Darwin in the Genome

Hi Percy,peter borger writes:
Dr Caporale may be unders the impresion that these new findings are fully consistent with Darwinism but it is not since I already mentioned that Darwin's extrapolation from pigeons and finches (and other organism) becomes unwarranted.Percy: But you've been claiming that Dr. Caporale's book overturns NDT, which is incorrect and misleading.PB: No, it is correct. That you don't admit it is misleading.percy: What you must instead say, if you're at all interested in accuracy, is that adding your insights to the information in Dr. Caporale's book overturns NDT. Dr. Caporale's book by itself does not support your conclusions, and Dr. Caporale herself is on record as rejecting them.PB: If evo's were interested in accuracy they wouldn't call several unequal phenomena 'evolution'.Percy: On a side-note, it may just be me, but even after reading your GUToB thread in the Welcome, Visitors! forum I can't say I understand it.PB: Let's stay on track.Quote (PB):
Only if one assumes that all the info was already present in the first cell (few cells is more probable) Darwinism is a possibility.Percy: We just discussed this in another thread. It was described in detail for you how even simple point mutations can add information to the genome.PB: No, this point mutations ACTIVATED preexisting information.Percy: See Message 166 of the Where is the evidence for evolution? thread in the Evolution forum, to which you replied, "In accord with GUToB rule 3. I forgot about rule and prediction 3." If even a simple point mutation can add information, then most certainly more complex mutations such as gene duplication can. To deny this would be akin to saying you can fill a barrel with water using an eyedropper but not a bucket.PB: It didn't add information. It activated a preexisting mechanism.Quote (PB): Genes do not duplicate and diverge randomly into novel genes. It is inferred from what we see in the genome: gene families. However, if we find only one family not in accord with this view, we know that it is false.Percy: Since duplication is only one of the processes by which unique genes are thought to arise, such a conclusion would be faulty.PB: Yep, there probably is 'gene generating' machinery in the MPG.Quote (PB): Recently, gene families that cannot have arisen through duplication have been described. I already demonstrated the alpha actinins...Percy: If you do a search on peter borger posts that mention "alpha actinin" or "alpha actinins" you'll see that all you did was claim you demonstrated this in some letter, after which you simply claimed that you'd demonstrated it. You've never actually made the argument here at EvC Forum.PB: This letter pretty much says it. If one has to explain a family through introduction of neutral selection it cannot be accepted as explanation. Otherwise you have to introduce NRM. It's up to you.Quote(PB):
There is no evolutionary explanation for such phenomena.Percy: Until you present your information here, I can't even guess what phenomena you're talking about.PB: this pertained the redundant family of src-phosphates. If you like me to open a new thread, please let me know.Percy:
Added by edit:Went through the search list one more time and found your actinin explanation in Message 28 of the scientific end of evolution theory (2) thread in the Evolution forum. From what I can tell it didn't receive much discussion. Unsupported assumptions necessary to your conclusions are:10-9/nucleotide/year neutral evolution rateOnly point mutations contributedThe gene was neutral from its inceptionIs the gene really neutral, or does it compensate for deactivated ACTN2 genes or some other gene?And that list is probably incomplete - Scott should take a look.PB: Yeah, that would be great. I mailed my questions to an evo-in-the-field-of-redundancies (Dr Wagner). Never got a response.Percy: Anyway, it may turn out that you're able to provide the necessary support for these assumptions, but until you do so your conclusions are premature.PB: Sometimes it pays to do some research and calculation yourself, instead of believing what others claim. The topic of redundancies is still open for discussion.best wishes,
Peter

