molecular genetic evidence for a multipurpose genome

[QUOTE]Originally posted by Fred Williams:
[B]minnemooseus:

quote:

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I personally can't seem to see a direct correlation between "increased diversity" and "increased information".

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I never said there necessarily was a direct correlation (in fact I can easily think of counter-examples to the above). Let’s deal with what I said, not what someone else said. What I said is that the cheetah has clearly lost genetic information from its pre-bottleneck parent population. For example, we know the cheetah has a deteriorated immune system and it is likely it has lost some gene segments (via crossover) and thus potential antibodies. This is clearly a loss of information, no way around it.M: And your evidence of specific gene losses in the immune system of cheetah' much less any other species? Ironic that the first study I post below (which you could not even find) says nothing about loss of gene segments and deteriorated immune systems due to loss by crossover.Immunol Rev 1999 Feb;167:133-44 Related Articles, LinksComparative genome organization of the major histocompatibility complex: lessons from the Felidae.O'Brien SJ, Yuhki N.Laboratory of Genomic Diversity, National Cancer Institute, Frederick, Maryland 21702-1201, USA. obrien@mail.ncifcrf.govThe mammalian major histocompatibility complex (MHC) has taught both immunologists and evolutionary biologists a great deal about the patterns and processes that have led to immune defenses. Driven principally by human and mouse studies, comparative MHC projects among other mammalian species offer certain advantages in connecting MHC genome characters to natural situations. We have studied the MHC in the domestic cat and in several wild species of Felidae. Our observations affirm class I and class II homology with other mammalian orders, derivative gene duplications during the Felidae radiation, abundant persistent trans-species allele polymorphism, recombination-derived amino acid motifs, and inverted ratios of non-synonymous to silent substitutions in the MHC peptide-binding regions, consistent with overdominant selection in class I and II genes. MHC diversity as quantified in population studies is a powerful barometer of historic demographic reduction for several endangered species including cheetahs, Asiatic lions, Florida panthers and tigers. In two cases (Florida panther and cheetah), reduced MHC variation may be contributing to uniform population sensitivity to emerging infectious pathogens. The Felidae species, nearly all endangered and monitored for conservation concerns, have allowed a glimpse of species adaptation, mediated by MHC divergence, using comparative inferences drawn from human and mouse models.Science 1985 Mar 22;227(4693):1428-34 Related Articles, LinksGenetic basis for species vulnerability in the cheetah.O'Brien SJ, Roelke ME, Marker L, Newman A, Winkler CA, Meltzer D, Colly L, Evermann JF, Bush M, Wildt DE.A population genetic survey of over 200 structural loci previously revealed that the South African cheetah (Acinonyx jubatus jubatus) has an extreme paucity of genetic variability, probably as a consequence of a severe population bottleneck in its recent past. The genetic monomorphism of the species is here extended to the major histocompatibility complex, since 14 reciprocal skin grafts between unrelated cheetahs were accepted. The apparent consequences of such genetic uniformity to the species include (i) great difficulty in captive breeding, (ii) a high degree of juvenile mortality in captivity and in the wild, and (iii) a high frequency of spermatozoal abnormalities in ejaculates. The species vulnerability of the cheetah was demonstrated by an epizootic of coronavirus-associated feline infectious peritonitis in an Oregon breeding colony in 1983. Exposure and spread of the coronavirus, which has a very low morbidity in domestic cats (approximately 1 percent), has decimated a heretofore productive and healthy captive population. The extreme genetic monomorphism, especially at the major histocompatibility complex, and the apparent hypersensitivity of the cheetah to a viral pathogen may be related, and provide a biological basis for understanding the adaptive significance of abundant genetic variation in outbred mammalian species.Proc Natl Acad Sci U S A 1993 Apr 15;90(8):3172-6 Related Articles, LinksDating the genetic bottleneck of the African cheetah.Menotti-Raymond M, O'Brien SJ.Biological Carcinogenesis and Development Program, National Cancer Institute, Frederick, MD 21702.The cheetah is unusual among fields in exhibiting near genetic uniformity at a variety of loci previously screened to measure population genetic diversity. It has been hypothesized that a demographic crash or population bottleneck in the recent history of the species is causal to the observed monomorphic profiles for nuclear coding loci. The timing of a bottleneck is difficult to assess, but certain aspects of the cheetah's natural history suggest it may have occurred near the end of the last ice age (late Pleistocene, approximately 10,000 years ago), when a remarkable extinction of large vertebrates occurred on several continents. To further define the timing of such a bottleneck, the character of genetic diversity for two rapidly evolving DNA sequences, mitochondrial DNA and hypervariable minisatellite loci, was examined. Moderate levels of genetic diversity were observed for both of these indices in surveys of two cheetah subspecies, one from South Africa and one from East Africa. Back calculation from the extent of accumulation of DNA diversity based on observed mutation rates for VNTR (variable number of tandem repeats) loci and mitochondrial DNA supports a hypothesis of an ancient Pleistocene bottleneck that rendered the cheetah depauperate in genetic variation for nuclear coding loci but would allow sufficient time for partial reconstitution of more rapidly evolving genomic DNA segments.Electrophoresis 1995 Sep;16(9):1771-4 Related Articles, LinksHypervariable genomic variation to reconstruct the natural history of populations: lessons from the big cats.Menotti-Raymond M, O'Brien SJ.Laboratory of Viral Carcinogenesis, Frederick Cancer Research and Development Center, MD 21702-1201, USA.The extent and nature of variation in hypervariable regions DNA have been used in the past as a means to infer the natural histories of populations. We review the interpretation of the extent of genetic diversity for minisatellite DNA in the cheetah to estimate the timing of a population bottleneck in the species and the potential application of a second class of hypervariable DNA, microsatellite DNA, as a molecular tool to examine the natural histories of felid populations. A calibration curve relating the degree of allele fragment sharing in individuals to relatedness in a captive pedigree of cheetahs is presented. This measurement has important applications for management of potential matings in captive management situations.FW:
Speaking of diversity, the information problem always spurs an incredible amount of diversity in answers evolutionists come up with when the hot potato is thrown in their lap!M: Then English is clearly not your first language.FW:
Check this thread and you will see that Quetzal & Mammuthus are now stumbing all over each other. Quetzal clearly implies in his response to your message that he does not believe the cheetah has lost genetic information from its parent population, while Mammuthus backpedaled and now agrees information was lost (he blamed me for not understanding him; yea). I suspect Quetzal also originally believed Mammuthus thought the opposite because of what he wrote: They have neither poor genetic content nor have they lost genetic information. Mammuthus apparently confused a lot of people with that statement.M: Keep trying Fred...maybe you will impress the other electricians..LOL!

