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Another Day; Another Bad Day for Darwinism: Pt. 43

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This is from a new study published in Nature Communications, and talked about at Phys.Org.

Oh, how difficult it is these days to be an “intellectually fulfilled” neo-Darwinian:

Humans don’t like being alone, and their genes are no different. Together we are stronger, and the two versions of a gene – one from each parent – need each other. Scientists at the Max Planck Institute for Molecular Genetics in Berlin have analysed the genetic makeup of several hundred people and decoded the genetic information on the two sets of chromosomes separately. In this relatively small group alone they found millions of different gene forms. The results also show that genetic mutations do not occur randomly in the two parental chromosome sets and that they are distributed in the same ratio in everyone.

Ouch!!!!!

The results show that most genes can occur in many different forms within a population: On average, about 250 different forms of each gene exist. The researchers found around four million different gene forms just in the 400 or so genomes they analysed. This figure is certain to increase as more human genomes are examined. More than 85 percent of all genes have no predominant form which occurs in more than half of all individuals. This enormous diversity means that over half of all genes in an individual, around 9,000 of 17,500, occur uniquely in that one person – and are therefore individual in the truest sense of the word.

Uh oh. What happened to “purifying selection”? Ouch!!!!

According to the researchers, mutations of genes are not randomly distributed between the parental chromosomes. They found that 60 percent of mutations affect the same chromosome set and 40 percent both sets. Scientists refer to these as cis and trans mutations, respectively. Evidently, an organism must have more cis mutations, where the second gene form remains intact. “It’s amazing how precisely the 60:40 ratio is maintained. It occurs in the genome of every individual – almost like a magic formula,” says Hoehe. The 60:40 distribution ratio appears to be essential for survival. “This formula may help us to understand how gene variability occurs and how it affects gene function.”

Double Ouch!!!!!

The gene, as we imagined it, exists only in exceptional cases. “We need to fundamentally rethink the view of genes that every schoolchild has learned since Gregor Mendel’s time. Moreover, the conventional view of individual mutations is no longer adequate. Instead, we have to consider the two gene forms and their combination of variants,” Hoehe explains. When analysing genomes, scientists should therefore examine each parental gene form separately, as well as the effects of both forms as a pair.

What’s that you say? Oh, you’re going to take your bat and go home now? I understand.

Yikes!!! Could it get any worse for the Darwinists? Just wait for tomorrow. . . . .