Hi Page,I am trying to understand genetic redundancies in the light of evolution as a random process (=random mutation plus selection).Redundant genes usually demonstrate only moderate sequence homology.
For instance the alpha-actinin genes. The a-actinins comprise a group of actin-binding proteins encoded by a multigene family. In skeletal muscle, they are a major structural component of the Z-lines that anchor the actin-containing thin filaments and maintain the spatial relationship between myofilaments. In humans, two genes (ACTN2 and ACTN3) encode the closely related a-actinin-2 and a-actinin-3 skeletal muscle isoforms. ACTN2 is expressed in all skeletal muscle fibres, whereas expression of ACTN3 is limited to a subset of type 2 (fast) fibres. A careful screening of muscle biopsies with dystrophic (118 specimens), myopathic (74), neurogenic (20) and normal (55) features demonstrated that all specimens contained normal a-actinin-2 expression. Deficiency of a-actinin-3 was identified in 51 of the 267 cases (19%), and was due to a common non-sense mutation that introduced a premature stop codon. So, the proper a-actinin-3 protein cannot be synthesised. Surprisingly, the deficiency was not associated with any particular histopathological or clinical phenotype [North et al, Nature Genet.1999, 21:353].What troubles me is that I cannot think of a molecular mechanism that gave rise to such genes. According to theory, duplication and divergence gave rise to the alpha-actinins. A close look at the redundant genes reveals that the differences are the result of single nucleotide mutations. Neutral evolution rate is about 10(exp)-9/nucleotide/year, and recent genome wide studies present evidence that purifying selection worked upon duplicated genes (Dr Wagner in Genome Biology). The ACTN2 and ACTN3 genes are approximately 3000 bp, and share 85% sequence homology. Moreover, the ACTN3 gene is highly conserved within mammals, suggesting ancient duplication and rapid diversion.I have a couple of questions regarding the evolutionary mechanisms involved in genetic redundancies. Since you are the PhD-ed evo biologist on the board they should be easy to address. I was hoping that you can find the time to address them:1) Do these data mean that approximately 450 bp changes occurred on neutral positions?2) Do these data mean that it would take about 10(exp)6 years for 3 random mutation to occur in the duplicated gene? And 150 million years for 450 neutral mutations?3) Do these data indicate that after each point-mutation there was (neutral) purifying selection? And, what exactly is it? I mean, what exactly is selection on neutral genes?3a) Is it independent from nearby genes? Independent from the rest of the genome?3b) Does this type selection take place on the level of the organism? How?4) Are recently duplicated genes present in the human genome?5) Is evolution of the a-actinins driven by random mutation, or rather NRM?I hope you can help me out with my questions. I would be very grateful. Thanks in advance.
(If you wish, we could discuss the src phosphatases later).Best wishes,
Peter

Page says:'Borger - an unanswered "letter" is more likely a sign that the recipient found its contents unworthy of reply, rather than the recipient being 'troubled' by the implications.'Borger says:'If such were true, why do I respond to your letters?'Best wishes,
Peter

Page and Paul,Paul's quote:
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If I remember correctly he didn't actually acknowledge that he WAS the asthma researcher. He certainly didn't volunteer the information, and I very much doubt that "our" "Peter Borger" (if that is his real name) has any real scientific qualifications. After all a medical researcher would probably have to know enough statistics to understand the importance of sample size, which this Peter Borger seems not to grasp at all.
--------------------------------------------------------------------------------PB: If I remember correctly (and I do), PaulK wasn't even registered to the board in those days.
And a bout sample size. It has nothing to do with the example. Ever heard of random tests? Statistics too.Page: You may have a point. Way back, when Borger first started posting here, there was some discussion on this. I felt that he just happened to have that name, or perhaps co-opted it for discussion purposes, and ran with it. Schraf I think it was posted a list of citations from Pubmed. Borger has since written that "someone posted my CV" on EvC. He says "part of it". The problem is, not all of the citations were by the same P. Borger. So he sould well be an imposter.
it would explain a lot.PB: From your little chat above, your 'psyches' become crystal clear. Thanks for providing clearance (although it was already obvious). It explains all.And, the problem is not whether the citations are from the same P. Borger or whether he is an imposter. The real problem is that evo's don't understand their own theory. That's the REAL problem and you don't wanna see it.[And I really don't understand you guys: if he's an imposter why waste your precious research time here? Why not follow Dawkins advice?]have a nice day,
Peter