Hi Peterthanks for your response, here is my reply:My pleasure..here we go.M: And the gene pools of Asians are poorer, better, equal to others based on this expression difference?PB: To my knowledge, no studies on this topic, yet. Considering the LDH and ADH genes, they are present in the gene pool but less expressed. A more obvious example is melanin in African and European population. The gene is present in both gene pools but differentially expressed.M: I think you missed my point on this. I am not arguing that there are no expression differences among populations. There are large differences among members of the same population. My question was related to the "quality" of the genomes by your definition. Are they better, worse, or equal?M: Lions which are not nearly as inbred as cheetah's also suffer from the above i.e. low sperm production etc. Which genes did the cheetah specifically lose...it should be obvious...you could try to PCR 18S rDNA and would not be there for example. Do cheetah's have more, less, equal numbers of ERVs as before? Are there chromosomes now shorter because of all this genetic loss you claim there is evidence for or do you mean genetic variation in the population? If you mean the latter it argues against multipurpose genome by the way.PB: 18S? Why 18S? It is an essential gene, so losing it will immediately be selected against. Why not tRNA genes? They are abundantly present, and can to a certain extent be lost.M: Why? In a multipurpose genome why wouldnt actin just take over the function of 18S? Why do you need selection in your hypothesis? And by the way, 18S is multicopy i.e. redundant.M: 3.3 billion nucleotide variation in an inbred strain of mouse? Considering they have a genome similar in size to ours that is way more than 10% Peter. You sure you were looking at mouse and not C. elegans in your comparison? As to Quetzal being vague..he has given the conditions under which one expects sequences to remain static or to vary. That you ignore it is not his problem.PB: the genomic content of mice varies between 3 +/- 0.3 billion nucleotides per diploid genome.M: This is then a completely different statement than the one before. You said laboratory (inbred) mice differ from one another by an amount an order of magnitude larger than what you are posting now. Or do you mean all lab mice in which case the number you post here is hardly surprising. M. musculus is at least 1 or 2 million years separated from M. spretus for example.PB: Explain, I don’t get it.M: Here is some homework: O'Brien SJ, Yuhki N. Related Articles, LinksComparative genome organization of the major histocompatibility complex: lessons from the Felidae.
Immunol Rev. 1999 Feb;167:133-44. Review.
PMID: 10319256 [PubMed - indexed for MEDLINE]3: Spencer JA. Related Articles, LinksLymphocyte blast transformation responses and restriction fragment length analysis in the cheetah.
Onderstepoort J Vet Res. 1993 Sep;60(3):211-7.
PMID: 7970577 [PubMed - indexed for MEDLINE]4: Miller-Edge MA, Worley MB. Related Articles, LinksIn vitro responses of cheetah mononuclear cells to feline herpesvirus-1 and Cryptococcus neoformans.
Vet Immunol Immunopathol. 1992 Jan 15;30(2-3):261-74.
PMID: 1317618 [PubMed - indexed for MEDLINE]5: Miller-Edge M, Worley M. Related Articles, LinksIn vitro mitogen responses and lymphocyte subpopulations in cheetahs.
Vet Immunol Immunopathol. 1991 Jul;28(3-4):337-49.
PMID: 1835214 [PubMed - indexed for MEDLINE]6: Yuhki N, O'Brien SJ. Related Articles, LinksDNA variation of the mammalian major histocompatibility complex reflects genomic diversity and population history.
Proc Natl Acad Sci U S A. 1990 Jan;87(2):836-40.
PMID: 1967831 [PubMed - indexed for MEDLINE]PB: It is elementary that the wild type gene is superior to a mutant gene in the genetic background of that gene. Denying that is denying biology.M: It is elementary that mutations can be beneficial...denying that is denying biology and common sense.PB: Due to such mechanism the genetic content of seperated population will not be the same. Soon, the differences between human subpopulation will be elucidated. It is already known that different subpopulations lost distinct genes. I already mentioned the alpha actin gene: completely lost in 18% of the Caucasian population. The CFTR gene: 1 in 25 are carrier of the inactivated (=loss) gene in Caucasian population, etc. Easy to understand from MG stance.
I also would like to see a completely new gene in a human subpopulation.M: Though what your saying would be easily latched on to by racists as a genetic basis for descrimination, the problem with this is there is more variation within human populations than between them..thus concepts like Caucasian, etc. are moot...one big happy species.M: How do you know they are new? Mammals by your definition only appear similar because non-random process. There is no reason for a mouse to be any more related to other mammals than to a liverwort. Or are you now backing away from your illusion of descent argument? You cannot on the one hand group mammals but then claim there is only identity by descent at the subspecies level.PB: Novel systems need novel genes and gene programs. The RAG2 doesn’t demonstrate homology with other known protein.M: And you did not answer the question.M: That is if one just ignores the science on the subject. Considering that I, Quetzal, and others have to post links to the topics and ALWAYS find scientific citations for all of the points you claim are unknown, not thought about, or not studied your above claim is rather dubious and your scholarship is rather poor in this matter. I find that strange as you appear to be rather passionate about this subject yet refuse to inform yourself in any depth.PB: I can find these references myself. I can read them myself, and discover that all data are discussed subject to evolutionism. Next, I object to the just so stories presented by the authors, post my comments here, provide another solution to the data, usually an equal solution and often a better solution. What happens? You deny it, Quetzals denies it, Dr Page denies it, and he scoffs it. So, what is the use of reading these severely biased evo-stories. I know the content already. There is nothing new in it for science, no challenge, nothing! And nothing at all for mankind. Meaningless nothingness.M: How convenient for you Peter. Just ignore everything everyone else writes or says and then claim that you are misunderstood and that there is a global conspiracy...megalomania would be an apt description. You have shown an almost exclusive inability to find articles on the subjects you debate and now claim that all scientist that publish are evil evolutionist trying to hold you down personally.At least I, Quetzal, and Page read what the other side has to say rather than using your "ignorance is bliss" argument.MY RESPONSE:
