molecular genetic evidence for a multipurpose genome

Dear Dr Page,
There we go again, my comments to the ZFY region. I challenge you to rebut them. Last time I mailed them the only response I had was from Percipient. It was irrelevant. So give it a try.The Y-linked zinc finger (ZFY) gene is located on the male-determining Y-chromosome and specifies a protein that regulates the expression of genes. The ZFY gene is actively transcribed in male and appears to be involved in sperm and testes maturation. A detailed study was recently performed that surveyed the 729 base pair intron present between the third and fourth exon of the human ZFY gene. The study was performed to provide a picture of the sequence polymorphisms in the Y chromosome, and 38 individuals were included representing a cross section of geographic origins. In addition, the homologous sequences of the intron was analysed in three primates: chimpanzee, gorilla and orang-utan.
The samples obtained from human subpopulations no polymorphisms were detected whatsoever. On the contrary, inspection of the corresponding homologous intron region in the primates reveals that several variable sites are distributed throughout the intron and include at least 39 substitutions (21 transitions and 14 transversions, and 4 indel mutations. Thus, at least 5% variation in this region is observed between human and great apes.
The absence of variation in the ZFY region in humans is very awkward, and, according to the authors, cannot be ascribed to a chance (=random mechanism). Introns are thought to be subject to neutral evolution, and variation within the human population is predicted on neutral positions. Confronted with the peculiar situation of the absence of variation, the authors must apply statistics to define an era when the common ancestor of all males lived. They estimate that ‘Y-chromosome Adam’ lived around 270.000 (range 0-800.000) years before present (REF1).It should be noted that the non-variant intron sequences in the ZFY region provides a severe problem for evolution biologists, since molecular rules demand some neutral evolution, and thus, variation on silent positions. But, he authors state that ‘the invariance likely may results from a selective sweep, a recent origin of modern Homo sapiens, or a historically small effective male population sizes’ (REF1).Because the X and Y chromosome have little sequence homology there is no recombination between the major part of these chromosomes, and most of the genes on the Y chromosome will behave as one linked genetic group. Hence, if an advantageous mutation occurs in a gene on the Y chromosome it will drag with it all the non-recombining parts of the chromosome. A rapid, natural selection driven fixation of any advantageous gene on the Y chromosome would therefore result in loss of variance throughout the entire Y chromosome (REF2). Because all non-recombining DNA sequences of the Y chromosome are replaced in a single sweep, this vision predicts that variability should be absent in all linked non-recombining Y chromosome genes. (A retrospective prediction?)A recent study in mice on the non-coding region flanking the SRY gene, which is directly responsible for inducing maleness, is revealing in this matter. The study compared the amount of variation within the species and related it to the amount of variation among species. Then, the authors compared this ratio to the ratio for a rapidly changing region in the mitochondrial DNA obtained in the same way.If any of the two regions were subject to a selective sweep, it would be demonstrated by a reduced variation within species. It was found, however, that the non-coding region of the SRY gene changed at a neutral rate. It implicates that, because of linkage of the major part of the Y chromosomal genes, the entire non-recombining part of the Y chromosome changes at a neutral rate. Therefore, it is unlikely that natural selection acts upon the Y chromosome (REF2).But if natural selection did not act upon the Y chromosome the high degree of variability of the Y chromosome between primates apparently defies the theory of evolution, since the coding region of the SRY gene is very stable within a species (as observed before), whereas considerable variation is observed between distinct species. Some part of the SRY protein show such high degree of variability between distinct primate species that one must conclude that part of the protein has NO function at all, or that the gene is subject to DIRECTIONAL selection, says evolution biologist Svante Pbo (REF2). However, directional selection is only demonstrated in cases involving intergenomic conflict, such as occur between host and pathogen, but is has never been observed for non-immune system related protein coding genes. Of course, one can always propose non-random, directed mutations. But, evolutionists will object to that.
The only remaining evolutionary explanation of the variability in the Y chromosome between species is by the mechanism of neutral evolution. Yet, the observation that more replacement substitutions than synonymous substitutions are present between species suggests that a neutral mechanism is not likely to be responsible for variation among species.The ultimate hypothesis evolutionists propose is that ‘these regions have been retained throughout the primate lineage without any requirement for sequence conservation, implying that the SRY protein is [] the HMG box alone’ (REF2).Do evolutionists really understand their own theories? The proposal that the sequence has been retained without conservation requirement would still imply that the SRY protein is expected to evolve at a NEUTRAL rate! The peculiar thing about the SRY proteins was, however, that they are much more variable than predicted by neutral evolution. To properly understand this one has to assume SELECTION ON NEUTRAL POSITIONS! I can imagine that evolution biologists really get frustrated solving the riddles around the SRY region. Despite several ad hoc hypotheses it all ends, again, in a paradox. Apparently, there is no evolutionary explanation for the high degree of dissimilarity of SRY region between distinct primates. It points in the direction of directed, non-random mechanism. It is clear that invariability of this haploid region in humans is ensured by specific DNA guarding and stabilising proteins. All in accord with the MPG hypothesis.REF1) Dorit R.L. et al. Absence of polymorphism at the ZFY locus on the human Y chromosome. Science 1995, Volume 268, p1183-1185.REF2) Svante Pbo. The Y chromosome and the origin of all of us (men). Science 1995, 268, p1141-1142.Best wishes, and I hope for a lot of discussion, not a lot of abstracts. I can find abstracts myself.
Peter[This message has been edited by peter borger, 11-11-2002]