Comments
Dionisio: Your "intrusions" are always appreciated! :)gpuccio
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Zachriel: "That’s not the opinion of the researchers, who state that the diplotypic proteome provides a “‘major modulating principle’ generating diverse cellular and physiological outcomes in individual organisms, and at the population level giving rise to phenotypic diversity, adaptive and evolutionary processes”. This is something that is subject to further investigation." And: "If it has a function, then it is subject to selection. This seems to contradict your previous comment." I think you have not taken the time to read my post carefully. OK, it happens to the best! I quote my answer to wd400:
Ehm, here you seem to mix two different arguments, and none of them is relevant to the thing you are commenting (“More than 85 percent of all genes have no predominant form which occurs in more than half of all individual”). The thing you are apparently commenting (“More than 85 percent of all genes have no predominant form which occurs in more than half of all individual”) is interesting. It is not really a surprise, but the quantification of diversity at the gene level is an important fact. However, you say nothing about that aspect. Instead, you comment on other aspects, mixing two arguments. First, you say that: “If you take genes that have many variant sites (including synonymous ones), mix those up by recombination then package them into sets of two. Most of the time no single set of two genes is going to occur in 50% of people.” Correct. That is basic probability in a random system. But there is no reason to get a rather repetitive ratio of about 60:40, and there is no reason at all that that ration be connected to function
. Emphasis added. So, here I am saying that if, as suggested by wd400, there is nothing special in having different proportions (because "Most of the time no single set of two genes is going to occur in 50% of people."), it is however certainly true that there is no reason to get a rather repetitive ratio of about 60:40, and there is no reason at all that that ratio be connected to function. This is one concept. Then I say:
Surprisingly, you go on: “The paper found very strong evidence for purifying selection, if you care to read it.” So, with an interesting jump of thought, now you are admitting that there is something to be explained, and you just assume that it can be explained by “purifying selection”. I need not remind you that: “In natural selection, negative selection[1] or purifying selection is the selective removal of alleles that are deleterious. This can result in stabilizing selection through the purging of deleterious variations that arise.” (Wikipedia) Therefore, purifying selection can have no role in finding a functional pattern. It can just maintain it. I think that you would have more chances if you tried to attribute the observed pattern to positive selection.
I can see no contradiction in what I say. And my final statement is:
The paper says that the combination of variants have specific recurring distributions, and that those distributions are connected to specific functional sets of genes and therefore to functional regulation. For good or bad (see the part about tumors). Now, true or false that it may be, that is not trivial. And it requires a rethinking. Therefore, I am interested. And I am available to rethink, even if for now I am not sure about how to rethink.
IOWs, I disagree with wd400 and I find the paper very interesting, and I don't think that we have an immediate explanation for those findings. That's why it is interesting.gpuccio
December 1, 2014
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So something that doesn't have a function isn't subject to natural selection? Really?Joe
December 1, 2014
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gpuccio: But there is no reason to get a rather repetitive ration of about 60:40, and there is no reason at all that that ration be connected to function. That's not the opinion of the researchers, who state that the diplotypic proteome provides a "‘major modulating principle’ generating diverse cellular and physiological outcomes in individual organisms, and at the population level giving rise to phenotypic diversity, adaptive and evolutionary processes". This is something that is subject to further investigation. gpuccio: The paper says that the combination of variants have specific recurring distributions, and that those distributions are connected to specific functional sets of genes and therefore to functional regulation. If it has a function, then it is subject to selection. This seems to contradict your previous comment.Zachriel
December 1, 2014
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gpuccio, Thanks for taking the time to 'surgically' dissect wd400's comment. You are a Dr. in more ways than one! :) A question, Does not the whole issue of the 60/40 split not strongly suggest that the gene is not nearly as important as Darwinists have maintained, and also that there is a top down control of genes that Darwinists did not, indeed that they could not, anticipate in their 'bottom up' scheme of reductive materialism? i.e. Does not the paper strongly support James Shapiro's, Richard Sternberg's, and others', contention that the traditional ‘Mendelian’ view of the gene, which the modern synthesis is built upon, is wrong? https://uncommondescent.com/intelligent-design/another-day-another-bad-day-for-darwinism-pt-43/#comment-533308bornagain77
December 1, 2014
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gpuccio Please, forgive me for my unsolicited intrusion into your discussion with your interlocutor. I just wanted to make sure that everybody sees clearly the important issues you pointed at in your insightful comments. Now, let's hope that your interlocutor responds with matching clarity and with the same level of attention to details. :)Dionisio
December 1, 2014
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Review of the insightful post #35 by gpuccio in reference to post #26 by wd400:
While I certainly agree that the press release is not a good description of the paper (which is not really surprising, that is usually the case), I have to disagree with other statements you [wd400] make:
“If you read the paper you’ll see they don’t actually detect de novomutations, just variants, so there results won’t tell us anything about the randomness of mutation. What’s more, when evolutionary biologists say mutations are random when mean random with respect to fitness — not “distributed in the same ration in everyone”.”[wd400]
But the most interesting part of the paper is exactly the connection of the differential distribution of variation with function.
“This is not even a little bit suprising. If you take genes that have many variant sites (including synonymous ones), mix those up by recombination then package them into sets of two. Most of the time no single set of two genes is going to occur in 50% of people. The paper found very strong evidence for purifying selection, if you care to read it.”[wd400]
Ehm, here you [wd400] seem to mix two different arguments, and none of them is relevant to the thing you [wd400] are commenting (“More than 85 percent of all genes have no predominant form which occurs in more than half of all individual”). The thing you [wd400] are apparently commenting (“More than 85 percent of all genes have no predominant form which occurs in more than half of all individual”) is interesting. It is not really a surprise, but the quantification of diversity at the gene level is an important fact. However, you [wd400] say nothing about that aspect. Instead, you [wd400] comment on other aspects, mixing two arguments. First, you [wd400] say that:
