Darwin in the Genome

It must also be recalled that this point is not mutually exclusive. And that I think is the NEW criticism from creationism. I simply refer to thermodectetion mutations in the antennae of Drosophila and the temperature vestigial wing mutants my gradfather got his Phd in in the 30s.The problem really does not exist for the existence of this variation but for assumed CONTINUTIY to the strata differences even while we continue to debate the internal (chemical) heirarchies involved which may or MAY NOT need natural selection. It is entirely possible that heiracrhies of levels of organization trump considerations of levels of selection diverse. To say that one "fancies" these 'mechanisms' is one thing but to argue just becasue one can be imagined that this is the first prioty of testing with regard to genes in nature is another.So while for instance Calculus could or was applied to show that some mutations could be more likely than others if Wolfram has his insistence it is possible that simple programs rather govern the faculty able to better the MENDELISM no matter the darwin(wallace)ism.

iT COULD strengthen it, but if my suggestion that DNA is the strongest CONTACT in Faraday's pair wise listing of metals later updated to liquids then it may be MENDELISMS that garner the larger pie of molecular biology than any recursion to Gould's Structure say to argue against Mayr as Croizat stewed the bag lunch (for)...

Shouldnt the mutations that DO happen as correlated or not with those that "might" (by whatever reasoning) first be identified not biologically but physcio-chemically (if possible) by design invariances say??? It seems that Synthesists because they want this unit all to "whomselves" do not try to find a protocol that realtes the biochemisty and biophysics involved to the genetics iteself. This may be done for some limited set of genes but I see nothing on this on the whole. I would try first with behavioral genetics of thermoregulation. Certainly if other "one way" functions than mutations are supramolecularly important it is important to know this BEFORE searching for mutations and what if classes of mutations were predicatble based on the actual one vs the potenial form ones (say by some theory of the evolution of dominance) (but again it need not only be used to support a FISHER-FORD natural selection first especially if these "random" mutations have different statistical distributions offering the relation of the acutual and possible more than a corelation but a calculus instead when nothing elese emprical arises?

Use a "relic"; what's the problem here?? you all think it is but a tease?

Cap, I was refering to Will Provine's understanding of population genetics. Do these links mean that you feel free enough to ignore my question about diffusion? I can see how one may think Bayesianism plus variable RATES covers the geometry but my guess is that rigorously when one must JUSTIFY to the Haldanes of the world IN Fisher's position on Wright that such covering (function) no matter how the integration was to work (or not) is not sufficent to diminish the possibility of even arguing for orthogeneis AGAINST wrights best intentions. Dont tell me this is "incomprehensible" for IF I WAS teaching this stuff it would be known in short order but for now I must deal with my own short hand that came from having to FIRST contend with WIll PROVINE's notion of "free will" which is false and all the while KNOWING the of and now the actual acutal genetics my grandfather was familiar with in the same LAB as Wright was once.If I can seperate birds and turtles this way its not my burden but the cladists who want to further divide crocs, squamates and and turtles without even LISTENING to what I and other herpetologists have or could have said.

Peter, (B) so far you have not explained your argument at all. YOu just contnue to make assertions without support.You have not explained how redundancy is related to how easy the genes are to knock out, nor do you supply any reasoning as to how your "GuToB" would explain the mechanisms if they were redundant (indeed so far as I can tell your GuToB renders these mechanisms not only unnecesary but a potentital liabilility so it is highly questionable if their very existence is compatible with your views).
Nor do you even say how the other mechanisms from _Darwin in the Genoome_ fit inot your views.As for your final paragraph to the best of my knowledge neither Darwin nor Wallace worked with your mechanisms at all and certainly they did not have the knowledge of molecular biology required to investigate those from _Darwin in the Genome_. Nor does the book validate your other assertions.The lack of discussion seems to be due to your preference for "just so stories". Certainly you do not seem willoing to go into the necessary details to back up your claims nor do you seem willing to discuss the refutation of your original claims that the "non-random" mechanisms refuted NDT (an error based on your failure to understand the very point of the theory you vlaim to have been falsified!).