Dear Dr Page,Your examples are all in accord with the multipurpose genome. Lets start with your reference:From the abstract:"Transgenic analysis of Cyp6 1 shows that overtranscription
of this gene alone is both necessary and sufficient for resistance. Resistance and up-regulation in Drosophila populations are associated wit a single Cyp6 1 allele that has spread globally. The allele is characterized by the insertion of an Accord transposable element into the 5' end of the Cyp6 1 gene."What does the MPG hypothesis predict (see mail #1):The concept 'multipurpose genome' holds that:
1) DNA sequences —although plastic-- are stable throughout time,
2) organisms demonstrate genetic redundancies that reside in the genome without selective constraint,
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],
4) the function of natural selection is to remove degenerate organisms, and
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).Point #3 predicted your observation.So, I do not see a problem for the MPG hypothesis here. The other examples are similar. They all involve differential gene regulation. As predicted by the MPG hypothesis.The ball is back in 'your' ZFY region. Best wishes,
Peter

Dear Mammuthus,M: You will have to tell me then why they are not explanatory. You have shown on several occassions profound misunderstandings of the papers,PB: By "profound misunderstanding" you must mean "comments on evolutionism just-so stories". By now you should have known that I prefer to think for myself. I can analyse the data for myself, and I can interpret the data for myself. The data that are not in accord with molecular mechanism of evolutionism, I mailed to this site. You choose to deny them. I don't mind. Deny as often as you like. It doesn't make your pet theory a better theory.M: 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.PB: I mailed my comments on the ZFY region again. Maybe you can respond a bit on it, now. Haven't had any substantial responses, yet.PB: According to neutral theory at least a couple of mutations would have been expected in the ZFX region gene analysed by DR Kim. Of course, you will not find this in discussion of evolutionary papers. You have to find out for your self from the raw data. Therefore, I mailed Dr Kim for a copy of the paper. He was very kind to send me one, so I could have a close look at their data. The data show NO variation in this region for 20.000.000 years. What kind of evolution is that?
Similar things have been obsrved for the ZFY region in human and great apes. The observations can only be interpreted as NON-RANDOM evolution. I mailed this months ago and never got a response. Percy was the only one with an (irrelevant) remark. The ZFY region is also still open for discussion/rebuttal.M: Sounds like selection not non-random evolution. As to expectations of mutations...there is a probability of mutation not an expectation that they occur. A perfectly weighted coin is expected to give heads and tails 50:50 but it seldom meets this expectation...try it and see. Erlandsson found point muations, deletions, and transpostion events throughout the ZFX/ZFY region...you can look at their raw data to...thus, the available data does not falsify evolution.PB: Selection on neutral positions? Dear Mammuthus, at least 20% of this region is neutral. Ever heard of the neutral third codon positions of the redundant genetic code? The odds are against your simplistic presentation, as demonstrated on this site by your friend Fred. If you throw often enough the odds will be 50:50.PB: So, you don't believe that DNA evolves in a clocklike manner. How does it evolve than? Through punctuated equilibrium, I guess? Sometimes it evolves, sometimes it doesn't? Pretty good theory. Dear mammuthus, maybe you didn't get it yet but according o neutralists DNA is ALWAYS evolving on neutral positions. It is a random phenomenon, they say. Probably you don't agree with the neutralists, and are a selectionist. If so, let me know and we will discuss how these redundant genes were selected than. I will let you introduce neutral selection.M: Build up as many strawmen as you like Peter. I do not believe in an accurate clock because of selective sweeps, bottlenecks, and founder events among lineages that can completely screw up the coalescence time and give an inaccurrate date. Also, since it is a random process, there is only a probability of the clock ticking, not that it actually will for a given sequence. A real clock does not have this type of statistical fluctuation as a variable. If you actually would read some literature on the subject you would see why this is the case but...you won't. Your claims as to WHAT neutral evolution says are meaningless as you have steadfastly refused to educate yourself regarding evolutionary theory or population genetics...I could do the same as what you are doing as follows..creationism posits that big hairy priests insert bananas in their rectums thus causing the creation of kinds..why do you hold to this rectal banana theory Peter? Is it your evil oppressive christian imperialism that blinds you?...(M exits creationism mode)PB: Maybe you don’t believe in an accurate clock. But the HVR-1 mtDNA sequences presented by Adcock et al (PNAS 2001, 98:537-542) demonstrate with respect to human reference sequence 29 differences for bonobo, 24 for chimp, 27 for neanderthaler. I do not even see a RUDIMENTARY clock in these data. How about you? It should also be noted that an ancient homo sapiens (dated 62,000 BP) demonstrates 10 differences compared to reference sequence. Let me guess, bonobo/chimp and man have a common ancestor around 150.000 years ago? Nice believes you're holding to.PB: Selection on redundant genes? If a gene is inactivated in a population it clearly demonstrates that it doesn't have any selective advantage. That's the evolutionary problem with redundant genes, they are in the genome without selective constraints. How many times do I have to reiterate this observation? Also, redundant genes do NOT evolve faster than essential genes. How many times do I have to reiterate this observation?M: How many times do I have to re-iterate that you don't know anything about evolution or population genetics?PB: It is a known that evolutionism is so difficult to understand that not even evolutionists understand it.M: How do you know