Novel genes is primates doesn't make it easier for evolutionists. Now you have to explain them. Duplication and random mutaion would be my guess. If so, let's discuss the redundant alpha actinin genes. It immediately falsifies this vision.M: I have already provided a reference (more than once on this topic)...so go ahead..start the dicussion....PB: Refernce? Where can I find it, I will discuss it with you.M: Since you keep making me do your homework I will make you do some of your own...it is in two of the posts that I bumped and you ignored...have fun looking.M: You still don't understand the concept of fitness do you?PB: Again, you do not respond to my statements. You are starting to behave like Dr Page. He's got a degree in elusiveness.M: I don't respond? You have left almost all of my questions hanging without answers for weeks now so you are being rather hypocritical. I have explained this point to you before and get tired of repeating it. Do you understand what fitness is? From your answer I assume no, but I am getting sick of doing your homework for you.PB: If you mean the letters 94-96, I missed them, but will repond to them soon. Sick of doing my home work? If you wanna back up your assertions you have to do your homework.M: I do my homework but end up having to provide YOU with references you cannot seem to find for yourself in addtion to having to hunt down posts you ignore repeatedly. If you want to make up silly hypothesis to defend why is it that I have to support all the data for it exactly?PB:
It is you who claims that all life we observe came about by pure coincidence and randomness, so you better provide me with compelling evidence, instead of the stuff usually provided by evo’s. As demonstrated these data can be explained according to the multipurpose genome equally well or better.M: Well then get started explaining including all the posts you ignored. And why should I provide you with any more refrerences? Above you claimed you refuse to read anything by anyone who actually studies the subject as they are all conspiring against your non-existent god?PB:
Back to start, Mammuthus. You didn't read or didn't understand, what I wrote in mail #1. If you reread it you will notice that stability of DNA sequences is secured by DNA stabilising and repair proteins. That's a prediction of the hypothesis of multipurpose genome and it has been demonstrated to be correct in even the simplest organisms studied.
Why would I post exactly the same sentence? I know what I am talking about and I can explain all biological phenomena with the hypothesis of the MG.M: Then you have failed to explain variation in the genes encoding the repair proteins, the variation in repair mechanisms, the extreme variation in repair fidelity among repair enzymes etc etc...which explains why DNA can vary as much as it does...hardly argues for your stabilizing by repair...in fact it falsifies it.PB: Ever heard of entropy? Differential regulation of gene expression due to Shuffling DNA elements? All provided by the MPG hypothesis. Yes, Mammuthus, it explains all biological observations.M: First, you did not answer the question, second you abandoned your repair enzyme fantasy and came up with a new argument..guess you must have also realized how uncompelling an argument it was....interesting that you think "DNA element" shuffling explains all biological phenomenon..please explain genomic imprinting of the H19 locus using genomic shuffling and entropy M: Except that you would have to postulate that humans do not reproduce sexually and are not diploid since transfer of ALL variation from one generation to the next does not happen in a two sex diploid system...it does not work with any reproductive system known...hey, you do believe that storks bring babiesPB: Why would I have to postulate non-sexual reproduction of humans? Why would it be necessary to transfer ALL variation at once? It is merely your introduction of a straw man.M: How so? You claim that there was a multipurpose genome with all variation and since that point there has been no more variation only loss (though ironically you also say that variation is generated by shuffling and entropy). How many genomes were there? How much was lost? How do you distinguish gain then loss then gain of variation?
Why do ancient DNA studies of Native Americans show haplotypes that exist today? Shouldn't they all be novel entropy lost?
Where did the variation in the original population come from?M: Agree with most of this paragraph...wow,imagine that..except for the part about the variation always being there..I thought you said it gets lost by entropy..now you say it has to be maintained by cross species hybridization? Where is that stabilizing of the repair system? There should be no variation at all? Selection is not in doubt???M: No answer here?PB:
Cross breeding will restore genetic variability. In addition, you have to explain the beak in the first place. I mean an evolutionary explanation for the genetic program that gave rise to the first beak.M: Why do I have to explain the origin of the beak to explain beak evolution in Galapagos finches??? We can debate the subject if you wish but it is off the topic at hand.PB: If you want to discuss minor beak variations between subpopulations of finches, you first have to explain the beak, since the beak has an evolutionary origin too, according to your worldview. So, please explain. Other wise we simply discuss population genetics and that’s NO evolution. That is frequency changes of preexisting DNA elements over time.M: LOL! You claim refuse to read anything about evolution because it is against your worldview but then claim you can define evolution as not being population genetics? Wake up Peter...evolution is population genetics over long periods of time....ok, if I have to explain the beak before we can talk about Galapagos finch beak evolution then you have to show me a picture of god poof banging the entire human gene pool into existence...fair enough?...Hartl and Clark...use the eyes, flip the pages, learn M: So yet again I have to do your freaking homework...you must be the laziest anti-science person I have ever met. Even Behe does his own background research....na ja.PB: No, you have to back up your extraordinary claim that all life evolved from nothing through randomness and selection. I will look up your references. Probablyy, the reduced fitness is related to an incompatible secondary DNA code, or maybe incompatible transcriptional code. Will read them. Thanks.M: Oh, so now you will read references? Which is it? Deny all the biological sciences or actually inform youself whether you agree with the authors or not...up to you.M: Ok, so if I cross two species or subspecies, they should be genetically more similar to their ancestor?....care to show some evidence that donkeys or wolf-dog hybrids are more like their last common ancestor? If an Asian and an African have a kid, are you saying the genotype will be closer to cro magnon? What about all the stabilizing repair enzymes preventing any change backwards or forwards..so much for your hypothesis being the easiest answer to everything.PB: Cro magnon was probably already another subspecies of the human archetype. But, anyway, you show that you are beginning to understand the MPG hypothesis. Your idea is okay.M: Actually I was joking...Kind of scary that you think this is how genetics works...how about this, Finnish man has a child with a Chinese woman...will the mtDNA look more like cro magnon, Finnish haplotype, Chinese?M: Does not look like this holds up either....