Dear Paul,[Edited irrelevant stuff]PK: Peter, (B) so far you have not explained your argument at all. YOu just contnue to make assertions without support.PB: That is because you are new here. I've explained my stance over and over and over in several threads on this board. Before Dr Caporale posted her link to her book 'Darwin in the Genome' (with exactly the same conclusion I've been repeating for months now: nonrandom mutations) several evolutionists on this board (in particular dr Page is very rude ) kicked my but, scoffed, mocked... well, the usual childish behaviour. So, I recommend to get acquianted to what I have contributed to this board over the last six months.PK: You have not explained how redundancy is related to how easy the genes are to knock out,...PB: the more redundant the gene, the easier lost through inactivating mutationsPK: ...nor do you supply any reasoning as to how your "GuToB" would explain the mechanisms if they were redundant (indeed so far as I can tell your GuToB renders these mechanisms not only unnecesary but a potentital liabilility so it is highly questionable if their very existence is compatible with your views).PB: This sounds interesting, so could you please expand. I am aware that the GUToB requires some tiny aesthetic additions, so please elaborate.PK: Nor do you even say how the other mechanisms from _Darwin in the Genoome_ fit inot your views.PB: I will fit them in. The are part of the GUToB and will find their place in the MPG. Dr Caporale's work is very timely.PK: As for your final paragraph to the best of my knowledge neither Darwin nor Wallace worked with your mechanisms at all and certainly they did not have the knowledge of molecular biology required to investigate those from _Darwin in the Genome_. Nor does the book validate your other assertions.PB: What D and W really observed was the MPG in action. Their extrapolation was entirely unwarranted. They observed an active mechanism already present in the genome (of course you are right they didn't kow about that) that generates variation over time. Now, the elucidaation of the underlying mechanisms demonstrate the extrapolation of evolution from microbe to man to be a nonsequitur. We are looking at two unequal phenomena here. The one that has been demontrated to operate in the genome to induce variation CANNOT be taken to demonstrate evolution from micobe to man. If you propose to do that than you have also to propose that evolution from microbe to man is mechanistically determined. That's creation.PK: The lack of discussion seems to be due to your preference for "just so stories".PB: I've explained my position over and over on this board; NONRANDOM mutations with repect to position and nucleotide are found in TH 1G5 gene, mtDNA and the ZFY region. All I got: denial and ignorance, so you can imagine that I am very glad with this new thread. And it confirms my opinion on evolutionism: unfair and outdated.PK: Certainly you do not seem willoing to go into the necessary details to back up your claims nor do you seem willing to discuss the refutation of your original claims that the "non-random" mechanisms refuted NDT (an error based on your failure to understand the very point of the theory you vlaim to have been falsified!).PB: I already did that and I am getting a bit tired of reiteraing the details over and over. They can be found on this board. However, I am very glad with the publication of Dr Caporale's book; it saves me a lot of time finishing my own.Best wishes,
Peter[This message has been edited by peter borger, 01-14-2003]

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Originally posted by peter borger:
Dear Primordial,

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PE: and are you able to share this knowledge? I'm sure Dr Caporale would be interested.

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PB: I discussed the consequences of non-random mutations for over six months now. All info can be found on this board. I've contacted Dr Caporale, and she concurs that such mutations indeed have implications for phylogenetics.
I already spelled out on this board in a letter to Dr Page how non-random mutations invalidate molecular evidence of common descent. It used to be the best evidence of molecular evolution, but due to the existence of non-random mutations not any more. For instance, the ZFY region is better exlained by NRM.
Not only Dr Caporale, but the entire evolutionary community should be interested.

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Best wishes,
Peter

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"Evolution? NO, GUToB!"

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[This message has been edited by peter borger, 01-13-2003]

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Peter,This is a very childish response, given that I would have expected you to be more than willing to post your conjecture as many times as possible, if you genuinely believed it had any value...something about the action of "creatons" on a "morphogenetic field" wasn't it?Given your obvious reluctance to describe your conjecture or subject it to any sort of scrutiny, your trite responses ("I have read the book and I know what it contains"), your dishonest and specious arguments on this thread, your persistent misunderstandings of the concepts you try to refute and your continual trolling, its very difficult to avoid the conclusion that you are simply seeking attention ("my theory's the best! my theory's the best!") without any kind of supporting argument or evidence. In short, you have no cogent theory which will revolutionise biology.My own opinion of your motives is that if you repeat this often enough, you're fervently hoping that it may get noticed by one of the less honourable creation science research foundations in the US who might give you a fat funding cheque for your "research" - if so, I don't know whether to wish you luck or not.PE

I must confess this isn't the direction I hoped this thread would take. I expected that PB and Dr. Caporale would engage in a longer dialogue. Dr. Caporale said that non-random mutations fit within a Darwinian framework, thereby disagreeing with PB's views on their origins. PB has ignored this but keeps painting a picture that attempts to make it seem like Dr. Caporale supports his views, like mentioning areas of inconsequential agreement such as the impact on phylogenetics and expressing support for her book. I would have liked to see a discussion about the origins of non-random mutations, which is the primary area of disagreement that evolutionists here have had with PB.--Percy