that there is no selective advantage?PB: How do you know that there is selective advantage? You are the propagator of an extraordinary claim. So you have to present the extraordinary evidence.M: How do you know that removal of the gene is not slighltly deleterious?PB: I know that your friends introduced very weak purifying selection, another meaningless term. For the redundant gene family of alpha actinins --as for the 1G5 gene-- you have to introduce neutral selection. As demonstrated. And as denied by evo's.M: Most mutations are yet are maintained in the population regardless.PB: So you are a neutralist?M: Survival of the fittest does not mean the best. It means that a population has reached an optima higher than its competitors and produces more offspring...not that there is no consequence of losing the gene on long term fitness when faced with subsequent selection. How much selection do you think is required to homogenize a gene?PB: You should know this, you are the evolutionist. However, how much selection does it require to purify a redundant gene?PB: Thanks for these references. If you read these articles properly, you will find out that concerted evolution was a concept to understand the uniformity of these high abundance genes, for instance the histon genes, TcR genes, ubuiquitin genes. However, it isn't tenable anymore and recently it was replaced by birth and death evolution. It's a meaningless term that doesn't explain anything. It's what you believe in. Explain what you believe in, maybe I can believe in it too.M: As I said, in some cases concerted, in others by selection.PB: Yes, and that makes it such fabulous theory. Sometimes a bit of this, than a bit of that. Evolutionism is like cooking, isn’t it. How to cook the one kind into the other. The stories get better and better.
What happened to Occam’s razor. Mark Pullen will object to such theories, is my guess. What about it, Mark?M: What did you not understand in my sentence. And what percicesly do you want to discuss? You claim that Nei's papers are meaningless i.e. you don't understand them at all...what specifically is it that you disagree with since it is not clear from reading the portions of the papers you posted and your response.PB: The whole discussion is meaningless. If I write discussions like that, I could forget about my papers. The peer reviewers would immediately return my manuscripts with the comment: Meaningless nothingness.PB: I checked out this reference. It is a model, a proposal. The authors do not provide a single example that demonstrates that duplication and cooption has been observed. In fact, the redundancy in the alpha actinin genes opposes the whole putative concept of cooption. What I like to see are genes in the human genome on their way to cooption. That is, show me expressed genes (pseudogenes are irrelevant for this concept) that are moving towards genes with a (slightly) different function through selection. A prediction could be that in distinct subpopulations these duplicated genes have accumulated distinct mutations.M: Actually the paper is based on experiments done by Carrol and others to support his model .....also not totally clear what kind of example you want...something like this perhaps?PB: Apparently these experiments have never been published. Or do you mean the reference below? If so, than I have to disappoint you. It is NOT an experiment it is interpretations of data. You know the difference, I hope. (If not, it explains a lot ).Evol Dev 2002 Mar-Apr;4(2):111-23 Related Articles, LinksGene expression and larval evolution: changing roles of distal-less and orthodenticle in echinoderm larvae.Lowe CJ, Issel-Tarver L, Wray GA.Department of Ecology and Evolution, State University of New York at Stony Brook, 11732, USA.We describe the expression of the homeobox genes orthodenticle (Otx) and distal-less (Dlx) during the larval development of seven species representing three classes of echinoderms: Holothuroidea, Asteroidea, and Echinoidea. Several expression domains are conserved between species within a single class, including Dlx expression within the brachiolar arms of asteroid larvae and Otx expression within the ciliated bands of holothuroid larvae. Some expression domains are apparently conserved between classes, such as the expression of Dlx within the hydrocoel (left mesocoel) in all three classes. However, several substantial differences in expression domains among taxa were also evident for both genes. Some autapomorphic (unique derived) features of gene expression are phylogenetically associated with autapomorphic structures, such as Dlx expression within the invaginating rudiment of euechinoids. Other autapomorphic gene expression domains are associated with evolutionary shifts in life history from feeding to nonfeeding larval development, such as Otx expression within the ciliated bands of a nonfeeding holothuroid larva. Similar associations between evolutionary changes in morphology and life history mode with changes in regulatory gene expression have also been observed in arthropods, urochordates, and chordates. We predict that recruitment of regulatory genes to a new developmental role is commonly associated with evolutionary changes in morphology and may be particularly common in clades with complex life cycles and diversity of life history modes. Caution should be used when making generalizations about gene expression and function based on a single species, which may not accurately reflect developmental processes and life histories of the phyla to which it belongs.PB: 5) Is evolution a phenomenon driven by random mutation?
YESPB: Apparently NOT, judging from examples like the alpha actinin genes, the ZFY region, the 1G5 gene, etcetera.M: Apparently so since NOT a single one of these demonstrates a non-random mechanism.M: I am going to let Quetzal have first crack at a response to your post to him but I found several deep flaws in your statements that I will address if he does not.PB: No worries about that.M: If by no worries you mean you will avoid answering Quetzal then I see what you mean by no worries.PB: You are lagging behind, I responded to all Quetzal’s points. He choose not to respond to all my replies. However, talking about avoidance. You are avoiding crucial questions of my mails with increasing frequency. Why, I wonder?Best wishes,
peter