Hi Page,I am still waiting. For the organisms that the abbreviations stand for and a phylo-tree. This is the third time I ask for it. I am not going to ask you another time (I have better things to do). So, if you wanna discuss your best evidence of commom descent in detail, this is your chance.best wishes,
Peter

dear Paul,PK: Firstly one can read the board without being registered as I did for some time.PB: Why? Dawkins' advice?PK: Secondly your lack of understanding of the importance of sample ssize is based on the discussions of human mtDNA where you dismissed the importance of using a larger sample.PB: My lack of understanding? What a poppycock. The only example of mtDNA sequences over time (0-62 Ky BP) we have at the moment can be regarded as a random sample. That this small is not in accord with evolutionism is tale telling and I predict that other ancient mtDNA sequences will demonstrate similar results as soon as they are published. I mentioned this before and you better listen to what I say.PK: Thirdly you are the one who does not understand evolutionary theory as indicated by your own refusal to explain the sense in which the theory requires mutations to be random, and thus support your claim that the "non-random" mutations contradict this.PB: No, since you are the evolutionist YOU are going to do that. Let's see what a man of the field makes of it. If you are defending your theory better explain it properly too.PK: In the absence of any such explanation it is clear that your "refutation" relies on a point of evolutionary theory that you do not even understand well enough to discuss.PB: I know all in and outs of this outdated theory and I know where and why it cannot hold in the light of contemporary findings.PK: Which demonstrates that you do not even understand your own argument. Your equation of purifying selection with some imaginary idea of "neutral selection" further underlines your lack of understanding.PB: The concept of 'weak purifying selection' has been introduced to "explain" genetic redundancies. For some families 'neutral purifying selection' has to be introduced to understand them in an evolutionary sense (as demonstrated, and denied by the evo-community, as expected). It is of course humbug, and evo's will not demonstrate such examples and that's why I do it.best wishes,
Peter

Dear paul,PK: I have no idea why you would think that I take advice from Dawkins on which internet fora I visit or how I approach them.PB: I can't understand why anybody would take advice from somebody who demonstrably does not know the most elementary stuff of the topic he discusses.PK: The section of mtDNA you considered cannot be considered a random sample - because it is not.PB: You owe the board an explanation.PK: And even a random sample has limitations which is why professional polling organsiations seek to obtain a balanced sample. And no, it is not the only relevant mtDNA that we have - as was mentioned in the thread. And of course you failed to even consider the significance of the fact that the sample offered by Dr. Page was of the same size.PB: Apparently you still don't get the example: it was on a 360 bp mtDNA region in ancient human mtDNAs (0-62 kY BP). Maybe you could provide the other references on ancient human mtDNA in several ancient human species. Maybe I should also mention that a good theory requires to be right in extreme conditions. For instance Einsteins' gravitational theory proven over and over through extraordinary predicted observation. The mtDNA could be such extraordinary case. It turns out to falsify evolutionary assertions. To me it is clear that evolutionism is a bad theory.PK: And I note that you still cannot explain the very point of evolutionary theory you claim to have refuted. What is even more amazing is that I have referred to it more than once and you still expect me to explain it again ! Clearly your claim to know "all the ins and outs" is false.PB: Great, I don't see your explanation. I offered you the opportunity but you simply let it go by.
And I did not claim to know that all ins and outs to be false, I said that contemporary biology has severe implications for evolutionary theory. You make a strawman, and next attack the strawman. Not much of an argument.PK: And even if there are evolutionists who refer to "neutral purifying selection" - which I doubt - this still does not change the fact that the term neutral selection does not refer to purifying selection.PB: Why do you keep misrepresenting what I say? I said that very weak purifying selection has been introduced, and that I introduced neutral selection for certain genetic redundancies to explain them in an evolutionary sense. I wonder, how can one discuss with people who keep making up strawmen and keep misrepresenting. It is a debating tactic to wear the opposite party out, so the attack will be ceased, I guess. However the attack will not stop, the more you object to my claims the more I will show where your pet theory goes wrong. One thing that biology has taught us is that everything has to be in balance.PK: In fact neutral selection is used to refer to the situation where neither purifying nor positive selection are operating.PB: So, at last we know what neutral selection is. It is though a contradiction in terminis. Besides, from evolutionary theory it is to be expected that genetic redundancies mutate faster than essential genes. As recently demonstrated they do not (and mentioned several times in the discussions and backed up by scientific literature).PK: And as the references I have discovered show, it is not the case that the knockout of the ACTN-3 gene is neutral even in humans (and it is certainly detrimental in other species).PB: The data I have recently encountered on a symposium in Sydney demonstrate that the presence of a-actinin MAY have a positive effect on sprint performance, but is only significant in large groups. This shows that it is not necessary for sprint performance in a considerable amount of athletes: redundancy. And redundancies are going to be inactivated over time, as predicted by the GUToB.Best wishes,
Peter