BMC Evol Biol 2002 Sep 10;2(1):16 Related Articles, LinksLittle qualitative RNA misexpression in sterile male F1 hybrids of Drosophila pseudoobscura and D. persimilis.Reiland J, Noor MA.Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA. mnoor@lsu.eduBACKGROUND: Although the genetics of hybrid sterility has been the subject of evolutionary studies for over sixty years, no one has shown the reason(s) why alleles that operate normally within species fail to function in another genetic background. Several lines of evidence suggest that failures in normal gene transcription contribute to hybrid dysfunctions, but genome-wide studies of gene expression in pure-species and hybrids have not been undertaken. Here, we study genome-wide patterns of expression in Drosophila pseudoobscura, D. persimilis, and their sterile F1 hybrid males using differential display. RESULTS: Over five thousand amplifications were analyzed, and 3312 were present in amplifications from both of the pure species. Of these, 28 (0.5%) were not present in amplifications from adult F1 hybrid males. Using product-specific primers, we were able to confirm one of nine of the transcripts putatively misexpressed in hybrids. This transcript was shown to be male-specific, but without detectable homology to D. melanogaster sequence. CONCLUSION: We tentatively conclude that hybrid sterility can evolve without widespread, qualitative misexpression of transcripts in species hybrids. We suggest that, if more misexpression exists in sterile hybrids, it is likely to be quantitative, tissue-specific, and/ or limited to earlier developmental stages. Although several caveats apply, this study was a first attempt to determine the mechanistic basis of hybrid sterility, and one potential candidate gene has been identified for further study.PB: I will spell this paper out. At fisrt sight I don’t see a problem here for the MPG hypothesis.M: Except that it falsifies most of the tenets.PB:
As if evolutionism is a testable hypothesis. It has been tested and falsifies over and over.
Preset by the multipurpose genome, of course. The Creator if you like.M: Besides your desperate attack on evolution you did not answer actually respond to this...what is the testable hypothesis? But thanks for your candor in eliminating the multipurpose genome from the realms of science and properly designating it as a religion (an interesting one granted).PB: The predictions made by the MPG hype can be tested. See mail #1 for predictions and falsifications.M: See all my immediate responses following mail 1.M: Yes I do...you going to answer my question first?PB: Wildtype genes are usually better than mutant genes. The major part of the genes is homozygously present, and reflects this observation. So this statement is not so farfetched. For instance, for Drosophila only approximately 30 % of the D. melanogaster genes is polymorph and only 11 % is heterozygous (Page, D.M, and Holmes, E.C. Molecular evolution. A phylogenetic approach. 1998. Blackwell Science Inc. ISBN 0-86542-889-1, p231).M: Better? How? Plenty of slightly deleterious alleles are stable in the population...plenty of lethal alleles also. Better than what? 30% is a huge amount of variation! What happened to your poor stablizing enzymes?M: Funny that there is no evidence for it...yet Monkenstick could easily find evidence for random mutations...show us your data.PB: Monkenstick’s graph showed nothing related to this subject.M: Sure, he provided evidence for random mutation...you have not provided evidence for non-random...why is this so difficult? Make a graph from a published data set or genbank showing non-random mutation...I want to know where and when my next P53 mutation will occur so that I can cut off any cancer before it can take hold...M: I sequenced two mammoths for 350 bp of cytb and they were identical...Oh, I believe in god/Elvis resurrected/creator...my belief in evolution is shattered! Dolly the clone is identical to the animal she was cloned from...Oh no...I have to go re-evaluate everything I ever did...thanks for the eye openerPB: Pretty stable DNA. Guarded by stability ensuring proteins I guess. It is a prediction of MPG hypothesis. Did you also determine the age of the samples? Same location finds?M: Oops addendum...found several more mammoths with differences in cytb and several nuclear genes...evolution safe again...whew Assuming the last part of your question is honest curiosity, I have about 100 mammoth samples I am working on. 40 or so are dated, locality varies. A large collection comes from the Taimyr peninsula and another group from Wrangel Island. Some are from Alaska. The rest are from all over the place in Siberia.M: Ah, so you don't think dogs are diploid either..or sexually reproducing. Storks bring them to? Earlier you said you could cross breed animals to get an ancestor..now you say you cannot. Interesting that suddenly your entire theory needs natural selection whereas beforer it was pure non-random pre adaptation...PB: Yeah the stork is also included in the multipurpose genome. Not as baby deliverer, however. No, it does NOT require natural selection. Here you refer to artificial selection. As should be obvious, artificial selection can not be compared to natural selection, since it involves intelligence (human intelligence).M: Read the Origin of species....dog and pigeon breeding were one of the key influences on Darwin's thinking about natural selection. How do you distinguish natural and artificial selection? Is selection due to industrial waste output natural or artificial?...by the way, where does the stork fit in the MG?PB: How can I back up my new hypothesis with peer reviewed science papers that are always discussed subject to evolutionism. As soon as I start to explain the data subject to another paradigm, you start to object. However, I already discussed the ZFX region in this forum with NO response at all. To explain the data between the specis it absolutely requires NON-RANDOM mutations.M: No response at all??? I freakin posted in response to your ZFX nonesense mutliple times with references!!!! So did SLPx. Let's stay honest here.PB:
None of the evo-explanations can hold (as discussed). Likewise, the redundant alpha actinin genes. (I will respond to your comments in mail 64-96 soon)M: OK, look forward to it.M: Um, so now you think that if you remove DNA polymerases from an organism it will survive? Have fun trying to generate that mutant strain. And please list the full quote and context for the quote you have posted. As you have it written it really does not make much of a point...and if non-random mutation is so obvious why can't you provide just simply something equivalent to Monkenstick's post?PB: I am talking about the alternative error prone polymerase. I am sure that it can be removed without affecting the organism. I guess, it is a redundant gene.M: Which one is it? Where is the evidence for it? What about the non error prone (less error prone I should say) polymerases? Repair enzymes?M: It does not appear to be so easy since you have not convinced any of the evolutionists on this board of anything...but keep trying.PB: Paradigms shifts do not come overnight.M: No they don't, and when they do come they require a lot of consistency in the new paradigm and reams of supporting data.Best wishes,
M

