Park, PA 16802, USA. oxp108@psu.eduHistones are small basic proteins encoded by a multigene family and are responsible for the nucleosomal organization of chromatin in eukaryotes. Because of the high degree of protein sequence conservation, it is generally believed that histone genes are subject to concerted evolution. However, purifying selection can also generate a high degree of sequence homogeneity. In this study, we examined the long-term evolution of histone H4 genes to determine whether concerted evolution or purifying selection was the major factor for maintaining sequence homogeneity. We analyzed the proportion (p(S)) of synonymous nucleotide differences between the H4 genes from 59 species of fungi, plants, animals, and protists and found that p(S) is generally very high and often close to the saturation level (p(S) ranging from 0.3 to 0.6) even though protein sequences are virtually identical for all H4 genes. A small proportion of genes showed a low level of p(S) values, but this appeared to be caused by recent gene duplication. Our findings suggest that the members of this gene family evolve according to the birth-and-death model of evolution under strong purifying selection. Using histone-like genes in archaebacteria as outgroups, we also showed that H1, H2A, H2B, H3, and H4 histone genes in eukaryotes form separate clusters and that these classes of genes diverged nearly at the same time, before the eukaryotic kingdoms diverged.: Proc Natl Acad Sci U S A 2000 Sep 26;97(20):10866-71 Related Articles, LinksPurifying selection and birth-and-death evolution in the ubiquitin gene family.Nei M, Rogozin IB, Piontkivska H.Institute of Molecular Evolutionary Genetics and Department of Biology, Pennsylvania State University, 328 Mueller Laboratory, University Park, PA 16802, USA. nxm2@psu.eduUbiquitin is a highly conserved protein that is encoded by a multigene family. It is generally believed that this gene family is subject to concerted evolution, which homogenizes the member genes of the family. However, protein homogeneity can be attained also by strong purifying selection. We therefore studied the proportion (p(S)) of synonymous nucleotide differences between members of the ubiquitin gene family from 28 species of fungi, plants, and animals. The results have shown that p(S) is generally very high and is often close to the saturation level, although the protein sequence is virtually identical for all ubiquitins from fungi, plants, and animals. A small proportion of species showed a low level of p(S) values, but these values appeared to be caused by recent gene duplication. It was also found that the number of repeat copies of the gene family varies considerably with species, and some species harbor pseudogenes. These observations suggest that the members of this gene family evolve almost independently by silent nucleotide substitution and are subjected to birth-and-death evolution at the DNA level.3b) Does this type of selection take place on the level of the organism? How?AGAIN; YOU REALLY NEED TO LEARN SOME POPULATION GENETICS OR AT LEAST GET A GRASP OF WHAT RELATIVE FITNESS MEANS. EVEN IF A MUTATION IS NOT IMMEDIATELY LETHAL; IF IT PUTS THE ORGANISM AT A DISADVANTAGE IT WILL BE SELECTED AGAINST. YES; IT IS AT THE LEVEL OF THE ORGANISM4) Are there identical (=very recently duplicated) genes in known genomes?Annu Rev Cell Dev Biol 2002;18:53-80 Related Articles, LinksGene co-option in physiological and morphological evolution.True JR, Carroll SB.Department of Ecology and Evolution, State University of New York at Stony Brook, Stony Brook, New York 11794-5245, e-mail: jrtrue@life.bio.sunysb.eduCo-option occurs when natural selection finds new uses for existing traits, including genes, organs, and other body structures. Genes can be co-opted to generate developmental and physiological novelties by changing their patterns of regulation, by changing the functions of the proteins they encode, or both. This often involves gene duplication followed by specialization of the resulting paralogous genes into particular functions. A major role for gene co-option in the evolution of development has long been assumed, and many recent comparative developmental and genomic studies have lent support to this idea. Although there is relatively less known about the molecular basis of co-option events involving developmental pathways, much can be drawn from well-studied examples of the co-option of structural proteins. Here, we summarize several case studies of both structural gene and developmental genetic circuit co-option and discuss how co-option may underlie major episodes of adaptive change in multicellular organisms. We also examine the phenomenon of intraspecific variability in gene expression patterns, which we propose to be one form of material for the co-option process. We integrate this information with recent models of gene family evolution to provide a framework for understanding the origin of co-optive evolution and the mechanisms by which natural selection promotes evolutionary novelty by inventing new uses for the genetic toolkit.5) Is evolution a phenomenon driven by random mutation?
YESI am going to let Quetzal have first crack at a response to your post to him but I found several deep flaws in your statements that I will address if he does not.Best wishes and thanks for responding to the posts
M

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

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