Dear page,Of interest:
J Mol Evol 2003 Jan;56(1):1-10The alpha-Actinin Gene Family: A Revised Classification.Dixson JD, Forstner MJ, Garcia DM.Southwest Texas State University, 78666, San Marcos, TX, USA, jamie.dixson@excite.comThe sequencing of a genome is the first stage of its complete characterization. Subsequent work seeks to utilize available sequence data to gain a better understanding of the genes which are found within a genome. Gene families comprise large portions of the genomes of higher vertebrates, and the available genomic data allow for a reappraisal of gene family evolution. This reappraisal will clarify relatedness within and between gene families. One such family, the alpha-actinin gene family, is part of the spectrin superfamily. There are four known loci, which encode alpha-actinins 1, 2, 3, and 4. Of the eight domains in alpha-actinin, the actin-binding domain is the most highly conserved. Here we present evidence gained through phylogenetic analyses of the highly conserved actin-binding domain that alpha-actinin 2 was the first of the four alpha-actinins to arise by gene duplication, followed by the divergence of alpha-actinin 3 and then alpha-actinins 1 and 4. Resolution of the gene tree for this gene family has allowed us to reclassify several alpha-actinins which were previously given names inconsistent with the most widely accepted nomenclature for this gene family. This reclassification clarifies previous discrepancies in the public databases as well as in the literature, thus eliminating confusion caused by continued misclassification of members of the alpha-actinin gene family. In addition, the topology found for this gene family undermines the 2R hypothesis theory of two rounds of genome duplication early in vertebrate evolution.PB: The paper is on gene classification. And the explicit assumption that the one gene arose from the other. However, my comments posted to you yesterday questioned this scenario. It is my comments that I would like to have addressed, pubmed abstracts I can find for myself. Anyway, the final addition is interesting and in accord with Austin Hughes work: genomes can not be explained by chromosome duplications (e.g. Genome Res 2001, vol11, p771-780; J Mol Evol, vol48, p565-576).So, the only remaining possibility for genome expansion is duplication of preexisting genes and other DNA elements. This scenario is based upon assertions that duplication and divergence of the duplicates yield new genes. If genes are around that can not be explained accordingly (and they are), I see a little evolutionary paradox. [Also, preexisting sound a lot like........yep, GUToB]Page wonders: Who to believe?PB: That's a very good question. Although I do not object to the data, the evolutionary interpretation is questionable (at the least).Have a good one,
Petey

Hi paul,In response to:The INMR report cited earlier claims that "We have also studied the a-actinin-3 gene throughout evolution and have demonstrated it appears to be essential in all other species — including mice, chickens, baboons and chimpanzees."PB says:These guys -and you- may be under the impression that they have studied evolution, but they didn't. If they really had studied the ACTN genes throughout evolution it would have taken them millions of years to perform the study.
In contrast, all they show is a study on the ACTN3 genes in several distinct organisms. MPGs if you like. Nothing evolved here. That they think they are studying evolution -while all they do is checking distinct sequences in distinct organism- is tale telling for you evo guys: conclusion jumping based upon assumptions.best wishes,
Peter

Hi Page,Page says:Borgerism.
Police develop a 'theory' about a serial arsonist. 100 fires have been set. They catch the crook in action. He admits to setting 99 of the 100 fires, but has a rock-solid alibi for the 100th.The police scratch their heads.."I guess we should let him go" one finally utters."Yup" says another "if he didn't do all of them, I guess he must not have done any. Our theory is refuted."PB: You do not have 99 sure cases. All you have is 99 biased interpretations. Even your best evidence of common descent is not free from NRM (as I will point out later), and thus not compelling. It should be obvious that you cannot convince me with such data. If you are going to claim common descent you have to exclude all other possibilities (that is the scientific method), since 'evolution-from-microbe-to-man' is an extraordinary claim. And as you know extraordinary claims require extraordinary evidence.best wishes,
Peter