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Originally posted by peter borger:
Dear mamumuthus,

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

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My response:
The Erlandson study doesn't rebut Dr Kim's observation that the assessed region of the ZFX gene is completly stable. No variability at all, not even at neutral positions.

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Best wishes,
peter

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********************************++Interesting Peter...you now had to change your statement from the ZFX region to the "assessed" region of ZFX. Erlandsson did a more thorough study that falsifies your statement...and now you are also demonstrating that SLPx was correct that you were mis-defining the region as you have here backpedalled.....at some point you will be looking at a single base pair of ZFX for support

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: So, you don't believ 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: 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? How do you know that there is no selective advantage? How do you know that removal of the gene is not slighltly deleterious? Most mutations are yet are maintained in the population regardless. 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: Thanks for these refernces. If you read these articles properly, you will find ou 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..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: 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?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: 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: No, by profound misunderstandings I mean you have shown a steadfast inability to grasp concepts in developmental biology, population genetics, and evolutionary theory (which is strange if you oppose it) coupled with an unwillingness to inform yourself and then handwaving about how evolution is wrong even though you don't know what it is. That does not amke your fantasy hypothesis any better either.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.M: I will..but I feel that you are not giving particularly substantial responses to many posts i.e. Quetzal's either.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.M: And that is where your arguement fails...if you throw often enough. How often do you think the die have been thrown here. Fred only demonstrated that he knows even less about this subject than you so I don't see your point with that comment. That is the problem for you..this is a demonstration of random mutation...not mutations where Peter wants to see them.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.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. I guess since your arguments are so pathetically weak this is the only strategy left to you. Did you even read how they calculated the clock rate in the damn paper? I explained why I don't put much stock in molecular clocks, particularly recent events (last million years). You clearly did not understand it. 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: It is a 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: 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. 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: 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: So you are a neutralist?M: What makes you say that?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: 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. Do you beleive the environment is constant everywhere always? 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 one
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: 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.M: Great clarification Peter...so I will take it to mean you could not understand Nei's papers as all.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: 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.cheers,
M

quote:

---

Originally posted by peter borger:
Dear Mammuthus,

​

You say:
Interesting Peter...you now had to change your statement from the ZFX region to the "assessed" region of ZFX. Erlandsson did a more thorough study that falsifies your statement...and now you are also demonstrating that SLPx was correct that you were mis-defining the region as you have here backpedalled.....at some point you will be looking at a single base pair of ZFX for support.

​

I say:
It was Dr Kim --the author of the paper-- who talked about the ZFX gene instead of exon and I was a bit sloppy of me not to notice that. Doesn't invalidate my example, however. The nitpicking begins, I presume. You could have saved yourself the mail, since Dr Page already nitpicked on this observation.
However, are you a neutralist or a selectionist?

​

Best wishes,
Peter

---

____________________--Hi Peter,
Thank you for the admission...but that was not acutally my point. You claimed nobody had responded to you on the issue of ZFX and ZFY and I was correcting you by saying I had posted to you on the subject.