Dear Quetzal,You write:Given the substance-less nature of your last two replies to me, perhaps you could detail - in simpler form for those of us without your "expertise" - exactly what assertion or question I have not addressed.I write:If you mean by 'substance-less nature' that I addressed all your nine issues in a succinct way, I agree with you.
You write:With 8000 plus words to wade through desperately seeking some actual argument, it is quite possible to have missed something inadvertently.I say:I concisely responded to your 9 issues in my previous letter.
I didn't use 8000 words in my previous mail, not even 800. What you do now is going off on a tangent. Irrelevant stuff. Even if I choose to rebut you in 8000 words, it still is a rebuttal. You choose not to reply to my responses, but rather send in 4 new issues. If these issues are your primary points --the essence to be addressed-- better prepare properly for my reply.You say:In the meantime, my previous post awaits your attention.I say:In the meantime, I am looking for Dr Peakalls email address. It seemed that you have it, and I wondered whether you could provide me with it. To find out whether or not he stands behind his words. I thank the audience will like that to. Since I am accused --and this is my last chance (before what happens? Execution?)-- I'd better call in some experts of the field. Let's get the information first hand. So, let's hear Peakall as the first witness. Thanks for your cooperation,See you in court Best wishes,
Peter

Dear Dr Page,I had a look at the sequences.
Easy to explain. Non-random in conjunction with random mechanisms give the illusion of common descent. I will study these sequences in detail, and respond to it next month (or so).Best wishes,
Peter

Dear Dr Page,
At least the MPG hypothesis predicts properly. Something NDT/evolutiomnism lacks completely.best wishes,
Peter