dear Paul,PK: I see that you still have not managed to offer an explanation of how mutatiosn are "random" according to NDT. THe best resposne you can manage is to demand that I do the work of explaining a basic point which you claim to understand - even though I have already done so more than once.PB: I did that several times. As expected, you won't buy whatever I say and thus I am still waiting for your evo vision.PK: I also notice that you feel the need to throw irrelevant personal attacks at Dawkins for no apparent reason. I suggest you keep your personal hatreds out of your posts.PB: If you had read my previous mails you would have known that I have nothing personal against Dawkins. I have something against his silly outdated claims and the propgation there of. I will have to object to that from a scientific stance.PK: I also notice that you defend your comments by falsely claiming that they have been misrepresented.PB: No, you have misinterpreted the content of my mail. (as described in my previous mail).PK: However rather than explain why your ideas were not the nonsense I suggest you instead claim that they are a strawman (since they do not represent the views of your opponents).
I also note that in a later post you drop the idea of explaining the data in an evolutionary context altogether - to answer data which points to a viable alternative (the non-redundancy of actinin-3 in other species).PB: If you make links to what you claim I can respond to it. Keep it scientific please.PK: Your admission that you did not knwo what neutral selection was is a further evidence of your general lack of knowledge in the area of evolutionary theory.PB: Neutral selection is a contradictio. It is nothing.PK: As to your final point your argument fails to deal with the fact that actinin-3 does seem to confer a benefit (that some individuals MAY gain that benefit by other means does not change the fact that the evidence shows that there is a benefit).PB: As a redundancy it is going to be inactivated over time.PK: And it seems that your argument agaisnt evolution also applies to your own GuToB - only more so. Why have non-random mutations not inactivated the ACTN-3 gene in the entire human population ?PB: Usually I don't do why-questions, since it is metaphysics. But to explain the GUToB I will make an exception. The GUToB holds that there are two types of mutations, random mutations (RM) and non-random mutations (NRM). Evo's think that RM do the trick, and deny NRM (probably they start to see now that they cannot longer deny NRM). The stopcodon that inactivates the ACTN3 gene is likely introduced by RM, not NRM. So, it is a loss of functional gene (=GUToB rule 3).Best wishes,
Peter

Hi Percy,You say:--------------------------------------------------------------------------------
Peter Borger in reply to PaulK writes:
I did that several times. As expected, you won't buy whatever I say and thus I am still waiting for your evo vision.Percy: It's hard to escape the feeling that you're being purposefully evasive.PB: I am not the evasive one. Evo's have to present compelling scientific evidence for their extraordinary claim of microbe-to-man-evlution, but I haven't seen anything that cannot be distincly interpreted. The NRM has been denied for 6 months or so, untill I got backed up by Dr Caporale. So, I can imagine that it is a bit of a nuiance. It demonstrated that my vision is tre right one.Percy: No one here, except you, is proposing anything other than the standard ToE, which you can find in any textbook on evolutionary biology.PB: They all talk about random mutation and selection.Percy: There is no need for you to wait for PaulK's personal "evo vision," because there is no such thing.PB: That there is no such thing I could have expected. Evolutionism is 'ad hoc-ism'. There is no standard evolutionary theory, I guess, otherwise my question was not so hard to address. Even the Futuyma argument mark24 provided last year falls.Percy: We're all waiting for some convincing evidence or argument supporting your views, but about the best you can muster is bald assertions with no supporting evidence or argument, such as this:Neutral selection is a contradictio. It is nothing.PB: This is a very typical remark for evo's. I have presented several lines of evidence and now you ask me to provide evidence. It is impossible to discuss with people who deny scientific data. It demonstrates that you don't care about science. All you care about is to keep up your worldview.
And about neutral selection, it is nothing. In our first encounter you even admitted that (in the case of the 1g5 gene).Percy: And evasive non-sequiturs like this:Usually I don't do why-questions, since it is metaphysics.PB: You forget to metion that next I discussed the inactivation of the ACTN3 gene in a GUToB way. It elegantly explained.Percy: Why can't Peter Borger muster any defense of his views? Must be metaphysics.PB: Why can't evo's give simple answers to even simpler questions? Since evolutionism = metaphysics, I guess.Best wishes,
Peter[This message has been edited by peter borger, 03-03-2003]