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)M: = Peter's misunderstanding of randomness not the authors.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).M: 1. the entire intron is not neutral..you do know that there are conserved features of introns?..guess not.
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:
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:
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?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!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.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:
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...Do evolutionists really understand their own theories?M: They do...you don't...to bad.PB:
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!M: Or to properly understand it one has to realize that different mammals have undergone different histories so one does not expect mice and men to be identical....nice try Peter...let's throw reptiles and Drosophila in (which have totally different sex determining mechanisms)..and maybe Daphnia which can reproduce parthenogenetically to confuse you some more.PB:
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.M: You mean that primate M. musculus PB:
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.M: If it is so clear, you should be able to find a citation for such a DNA repair enzyme....and since you claim you can find abstracts on your own (though ironically you seem unable in our other debates) I am sure you have read all of these papers (though it is only a small subset of the available literature of which you must clearly have read before jumping to conclusions) Note, they are not all primates either...i.e. goats are not primates and niether are cats.J Mol Evol 2002 Jan;54(1):54-61 Related Articles, Links
Comparison of substitution rates in ZFX and ZFY introns of sheep and goat related species supports the hypothesis of male-biased mutation rates.Lawson LJ, Hewitt GM.School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK. lori.lawson@ebc.uu.seThere is a growing body of evidence that males serve as the major generators of mutations, due to the larger number of cell divisions involved in sperm compared to egg production. In mammals, this hypothesis (referred to as "male-driven evolution") has been tested by comparison of nucleotide substitution rates on the X and Y sex chromosomes in a limited number of taxa, predominantly primates and rodents. This study asks whether male-driven evolution is a more general phenomenon among mammals, by comparison of paralogous ZFX and ZFY intron sequences in sheep and goat species (the tribe Caprini). The male-to-female mutation ratio, alpha(m), was estimated to be between 2.93 (95% CI, 1.51-8.61) and 3.94 (95% CI, 1.25-32.29) when calculated using pairwise distance and branch length, respectively, suggesting that the Caprini are subject to weak, male-driven evolution. Comparison to published values for primates, felids, and rodents implies that there may be some correlation with reproductive life span. However, this is difficult to test with current data because confidence intervals are large and overlapping. Nonindependent evolution of paralogous sequences and/or the presence of selective constraints could lead to inaccurate estimates of alpha(m). No evidence for gene conversion between the ZFX and the ZFY introns was found, and this suggests that they have evolved independently during the radiation of the Caprini. Finally, there was no apparent evidence that these introns are subject to selective constraints, although low levels of intraspecific polymorphism reduce the power of neutrality tests.Mamm Genome 2001 Jan;12(1):17-21 Related Articles, LinksSex determination without the Y chromosome in two Japanese rodents Tokudaia osimensis osimensis and Tokudaia osimensis spp.Sutou S, Mitsui Y, Tsuchiya K.National Institute of Bioscience and Human-Technology, Tsukuba, Ibaraki, Japan. sutou@nibh.go.jpBoth males and females of the species of spinous country-rats (Tokudaia osimensis osimensis, T.o.o., Rodentia: Muridae), which live on Amami Oshima Island, a southern Japanese island, have 25 chromosomes. Another species of spinous country-rats (Tokudaia osimensis spp., T.o. spp., which live on Tokunoshima Island 40 km south of Amami Oshima Island, also have an odd number of chromosomes, 45. Karyotypes of males and females by the G-band method were indistinguishable in both populations. The lesser number of chromosomes (25) of T.o.o. is likely to be a result of Robertsonian fusions of 45 chromosomes of T.o. spp. that seem to be the offspring of another spinous country-rat Tokudaia osimensis muenninki (T.o.m.), which live on Okinawa Island and have 44 chromosomes including the X and Y Chrs. The lengths of the non-paired, putative X-Chr of T.o.o. and T.o. spp. occupied roughly 3.2% and 1.7% of the total lengths, respectively, hinting at translocation or exchange of a part of the X Chr and thus in violation of Ohno's Law. Southern blot analysis with murine Sry as a probe indicated that these two animals do not have Sry. When Zfx from T.o. spp. was used as a probe, both males and females of T.o.o. and T.o. spp. showed two bands, suggesting possible translocation of Zfy from the Y Chr. Comparison of physical characteristics, constituents of chromosomes, and sex-determination methods of these three Tokudaia country-rat populations suggests that each is endemic to each island and constitutes an independent species. These specialized species would provide us with clues to elucidate the mechanisms of primary sex determination and karyotype evolution in mammals.Proc Natl Acad Sci U S A 2000 May 9;97(10):5307-12 Related Articles, LinksNovel gene conversion between X-Y homologues located in the nonrecombining region of the Y chromosome in Felidae (Mammalia).Pecon Slattery J, Sanner-Wachter L, O'Brien SJ.Laboratory of Genomic Diversity, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702, USA. Slattery@mail.ncifcrf.govGenes located on the mammalian Y chromosome outside of the pseudoautosomal region do not recombine with those on the X and are predicted to either undergo selection for male function or gradually degenerate because of an accumulation of deleterious mutations. Here, phylogenetic analyses of X-Y homologues, Zfx and Zfy, among 26 felid species indicate two ancestral episodes of directed genetic exchange (ectopic gene conversion) from X to Y: once during the evolution of pallas cat and once in a common predecessor of ocelot lineage species. Replacement of the more rapidly evolving Y homologue with the evolutionarily constrained X copy may represent a mechanism for adaptive editing of functional genes on the nonrecombining region of the mammalian Y chromosome.Mol Biol Evol 1999 Nov;16(11):1633-40 Related Articles, LinksIs selection responsible for the low level of variation in the last intron of the ZFY locus?Jaruzelska J, Zietkiewicz E, Labuda D.Institute of Human Genetics, Polish Academy of Sciences, Strzeszynska, Poland.DNA variability was investigated in the last intron of the Y-chromosome-specific zinc finger gene, ZFY, and its X homolog on Xp21.3, ZFX. No polymorphisms were found in the 676-bp ZFY segment in a sample of 205 world-wide-distributed Y chromosomes, other than a solitary nucleotide variant in one individual (nucleotide diversity pi = 0.0014%). In contrast, 10 segregating sites (pi = 0.082%) were identified within 1,089 bp of the ZFX sequence in a sample of 336 X chromosomes. Four of these polymorphisms, which contributed most of the diversity, were located within an Alu insert disrupting the ZFY-ZFX homology (pi Alu = 0.24%). The diversity in the homologous portion of the ZFX intron, although higher than that in ZFY, was lower than that found in genomic segments believed to evolve neutrally; interspecies divergence in both segments was also reduced. Although this suggests that the evolution of both ZFY and ZFX homologs may not be entirely neutral, both Tajima and HKA tests did not reject neutrality. The lack of statistical significance may be attributed to a lack of power in these tests (the low divergence and variability values reduce the power of the HKA and Tajima tests, respectively); furthermore, Homo sapiens has recently undergone a rapid population growth, and selection is more difficult to detect in an expanding population. Therefore, the failure to reject neutrality does not necessarily indicate the absence of selection. In this context, the phylogenetic argument was given more weight in out interpretations. The high level of sequence identity in ZFY and ZFX segments, in spite of their separation 80-130 MYA, reflects a lower mutation rate as compared with other segments believed to undergo unconstrained evolution. Thus, the possibility of weak selection contributing to the low level of nucleotide diversity in the last ZFY intron cannot be excluded and should be kept in mind in the population genetics studies based on Y chromosome variability.Mol Biol Evol 1993 Mar;10(2):271-81 Related Articles, LinksEvolution of the Zfx and Zfy genes: rates and interdependence between the genes.Pamilo P, Bianchi NO.Department of Genetics, Uppsala University, Sweden.A phylogenetic analysis of sex-chromosomal zinc-finger genes (Zfx and Zfy) indicates that the genes have not evolved completely independently since their initial separation. The sequence similarities suggest gene conversion in the last exon between the duplicated Y-chromosomal genes Zfy-1 and Zfy-2 in the mouse. There are also indications of conversion (or recombination) between the X- and Y-chromosomal genes in the crab-eating fox and in the mouse. The method for estimating synonymous and nonsynonymous substitutions is modified by incorporating the substitutions in the twofold-degenerate sites in a novel way. The estimates of synonymous substitutions support the generation-time hypothesis in that the obtained rates are higher in mice (by a factor of 4.7) than in humans and higher in the Y-chromosomal genes (by a factor of 1.9) than in the X-chromosomal genes.