Obviously, this would have to "nonrandom" with respect to *something*. I was trying to MAKE that something out to be a more unified herpetology BEFORE cladistics became popular.Let me explain. As a Freshman at Cornell in the Into Bio Lab we were assigned a paper on "thermoregulation in the honey bee". I was somewhat acquainted with thoughts on thermoregulation in herps and I even tried as a teen ager to build and test if frogs actively thermorulate by variable behavior in response to substrate temps. In the class we measured hive temps and rate of wing beating but we did not attempt to figure out how many bees were coming and going during the time of the expt. As students were were expected to write on REGULATION of the temperature merely because there appeared a correlation with increased wing motion but I pointed out that we can not CONCLUDE that this is thermoregulation because we only know about temperature changes and behavior changes we do not know this this CAUSES the regulation. For this I was told that I was not properly interpreting the expt and was not permitted to indicate this source of error. But indeed I was correct as other work in lizard thermoregulators have expressed that one needs a standard of STABILITY from which the "regulation" can be compared. This is possible to get from bees but our "simple" expt did not provide enough data for us to categoricaly support regualtion of the heat transfer relations about the organism.The same *kind* of reasoning applies for nonrandom mutations. We need to know nonrandom with respect to what STANDARD. I propose one. You are correct the direction does not seem to be going in the way needed to relate the answer to the question.Going a step futhter I would be interested in any homology in Dimetron (permian reptile) PERPENDICULAR vertebrae bone extension morphogeny in the "thermoregulatory" 'sail' as to this as a variance in histogeny such showing againt that Owen's homology is not a dead concept but the use of cladistic programming that does not loop back to a phenetic data warehousing (something panbiogeography could provide if it caught on) seems to inhibit this kind of work and thought that this thread is headed for could so be done AND THEN correlated with stratigraphy... But once again this web site shows that the steps needed to acutally work out a problem from the c/e area to acutal science IS MUCH TOO LONG for the economics of science as it is acutally practiced today.May the c/e sites continue to exist to show the rest of us the extent the work must progress before results begin to show.

Percy-
Thank you for serving as a facilitator to stimulate discussion of the material in the book.One set of examples of non-random mutation, given in Chapter 6, are regions of the genome that encode repeat sequences such as GGGGG or CAATCAATCAAT.These repeats tend to mutate by changing in length at a rate orders of magnitude higher than the genome's overall mutation rate, and can throw the reading [which depends on a triplet code] out of frame.Because they can inactivate genes, such repeats would be expected to be selected against in much of the genome, and yet they accumulate in certain places, such as in genes in certain bacteria that are involved in host interaction.By facilitating surface variation, such repeats have the selective advantage of varying the bacteria's range of options, in terms of which tissues they can adhere to, and also by enabling the bacteria to hide from the immune response.Thus, selection can favor the emergence of non-random mutation [ie mutation in repeats become more probable than mutation elsewhere] and the alignment of non-random mutation with a biological role that provides a selective advantage [ie relative accumulation of "slippery" repeats in host-interaction genes].Lynn Caporale[This message has been edited by caporale, 01-14-2003]

My guess is that any "adherence" that you wish to refer to can be modeled from heirarchies in Gladyshev's MAcrothermodyanmics and yet you reason FROM a dynamics of surface variation. How do you account for the purely arithimetic consequences of reproducation (let us say a by out Muslim participant) and have this IN GENERAL differntiated from a position on orthogenesis. Obvously by using ACTUAL examples there is no doubt that some such reference to PROPRIETARY DATA BASE can be made but the general problem from the c/e design point (even from biodiverisity informatic points) is that the research ought to be based on accesible data to all. You are not differentiating rotational limits from rotational contrainsts between the boundary and intital conditions. Maybe with more detail about the microbiology one could but then this would probably not refer to the actual dissucussion going on here.I had suggested something else for the relation of immune body-antibody knoweldge and base PAIRING.The particular argument works from this point set to molecular adaptations to somatic programming but that requires some significant interaction with my quantity of posting to continue to discuss however consider this:THE IMPORTANCE OF HYDROPHOBIC SIDES CHAINED MAY BE N O T FIT IN THE ACTUAL INCREASE IN IMMISIBILITY WITH WATER BUT PROVIDE A MEANS FOR THE THEORETICAL PHYSICAL LINES AND FARADAY LINES OF FORCE PENETRANCE CLOSER TO THE ORGANISM (BACTERIA OR OTHERWISE). SINCE HYDROGEN BONDS AND IONICS BONDS ARE STONGER THAN THIS PROPOSED TENSE PRESSURE THE FUNCTIONAL GROUPS SUCH ARE FOUND MORE INTERNAL TO THE PROTEIN 'ANATOMY' BUT THIS DOES NOT DEPRECIATE THE PROTEINS' EFFECT (?) AS THE sIze OF THE PROTEIN COULD GET 'FAT' NONTHELESS BY MUTATIONS THAT AFFECT ONLY THE HYDROPHOBIC SIDE CHAINS.The standard would be made not to the genomic homeostasis but to the gene pool as a vapor model where repulsions as well as attractions are considered and dependent not on the proximate molecular biology but by the actual selection (not genetically engineerred kind possible by selecting homozygotic lines with hydrophic side chain breeding) that occurs in nature of the amino acid content of proteins no matter how bacteria interact with the immune system.Again what you say IS POSSIBLE but by "THUS," you reason in a way that another logic carrier could supply. I think "emergence" is a false realistic philosophy influenced by the ideology of post-Communist Marxists in actual infinity. Not all problems in genetic engineering are reducible to issues with Kuhn over gravity.What if instead the centromere acutally obeyed Newton's bucket expt for absolute force to a T?? The notion of "slip" would then confuse Maxwell's term of bodies brittle, mild and hard.Slipperly ness cognitively is a tactile notion and yet tempertature still could be more important for the uniform association you PRESUME in the repeat. Repeats may not only be about MORE Gene expression but could be entropic teleomatic program fragements for bioentropisms as adapations. Also maybe even the mean free path motions can be altered if the Dieledtric around the protein is by Newton's third law reacting. Why do you refuse to post under any of my comments??? Do you jsut think I am "reactionary"? I can accept an YES. I would disagree then.