Percy,--------------------------------------------------------------------------------Re: borgerisms
--------------------------------------------------------------------------------PB: I notice that I almost made it into the dictionary Percy: So many fallacies packed into so little space.Peter Borger writes:
Even your best evidence of common descent is not free from NRM (as I will point out later), and thus not compelling.Percy: No one is claiming that common descent is free of NRM.PB: And since you cannot exclude the alignment being caused by NRM the evolutionary conclusions are invalid. Conlusion jumping.Percy; You're issuing a valid defense, but it's of a challenge that wasn't made. It is your claim that the presence of NRM invalidates the ToE that is being challenged, and which you seem unable to defend.PB: No, here I am challenging evidence of common descent based upon alignments of shared mutations. As long as you don't exclude NRM, the conslusions are invalid. As you should know by now, I demonstrate over and over that evo claims are founded on outdated scientific views.Percy: Hence you defend that which was not challenged and ignore that that was.PB: No, I was challenging common descent. That is evolutionary theory isn't it?PB: It should be obvious that you cannot convince me with such data.Percy: It does not matter whether we can convince you or not. What is important is that the ToE is the accepted theory of the vast majority of scientists working in evolutionary biology, while your views seem to be confined to you alone.PB: So what. Even if the pope accepted evolutionism, or the dalai lama or president Bush, Dr Watson and Dr Crick, I really don't mind. As long as it can be demonstrated to be wrong I do not see the point propagating it as fact. It is not much more than a 19th/20th century hypothesis most likely to be wrong.Percy: In other words, the explanatory power of the ToE has convinced many, while your view has convinced only you. By this measure your proposals fall far short of the ToE.PB: Where has it explanatory power? I am not aware of it. It doesn't explain the fossil record, it doesn't explain molecular biology. It doesn't even explain Page's best example of common descent (soon to be discussed here). So, please expand.
If I were you I wouldn't bet on your claim that I convinced only myself. I'd rather bet I already convinced more than 1.PB (quote): If you are going to claim common descent you have to exclude all other possibilities (that is the scientific method),...Percy: Science is tentative. There is no way to permanently exclude all but one possibility. You are incorrect to state that the scientific method includes such a requirement.PB: No, one has to exclude other possibilities. Therefor, I recommed that unbiased agnostic scientists have to reanalyse all biological data available. And find the most likely explanation for the data: evolutionism or GUToB. As an unbiased sciecntist I did that, and the data superfacially can stand the evolutionary vision. A carefull scrutiny, however, reveals unexpected things and can often not be explained by the standard ToE (as discussed on this board). I've set up the GUToB to explain all biological phenomena. That is what we should be interested in with respect to a scientific theory: its explanatory power.PB (quote): ...since 'evolution-from-microbe-to-man' is an extraordinary claim. And as you know extraordinary claims require extraordinary evidence.Percy: The extraordinary claim is that which is out of the ordinary. Since the ToE is the ordinary everyday theory accepted by most scientists and described in all textbooks and supported by mountains of evidence gathered over a couple centuries, it is therefore your claims that are the extraordinary ones and require extraordinary evidence.PB: This is simply untrue. Evolutionism (=evolution-from-microbe-to-man) is a non sequitur from the variation observed within the MPG.
What kind of evidence do you refer to? Shared mutations and alignments? Most likely caused by NRM. Molecular biology? Not to be explained by ToE. And the fossil record is simply not in accord with evolutionism, unless you accept Gould's view. But, his ideas are merely a claim not backed up by contemporary knowledge on biology.What is your best evidence of evolutionism? I am very curious what convinced you.Best wishes,
Peter

Dear Mark,You were the one that wanted to set up definitions and it is known that it always takes a long time. Usually debates involving two (opposing) parties are about definitions. I thought I told you that in a previous mail.best wishes,
Peter

Hi Percy,You, Page and PaulK will have all your responses soon, but since you have chosen for a massive (instead of a substantial) counter attack of your outdated views on life, it will take a bit of my time to address all your mails. First, I will finish off with Page's best example of common descent: the alignment in primates. And that requires a bit of attention. I hope you understand. Thanks in advance.best wishes,
Peter