PB:
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.M: Friendship in drawing scientific conclusions is irrelevant. No, he is not my friend. We know each other.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: What kind of logic is that? 1. why would conserved features in introns invalidate neutral evolution? There are conserved features of hypervariable region I as well...old hat..read up on it. And you should read Kimura...he did not state that the entire genome evolves neutrally.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?M: And I see you are a racist as well..good job. Nope, this is not what I am referring to...see below.PB:
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.M: Dominant males (whether through power, wealth, violence) in many cultures disproportionately father more children. Humans lived in smallish bands thousands of years ago. It is unlikely given current practices that all males had an equal probability of producing offspring. This is seen directly in some populations such as small nomadic groups today, and the Yanomamo (who I guess you would like to exterminate), and shows exactly the effect on the Y chromosome we observe in the broader human male population.PB:
This is what I found in pubmed on paternity in Yanomami Indians. (I could find Jim Neel, do you have the reference? Thanks):M: He presented the data in a seminar. I don't know if he published the data set or not...can't ask him since he is dead. But you can search medline yourself for plenty of other examples. Or do Y chromosome, Yanomamo as search terms.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).M: What's the matter Peter...hate the idea that you might be an African descendant ? Do you know what the effective population size is for humans? It is a lot smaller than you think. Conservationists stress small effective populations size is bad for survival..that is true. We are talking about the males that contribute to the next generation which does not imply the effective population size is small...or do you not count woman as human?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).M: No, I pointed out that you were using the mouse data as an example of human Y chromosome variation which is false.M: So there was no selective sweep in the mice...whoo hoo!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.M: Not my friends...are you in love with Spetner so you have to accept what he says..and my point was and still is that if you sequence a mouse gene and call it human you are wrong just as if you take the mouse genetical history for the Y and say that it represents humans....I may not be a primatologist like SLPx but even I know that mice are not primates.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.M: Funny that you call HERV's "degenerate" since most of the ones transposing have a full complement of viral genes...not very degenerate...MPG yet again fails.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.M: You obviously did not read any of the primary literature I posted since Svante wrote a review...and then you claim that the data from mice should be applied to humans.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 ).M: You have actually shown complete ignorance of the fundamentals of the NDT and population genetics so your claims to understanding molecular mechanisms are highly suspect.PB:
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.M:
Interesting that you missed this direct comment to Svante's 1995 review Absence of polymorphism at the ZFY locus on the human Y chromosome.Dorit RL, Akashi H, Gilbert W.Department of Biology, Yale University, New Haven, CT 06511, USA.DNA polymorphism in the Y chromosome, examined at a 729-base pair intron located immediately upstream of the ZFY zinc-finger exon, revealed no sequence variation in a worldwide sample of 38 human males. This finding cannot be explained by global constraint on the intron sequence, because interspecific comparisons with other nonhuman primates revealed phylogenetically informative sequence changes. The invariance likely results from either a recent selective sweep, a recent origin for modern Homo sapiens, recurrent male population bottlenecks, or historically small effective male population sizes. A coalescence model predicts an expected time to a most recent common ancestral male lineage of 270,000 years (95 percent confidence limits: 0 to 800,000 years).PB:
In conclusion, the falsification still stands.M: In conclusion, you have provided nothing substantive...try again and don't beat up any of those Yanomamo on the way home...cheers,
M

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: Nope not prickly but if your tactic is to attribute statements to me that I did not make then it is clear that you have completely lost this debate. Other than your offhand remark about the data being a clearcut falsification, you will have to actually explain why...you avoided this issue completely when SLPx presented raw data (which you claim to prefer) and asked you to point out the non-random mutation. So go for it...we have all only been waiting for about half a year for this.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: Pathetically weak is an apt characterization as you have not yet again attributed to me, the polar opposite of what I initially stated..I claimed I do NOT see why evolution, even neutral evolution should provide a reliable clock. Do your homework and you might even find out why yourself.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: How perceptive of you...the paper was just a picture of the sequence I take it? And all those funny little objects around the figures..most of us call them words...what did they say about it?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.]M: Wow are you one heck of a megalomaniac...you think I registered on EvC to educate you...yes I have been searching the internet all my life for Peter Borger to bring him out of the dark ages of ignorance that he is clinging to...LOL!!!! You are so freaking lazy Pete. You want to claim you have easily refuted evolution yet you are unable to even find references on your own...I really hope your scholarship is many orders of magnitude more thorough for your asthma research.My claims are completely mainstream Peter...you are the one making claims to morphogenetic fields, creatons, and non-random mutations. The first two you have refused to even debate much less provide support for and the last you have been unable to support since your entry on this board...I suggest YOU support your claims with a nice big post full of citations (not reviews not novels) from primary literature supporting each one of your thus far unsupported claims.Well..here is Mommy to spoon feed Petey Wetey again...Ayala FJ. Related Articles, LinksMolecular clock mirages.
Bioessays. 1999 Jan;21(1):71-5. Review.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.M: And I see you still have no answer to my question...I know Peter, science is tough..maybe you will get it some day.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!M: What is a deep dark inside? Anyway, you are accusing me of not answering questions that You did not answer and attributing positions to me that I did not take...so you keep it scientific...and answer the question. I will then gladly answer.....and who I am would not really be so unbelievably difficult to figure out 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.M: Not sure what you are talking about here...I posted papers from Nei not Gunther Wagner. You also seem to find some need to attribute lots of friends to me....I mean, I am a popular guy but hey..not that popular.PB: Your remark on stuff residing in the genome waiting for someting.M: Oh, that remark that I never made..I see.PB: I am rather curious about how much selection purification of redundant genes require. You are the proponent of an extraordinary claim....M: As much as they need ....wow Peter...it so much easier if I just make my posts like yours.PB: Dim? I'd rather call it bright.M: I don't think the tactic is particularly bright (note: I am not calling you generally dim or claiming that you are otherwise not bright)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: You think the environment does not change a lot and that ice ages are overnight?? LOL!!!!!!!!!!!!!!!!!
As to the second part...show us the evidence.PB: 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: No wonder you have so much trouble with understanding population genetics and evolution...you think selection is constant...well, that explains a lot of the conceptual problems you have...it also is the underpining of your strawman arguments.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).M: Do a PCR with a repair deficient Taq, clone the product and sequence the clones....after multiple replication cycles the sequence will remain stable without repair and with accumulation of RANDOM mutations in some individual clones...your claim is false. You claim that the appearance of identitiy of descent is due to non-random processes yet all data sets you have seen you claim are random mutations masking non-random...thus, no evidence for your model. In addition, there is no such thing as a "complete" set of repair enzymes...bacteria have different repair mechanisms from humans...which one of us is complete?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.M: I understand that you are proposing a hypothesis with several non-testable components (creatons etc), that is internally inconsistent (non-random with random, stable yet plastic), with several of the initial claims falsified...it needs a lot of work Peter.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.M: Great further clarification Peter...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.M: So you mean now that it is ok for YOU to do inferrential work but not Caroll et al.? Interesting....peer review Tuesday, Peter review Thursday?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.M: The thread was unanswered, bottom line...I bumped it repeatedly..and this does not address the other posts that I made that went to this day unanswered.PB:
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.M: I prefer to have the debate on the public forum where others can contribute to both our sides....though given the length of our posts to each other, I find it hard to imagine anybody reads them but the two of us.PB:
Best wishes, and have a nice weekend,
[I hope you're not so prickly next week.]M: Have a nice weekend to....no promises about being prickly (I see you liked that word) How do you say ciao in Dutch?ciao
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?