Dear Quetzal,You say:--------------------------------------------------------------------------------
I don't give out anyone's email address on-line, even if they are freely available. However, as was pointed out, he's at the ANU, feel free to look it up. Here's the ANU website: ANUI say:
Thanks I will look it up and write him a letter.You say:
Oh, and btw, you appear to have misunderstood me. Although you responded to my post 171 the response can in no way be considered substantive - indeed, you merely repeated your original assertions and collected a few more ad hominems to your credit.I say:
That is what you do too. What's the difference?You:
That being the case, I tried to make it easy on you in post 205 by succinctly restating the question and the arguments I have used over the course of now 15 pages so that there could be no confusion on your part. You have not answered. Answer the specific question in post 205. Discuss the four explanations, formally and in sufficient detail to show your self-proclaimed expertise on the subject.I say:
Understanding biology is not as hard as you think it is. It depends on the paradigm. If one tries to explain things subject to a false paradigm things get hard indeed. That's the is the isue here. However, I will answer your 4 points as soon as I got Dr Peakall's response.Best wishes,
Peter

dear Mammuthus,I don not quite understand your reponses. You are attacking Svante Paabo's explanations on this region, not mine (see: REF2 in my previous mail). I was under the impression that Svante is your friend. So, please explain.My comments:M: 1. the entire intron is not neutral..you do know that there are conserved features of introns?..guess not.PB: And that would invalidate all studies on neutral evolution, isn't it? So, you have to either deny Kimura's theory or you have to deny common descent.M: The rest is easy. Jim Neel for example studied kinship among the Yanomamo and demonstrated that one male fathered about 95% of the children in one tribe...what do you think that does to Y chromosome variation? Gorillas live in single male dominated groups where the dominant silverback has almost exclusive mating priveleges...what do you expect the Y chromosome to look like?PB: You mean the rape-and-run cultural practice of the Yanomami Indians? And this cultural aberration is taken as a common human trait to explain the invariable ZFY region? I would call that conclusion jumping. In addition, you are talking about one Indian tribe; I was talking about the complete absence of variability throughout the human population.This is what I found in pubmed on paternity in Yanomami Indians. (I could find Jim Neel, do you have the reference? Thanks):Microsatellite and HLA class II oligonucleotide typing in a population of Yanomami Indians.Roewer L, Nagy M, Schmidt P, Epplen JT, Herzog-Schroder G.Institut fur Gerichtliche Medizin, Humboldt-Universitat, Berlin, Germany.We have used three different microsatellites (on chromosome 12 and Y) together with HLA class II oligonucleotide typing (DQA and DQB) to analyze families of Yanomami indians settling in villages in Southern Venezuela. There exist complex networks of biological relationship between villages as a result of wife exchange, village fissioning and changing patterns of alliances associated with inter-village warfare. Social status in this society is largely determined by the kinship system. Polygyny is common, especially among headmen, with additional wives, frequently being chosen among the sisters of the first wife. Our preliminary results mainly obtained from inhabitants of the village HAP show the expected allele distribution in populations with a high degree of consanguinity: (i) deficiency of observed heterozygotes at the autosomal loci and (ii) almost all men carry the same Y chromosomal allele. Nevertheless in the Yanomami village two thirds of the described autosomal microsatellite alleles were identified. Several paternities were clarified.PMID: 8400691 [PubMed - indexed for MEDLINE]PB: A rapid, natural selection driven fixation of any advantageous gene on the Y chromosome would therefore result in loss of variance throughout the entire Y chromosome (REF2). Because all non-recombining DNA sequences of the Y chromosome are replaced in a single sweep, this vision predicts that variability should be absent in all linked non-recombining Y chromosome genes. (A retrospective prediction?)M: Nope, an observation and one you could falsify Peter. Take a group of genetically diverse mice and only let one male mate for 10 generations and then measure the Y chromosome versus mtDNA variation...I can already tell you what you will see...hardly a retrospective prediction.PB: First of all 10 generation is not 10.000 generations. You assume that the cultural thing of Yanomami Indians is representative for the entire human population. You are free to have these believes, but it is conclusion jumping. You can never present it as fact. And thirdly, what about inbreeding? Evolutionary conservationists keep stressing that small effective populations are bad for survival (ask Quetzal).PB:
A recent study in mice on the non-coding region flanking the SRY gene, which is directly responsible for inducing maleness, is revealing in this matter. The study compared the amount of variation within the species and related it to the amount of variation among species. Then, the authors compared this ratio to the ratio for a rapidly changing region in the mitochondrial DNA obtained in the same way.M: Okey....now we have gone from humans to mice...why do I expect exactly the same result?PB: This was introduced by Svante Paboo, not me. I referred to it. (REF2).If any of the two regions were subject to a selective sweep, it would be demonstrated by a reduced variation within species. It was found, however, that the non-coding region of the SRY gene changed at a neutral rate. It implicates that, because of linkage of the major part of the Y chromosomal genes, the entire non-recombining part of the Y chromosome changes at a neutral rate. Therefore, it is unlikely that natural selection acts upon the Y chromosome (REF2).M: So there was no selective sweep in the mice...whoo hoo!PB: According to Svante Paabo (REF2).But if natural selection did not act upon the Y chromosome the high degree of variability of the Y chromosome between primates apparently defies the theory of evolution, since the coding region of the SRY gene is very stable within a species (as observed before), whereas considerable variation is observed between distinct species.M: Note to Peter, though you seem to not realize it...mice are not primates.PB: According to the Science paper (REF2). All this information is from REF2. You are now doubting your evo-friends, not me.Some part of the SRY protein show such high degree of variability between distinct primate species that one must conclude that part of the protein has NO function at all, or that the gene is subject to DIRECTIONAL selection, says evolution biologist Svante Pbo (REF2). However, directional selection is only demonstrated in cases involving intergenomic conflict, such as occur between host and pathogen, but is has never been observed for non-immune system related protein coding genes. Of course, one can always propose non-random, directed mutations. But, evolutionists will object to that.M: The Y is full of HERVs to that are replicating and otherwise evolving at a completely independent rate i.e. in conflict.....and please show the citation that directional selection is exclusively demonstrated by intergenoic conflict.PB: First of all, it is Svante Paabo remark in REF 2. Apparently you didn’t read REF2. What have HERV to do with the observation that no polymorphism are observed in this non-recombining region? Nothing, I know what HERV are. In the MPG hypothesis, they are (degenerate) jumping preexisting DNA elements in the genome to introduce variation due to differential regulation of gene expression.PB:
The only remaining evolutionary explanation of the variability in the Y chromosome between species is by the mechanism of neutral evolution. Yet, the observation that more replacement substitutions than synonymous substitutions are present between species suggests that a neutral mechanism is not likely to be responsible for variation among species.M: Well, that would be true if all of us used data from mice to determine what is happening in primates...but then you have proposed that fish should be just as genetically similar to chimps as to each other so what the hey...PB: Again you doubt the references. Not me. It can all be found in REF2.Do evolutionists really understand their own theories?M: They do...you don't...to bad.PB: I do understand molecular mechanisms that should be responsible for evolutionism, apparently you don’t understand them or you deny them (Denying physics to keep the hype alive, you can't do that Mammuthus ).Read this one more time:REFERENCE 2 says that the only way to understand the region is:‘these regions have been retained throughout the primate lineage without any requirement for sequence conservation, implying that the SRY protein is [] the HMG box alone’ (REF2).It immediately implies NEUTRAL EVOLUTION in the whole region, since there is NO constraint on the region. And the funny thing on the region is that there has been DIRECTED EVOLUTION. It all ends, as usual, in a PARADOX. Is't a characteristic of false paradigms.In conclusion, the falsification still stands.Try again Best wishes,Peter[This message has been edited by peter borger, 11-13-2002]