Brad-
If you would like to examine the data for yourself, the book has extensive references to the original articles. Many of these are available on line, the rest in libraries.
Lynn

Thanks, Indeed this (is) the BOOK NOOK. I was hoping you would be interested in threading some of "our" site specific inductions in addition to promoting your own contribution. But if not, thanks again for the interaction. THAT is all I was looking for!

Dear PE,quote:
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Originally posted by peter borger:
Dear Primordial,
PE: and are you able to share this knowledge? I'm sure Dr Caporale would be interested.PB: I discussed the consequences of non-random mutations for over six months now. All info can be found on this board. I've contacted Dr Caporale, and she concurs that such mutations indeed have implications for phylogenetics.
I already spelled out on this board in a letter to Dr Page how non-random mutations invalidate molecular evidence of common descent. It used to be the best evidence of molecular evolution, but due to the existence of non-random mutations not any more. For instance, the ZFY region is better exlained by NRM.
Not only Dr Caporale, but the entire evolutionary community should be interested.Best wishes,
Peter"Evolution? NO, GUToB!"[This message has been edited by peter borger, 01-13-2003]--------------------------------------------------------------------------------PE: This is a very childish response, given that I would have expected you to be more than willing to post your conjecture as many times as possible, if you genuinely believed it had any value...something about the action of "creatons" on a "morphogenetic field" wasn't it?PB: I think childish is not the right term, but anyway. If you are interested I will make the links. It has nothing in common with creatons and morphogenetic fields, that's what some evo's on this board made of it, so they had a straw man. The GUToB I referred to is about non-random mutations in a multipurpose genome. Here you can find a brief summary of the GUToB:http://EvC Forum: molecular genetic evidence for a multipurpose genome -->EvC Forum: molecular genetic evidence for a multipurpose genomePE: Given your obvious reluctance to describe your conjecture or subject it to any sort of scrutiny, your trite responses ("I have read the book and I know what it contains"), your dishonest and specious arguments on this thread, your persistent misunderstandings of the concepts you try to refute and your continual trolling, its very difficult to avoid the conclusion that you are simply seeking attention ("my theory's the best! my theory's the best!") without any kind of supporting argument or evidence. In short, you have no cogent theory which will revolutionise biology.PB: I postulated an alternative to evolutionism, that’s all I did. Is that a crime? Everybody objective scientist knows that evolutionism is NOT explanatory. So we need something else: the GUToB. And since we are not able to scientifically explain the origin of genes from scratch (and due to ‘genetic uncertainty’) the GUToB does not address it. Although creatons and morphogenetic fields could be introduced to explain the origin, I’d rather not use these concepts for obvious reasons (=straw man attack).PE: My own opinion of your motives is that if you repeat this often enough, you're fervently hoping that it may get noticed by one of the less honourable creation science research foundations in the US who might give you a fat funding cheque for your "research" - if so, I don't know whether to wish you luck or not.PB: My motifs are NOT materialistic (I already have a very satisfying job). I simple demonstrated scientifically the validity of my theory. That’s not prohibited, is it? And the book of Dr Caporale confirms what I and others have been thinking about the genome.Best wishes,
Peter