FW:
We have done countless experiments in the lab over many years on organisms with rapid reproductive cycles, yet we cannot find ONE single example of increased genetic information. If evolution is true, we should be able to produce literally millions of examples.M: We have done countless expermeints??? I can count the number of experiments you have done....ZERO..LOL!

Most evo here realize I’ve been asking for observed examples. Giving me examples of duplications that allegedly happened millions of years ago is begging the question.We have done countless experiments in the lab over many years on organisms with rapid reproductive cycles, yet we cannot find ONE single example of increased genetic information. If evolution is true, we should be able to produce literally millions of examples. But you guys can’t even produce ONE.
**********************This is just two of about 20 papers from just this ONE lab on the subject...you can do your own homework from now on ( or are you to busy doing countless experiments LOL!) and look up the rest yourself.You can continue to ignore the reality of what experiments have been done as you have persistently done on this board or you can actually learn about the subject and actually adopt an alternative to your ignorance is bliss tactic.Proc Natl Acad Sci U S A 2001 Sep 25;98(20):11388-93 Related Articles, LinksContribution of individual random mutations to genotype-by-environment interactions in Escherichia coli.Remold SK, Lenski RE.Center for Microbial Ecology, Michigan State University, East Lansing, MI 48824, USA. remold@msu.eduNumerous studies have shown genotype-by-environment (GxE) interactions for traits related to organismal fitness. However, the genetic architecture of the interaction is usually unknown because these studies used genotypes that differ from one another by many unknown mutations. These mutations were also present as standing variation in populations and hence had been subject to prior selection. Based on such studies, it is therefore impossible to say what fraction of new, random mutations contributes to GxE interactions. In this study, we measured the fitness in four environments of 26 genotypes of Escherichia coli, each containing a single random insertion mutation. Fitness was measured relative to their common progenitor, which had evolved on glucose at 37 degrees C for the preceding 10,000 generations. The four assay environments differed in limiting resource and temperature (glucose, 28 degrees C; maltose, 28 degrees C; glucose, 37 degrees C; and maltose, 37 degrees C). A highly significant interaction between mutation and resource was found. In contrast, there was no interaction involving temperature. The resource interaction reflected much higher among mutation variation for fitness in maltose than in glucose. At least 11 mutations (42%) contributed to this GxE interaction through their differential fitness effects across resources. Beneficial mutations are generally thought to be rare but, surprisingly, at least three mutations (12%) significantly improved fitness in maltose, a resource novel to the progenitor. More generally, our findings demonstrate that GxE interactions can be quite common, even for genotypes that differ by only one mutation and in environments differing by only a single factor.Proc Natl Acad Sci U S A 1999 Mar 30;96(7):3807-12 Related Articles, LinksGenomic evolution during a 10,000-generation experiment with bacteria.Papadopoulos D, Schneider D, Meier-Eiss J, Arber W, Lenski RE, Blot M.Abteilung Mikrobiologie, Biozentrum, CH-4056 Basel, Switzerland.Molecular methods are used widely to measure genetic diversity within populations and determine relationships among species. However, it is difficult to observe genomic evolution in action because these dynamics are too slow in most organisms. To overcome this limitation, we sampled genomes from populations of Escherichia coli evolving in the laboratory for 10,000 generations. We analyzed the genomes for restriction fragment length polymorphisms (RFLP) using seven insertion sequences (IS) as probes; most polymorphisms detected by this approach reflect rearrangements (including transpositions) rather than point mutations. The evolving genomes became increasingly different from their ancestor over time. Moreover, tremendous diversity accumulated within each population, such that almost every individual had a different genetic fingerprint after 10,000 generations. As has been often suggested, but not previously shown by experiment, the rates of phenotypic and genomic change were discordant, both across replicate populations and over time within a population. Certain pivotal mutations were shared by all descendants in a population, and these are candidates for beneficial mutations, which are rare and difficult to find. More generally, these data show that the genome is highly dynamic even over a time scale that is, from an evolutionary perspective, very brief.

FW:
I looked at this paper, and this is hardly an example of new genetic information. It is pretty much no different than Mark’s nylon muncher. Here’s an important passage from your citation (emphasis mine):M: And you clearly did not read the entire paper nor the other paper I cited...your problem...not mine...or evolutions for that matter.FW:
What does this all mean?M: We know Fred...you have trouble understanding even the basics...FW:
The parent population was near a fitness peak in the glucose environment; in the maltose environment it was in a valley, having lost fitness. The subsequent experiments with the mutant strains only showed selection moving the maltose bacteria back up the maltose peak. There is clearly no new genetic information here.M: Oh, so they were magically shoved up the adaptive peak without selection for specific genotypes...LOL!FW:
Informed evolutionists who are aware of the information problem propose gene duplication followed by mutation as the mechanism of increasing information in the genome.M: What would an electrician part time keyboard player who knows nothing about biology know about what "informed" evolutionists propose?FW:
Fine. Any observed examples? Scott tried "begging the question" by giving a hypoethetical, unobserved example that allegedly occurred millions of years ago, and then protested after his logic was exposed and declared it an impossible challenge. But if evolution is true, there should be plenty of observed examples of this in the literature. Why can’t you give me even one provocative example?M: You have been given several but just deny them in your complete ignorance. And the two citations were just two of about 20 from one research group alone...so much for what you know about informed evolutionists.FW:
Evolution, the "impossible dream"....impossible when one is to dense to understand even the basics.

quote:

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Originally posted by peter borger:
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

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+++++++++++++++++++++++++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 well

PB:
Similarly, it has been demonstrated that chromosomal duplications do not play a role in construction of (the human) genome(s) (Huges et al).To bad you are wrong van Geel M, Eichler EE, Beck AF, Shan Z, Haaf T, van der Maarel SM, Frants RR, de Jong PJ. Related Articles, LinksA cascade of complex subtelomeric duplications during the evolution of the hominoid and Old World monkey genomes.
Am J Hum Genet. 2002 Jan;70(1):269-78.
PMID: 11731935 [PubMed - indexed for MEDLINE]16: Hughes JF, Coffin JM. Related Articles, LinksEvidence for genomic rearrangements mediated by human endogenous retroviruses during primate evolution.
Nat Genet. 2001 Dec;29(4):487-9.PB:
These actual facts and observations on microorganisms severely limit (bacterial) genome growth and thus evolutionism in general. I really wonder, do evolutionists ever read books on molecular biology?M: One has to wonder if you ever have......