Dear dr Page,In reposne to--------------------------------------------------------------------------------quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
However, are you a neutralist or a selectionist?Best wishes,
Peter----------------------------------------------------------------------
----------You say:Informed scientists understand that the two are not mutually exclusive.My reponse:Could you please point out where I say that they are mutually exclusive? It is a common characteristic of evolutionism to conlusion-jump. You once more proof it here,Best wishes,
Peter

Dear mammuthus,[no comments to the first part]PB: Maybe you don’t believe in an accurate clock. But the HVR-1 mtDNA sequences presented by Adcock et al (PNAS 2001, 98:537-542) demonstrate with respect to human reference sequence 29 differences for bonobo, 24 for chimp, 27 for neanderthaler. I do not even see a RUDIMENTARY clock in these data. How about you? It should also be noted that an ancient homo sapiens (dated 62,000 BP) demonstrates 10 differences compared to reference sequence. Let me guess, bonobo/chimp and man have a common ancestor around 150.000 years ago? Nice believes you're holding to.M: You know Peter, you are developing a Fred like habit of putting words in my mouth since your last sentence is utter bullshit and I never made the above statement.PB: A bit prickly today? However, I am not putting words in your mouth, I was drawing a conclusion from the data in the PNAS paper. These data are a clearcut falsification of common descent and the molecular clock.M: I guess since your arguments are so pathetically weak this is the only strategy left to you.PB: Please mind your words, Mammuthus. "Pathetically weak... left to you" does not sound like an argument. Better explain how you see the molecular clock, and convince me with scientific arguments that your visions are right.M: Did you even read how they calculated the clock rate in the damn paper?PB: All the paper showed are the polymorphisms in the HVR-1 region of mtDNA and according to these data there is NO molecular clock.M: I explained why I don't put much stock in molecular clocks, particularly recent events (last million years). You clearly did not understand it.PB: I fail to see why the molecular clock wouldn't be valid during the last million years. Moreover, why would it become valid after a few million years? Is it hiding behind non-falsifiable experiments?
What is clear from this PNAS paper, is that the mtDNA demonstrated 10/62.000 years in one analysed ancient human, or 3-7/10.000-15.000 years for the other ancient humans. Considering human, Neanderthaler, bonobo and chimp it implicates that either they have a common ancestor around 150.000 years ago (or even earlier), OR polymorphisms are always introduced at the same spot. The latter is a NON-RANDOM mechanism. I don't understand it. You are the evolutionist so please explain.M: I am not your Mommy and am not going to do your homework for you( again) look up molecular clocks and the controversy surrounding them yourself...otherwise stop arguing from ignorance..it is unbecoming of you.PB: Are you a bit prickly today? However, although it is not compulsory to addressing questions I would appreciate it. The EXTRAORDINARY evolutionary claims require EXTRAORDINARY scientific evidence.
If you don't want to discuss evolutionary topics, why did you register to this board? I am under the impression that you registered to educate me on evolutionism (remember your first letter?). So, here is an excellent challenge to help me understand evolutionism. Please explain how you see it. [Or, maybe you could recommend a review on the controversy. Thanks.]PB: It is known that evolutionism is so difficult to understand that not even evolutionists understand it.M: And I see you had no answer to my question. My understanding is fine. That you do not is obvious.PB: If it is not difficult to understand, please explain the PNAS data to me.PB: How do you know that there is selective advantage? You are the propagator of an extraordinary claim. So you have to present the extraordinary evidence.M: Ok Fred..I mean Peter.PB: You are prickly! So, these are the questions you get prickly about? Why, I wonder?M: This is how you want the debate to go? Let me know and I can change the tone of this very quickly and we can have a nice flame war.PB: A nice flame War? Who are you really Mammuthus? A deep dark inside? Keep it scientific please. Besided, you claimed selection so proof it!PB: I know that your friends introduced very weak purifying selection, another meaningless term. For the redundant gene family of alpha actinins --as for the 1G5 gene-- you have to introduce neutral selection. As demonstrated. And as denied by evo's.M: And another non-answer.PB: Your friend Wagner, among others. Evolutionary theorists on genetic redundancies introduced this concept. I introduced the concept of neutral seletion for the alpha actinin genes. You need this concept to explain these redundant genes. If you don't need this concept, please explain.PB: So you are a neutralist?M: What makes you say that?PB: Your remark on stuff residing in the genome waiting for someting.PB: You should know this, you are the evolutionist. However, how much selection does it require to purify a redundant gene?M: Are you actually going to respond to my posts in context. What the hell does this have to do with what I said?PB: I am rather curious about how much selection purification of redundant genes require. You are the proponent of an extraordinary claim....PB: Yes, and that makes it such fabulous theory. Sometimes a bit of this, than a bit of that. Evolutionism is like cooking, isn’t it. How to cook the one kind into the other. The stories get better and better.
What happened to Occam’s razor. Mark Pullen will object to such theories, is my guess. What about it, Mark?M: You are being really dim today Peter.PB: Dim? I'd rather call it bright. M: Do you beleive the environment is constant everywhere always?PB: Usually the environment does not change a lot. Sometimes, environments change overnight. For instance after meteor impacts, ice ages, total earth crust crushes, etc. Fortunately organisms have a multipurpose genome that interacts with creatons, so they can immediately adapt. M: Do you think selection acts at all times? Do you know if humans are under selective pressure now or not..I bet you don't know the answer to that onePB: Of course! There is always selection. Selection AGAINST. The issue here is, since I reason from a distinct paradigm, we can never come to the same conlusions.M: As to weaknesses of theories...your MPG is as weak as they come..stable but variable because of repair enzymes...falsified before it even gets to the starting blocks.PB: Dear mammuthus, it is elementary that stable DNA sequences can't reside in the genome longer than one generation without repair mechanism. Even the simplest organisms have a complete set of repair enzymes. It is a prediction of MPG hypothesis. I checked it and it is true (PNAS 2002, 99:9509).PB: I have the feeling that you don't understand the concept of the MPG. Maybe, you don't want to understand or you cannot think beyond the paradigm of evolutionism.PB: The whole discussion is meaningless (Nei's paper). If I write discussions like that, I could forget about my papers. The peer reviewers would immediately return my manuscripts with the comment: Meaningless nothingness.M: Great clarification Peter...so I will take it to mean you could not understand Nei's papers as all.PB: Only just-so statements. Not much of a discussion. So, meaningless.PB: Apparently these experiments have never been published. Or do you mean the reference below? If so, than I have to disappoint you. It is NOT an experiment it is interpretations of data. You know the difference, I hope. (If not, it explains a lot ).M: So I guess you are willing to retract all of your papers now to Peter..I mean you did not actually see the change in gene expression..you inferred it from your experiments..I look forward to the retraction letter...PB: If I have to retract, all inferred papers have to be retracted.PB: You are lagging behind, I responded to all Quetzal’s points. He choose not to respond to all my replies. However, talking about avoidance. You are avoiding crucial questions of my mails with increasing frequency. Why, I wonder?M: Me? I bumped both an entire thread and multiple posts multiple times without EVER getting an answer from you other than " oh, I missed that"...you are becoming an expert at avoidance. I have responded to all of your points in all of your mails...I have even responded to mails of yours to other people. So you are either being lazy or dishonest.PB: This thread was posted by Quetzal, not me. If time is there I will expand on this topic, but not now. I can make up my own thread, I don't need Quetzal's help.
And, it is true that I often mis reponses since I do not get a message in my postbox. If you want to have an immediate response, please send a direct mail.Best wishes, and have a nice weekend,
[I hope you're not so prickly next week.]Peter[This message has been edited by peter borger, 11-14-2002]

dear Dr Page,In reponse to:quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
M: 1. the entire intron is not neutral..you do know that there are conserved features of introns?..guess not.PB: And that would invalidate all studies on neutral evolution, isn't it? So, you have to either deny Kimura's theory or you have to deny common descent.--------------------------------------------------------------------------------You say:You have never read even one of Kimura's papers, have you?
For if you had, you would know that NT does NOT deny selection, nor does selection deny neutrality.And you wonder why I don't take you seriously?--------------------------------------------------------------------------------I say:Maybe you didn't get how evolutionism works. In brief, since I have not so much time, the intron sequences are assumed to be evolutionary neutral sequences. If the exons of a particular gene change with the same rate as the introns of that gene the sequence is said to be in accord with neutral evolution. [And with the assumption of common descent, of course.]
However, if introns are not neutral --as Mammuthus claims, and I agree-- the major part of evolutionary papers on this topic can be considered useless.Best wishes,
Peter[This message has been edited by peter borger, 11-14-2002]

Dear Dr Page,In mail #10 (thread: molecular genetic proof against random mutations) you wrote:I believe you have make an entirely unwarranted and somewhat bizarre extrapolation."a comparison between fixed and polymorphic sites between the two species shows also no significant deviation from the assumption of a neutral evolution in this region.Apparently, you have never heard of the Neutral Theory?MY RESPONSE:From your response above it is immediately clear that it is YOU who apparently never heard of neutral theory since you attacked the authors of the paper (!!).The sentence you quote above is a quote of Karl J. Schmid and Diethard Tautz in their paper A screen for fast evolving genes from Drosophila.Your responses get sloppier and more inconsistent. If you have nothing to contribute to the discussion, why do you mail me this non-sense? It really puzzles me.Best wishes,
Peter

Dear Mammuthus,PB:However, if introns are not neutral --as Mammuthus claims, and I agree-- the major part of evolutionary papers on this topic can be considered useless.M: Read what I said. I never said that introns are not neutral. I said that not every site in an intron is neutral. Did you ever learn anything about intron splicing?PB: What sites (in addition to sensible sites involved in splicing) do you mean? How do you determine these sites? It is non-coding DNA, remember.Best wishes,
Peter

Dear Itz,I was not referring to sensible splicing sites. They are, of course, non-neutral, and we know how the sequences look like.Best wishes,
Peter

Dear Mammuthus,You say:If you don't know how splicing works Peter then you are in more professional trouble than I realized and really need to take a basic biology class.oh yeah...and what is an unsensible site? Are there coming to their senses sites as wellI say:As mentioned before sensible DNA sequences are sequences that have a function, for instance in splicing, gene regulation, stabilisiation of DNA and/or mRNA, etc. The fact that introns demonstrate conserved regions within species points in the direction of 'sensible sequences' involved in gene regulation. As a matter of fact, sometimes I have to invent a term to describe properly what is observed in the genome. Since 'sense-' and 'antisense sequences' already have a well defined meaning, I rather use 'sensible sequences' for DNA sequences that serve a function.best wishes,
peter