“If you take genes that have many variant sites (including synonymous ones), mix those up by recombination then package them into sets of two. Most of the time no single set of two genes is going to occur in 50% of people.”[wd400]
Correct. That is basic probability in a random system. But there is no reason to get a rather repetitive ration of about 60:40, and there is no reason at all that that ration be connected to function. Surprisingly, you [wd400] go on:
“The paper found very strong evidence for purifying selection, if you care to read it.”[wd400]
So, with an interesting jump of thought, now you [wd400] are admitting that there is something to be explained, and you [wd400] just assume that it can be explained by “purifying selection”. I need not remind you [wd400] that: “In natural selection, negative selection[1] or purifying selection is the selective removal of alleles that are deleterious. This can result in stabilizing selection through the purging of deleterious variations that arise.” (Wikipedia) Therefore, purifying selection can have no role in finding a functional pattern. It can just maintain it. I think that you [wd400] would have more chances if you [wd400] tried to attribute the observed pattern to positive selection. You [wd400] say:
“Such nonsense is pretty common — the only question is anyone think these results require such a rethink. All they’ve shown (as far I can tell, parts of the paper are nearly unparsable) is that for any gene there are more combinations of two variants than there are variants, which is not really groundbreaking…”[wd400]
No. The paper says that the combination of variants have specific recurring distributions, and that those distributions are connected to specific functional sets of genes and therefore to functional regulation. For good or bad (see the part about tumors). Now, true or false that it may be, that is not trivial. And it requires a rethinking. Therefore, I am interested. And I am available to rethink, even if for now I am not sure about how to rethink. Are you [wd400]?
Obviously, now the ball is in wd400's court. :)Dionisio
December 1, 2014
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Please, let's read carefully gpuccio's post #35, so we all, specially onlookers/lurkers can see clearly what is discussed here. Thank you.Dionisio
December 1, 2014
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Post #35 is a very important correction of mistakes found in post #26. The grammar/syntax issues highlighted in post #36 are irrelevant in comparison to the more relevant issues indicated in post #35. The author of post #26 may disregard my post #36 and better figure out how to answer the questions raised by post #35. :)Dionisio
December 1, 2014
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@26
If you read the paper you’ll see they don’t actually detect de novomutations, just variants, so there results won’t tell us anything about the randomness of mutation.
there results? "..., so there results won’t tell..." Should it read "their results" ? Also, where it reads "...de novomutations..." should it say "...de novo mutations..." ? [It's not easy to post comments from a mobile device with an 'autocorrect' feature on. Words get replaced by unintended ones. This blog has added an editing feature that allows corrections a few minutes after posting the comments. However, grammatical/syntactical errors can be found in my comments too. Please, bring them up to my attention. Thank you.] :)Dionisio
December 1, 2014
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wd400: While I certainly agree that the press release is not a good description of the paper (which is not really surprising, that is usually the case), I have to disagree with other statements you make: "If you read the paper you’ll see they don’t actually detect de novomutations, just variants, so there results won’t tell us anything about the randomness of mutation. What’s more, when evolutionary biologists say mutations are random when mean random with respect to fitness — not “distributed in the same ration in everyone”." But the most interesting part of the paper is exactly the connection of the differential distribution of variation with function. "This is not even a little bit suprising. If you take genes that have many variant sites (including synonymous ones), mix those up by recombination then package them into sets of two. Most of the time no single set of two genes is going to occur in 50% of people. The paper found very strong evidence for purifying selection, if you care to read it." Ehm, here you seem to mix two different arguments, and none of them is relevant to the thing you are commenting ("More than 85 percent of all genes have no predominant form which occurs in more than half of all individual"). The thing you are apparently commenting ("More than 85 percent of all genes have no predominant form which occurs in more than half of all individual") is interesting. It is not really a surprise, but the quantification of diversity at the gene level is an important fact. However, you say nothing about that aspect. Instead, you comment on other aspects, mixing two arguments. First, you say that: "If you take genes that have many variant sites (including synonymous ones), mix those up by recombination then package them into sets of two. Most of the time no single set of two genes is going to occur in 50% of people." Correct. That is basic probability in a random system. But there is no reason to get a rather repetitive ration of about 60:40, and there is no reason at all that that ration be connected to function. Surprisingly, you go on: "The paper found very strong evidence for purifying selection, if you care to read it." So, with an interesting jump of thought, now you are admitting that there is something to be explained, and you just assume that it can be explained by "purifying selection". I need not remind you that: "In natural selection, negative selection[1] or purifying selection is the selective removal of alleles that are deleterious. This can result in stabilizing selection through the purging of deleterious variations that arise." (Wikipedia) Therefore, purifying selection can have no role in finding a functional pattern. It can just maintain it. I think that you would have more chances if you tried to attribute the observed pattern to positive selection. You say: "Such nonsense is pretty common — the only question is anyone think these results require such a rethink. All they’ve shown (as far I can tell, parts of the paper are nearly unparsable) is that for any gene there are more combinations of two variants than there are variants, which is not really groundbreaking…" No. The paper says that the combination of variants have specific recurring distributions, and that those distributions are connected to specific functional sets of genes and therefore to functional regulation. For good or bad (see the part about tumors). Now, true or false that it may be, that is not trivial. And it requires a rethinking. Therefore, I am interested. And I am available to rethink, even if for now I am not sure about how to rethink. Are you?gpuccio
December 1, 2014
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wd400:
PaV You summarised the press release about the paper because you thought it presented a problem for “Darwinism”. In fact, it doesn’t, and it’s not even about what you thought was about. Given that, I think it’s probably not a good idea to go casting aspersions on other people.
In my opinion information that is none the less helpful to a serious Theory of Intelligent Design is a problem for the belief system known as “Darwinism”, which teaches that such a theory is scientifically impossible. wd400:
But I don’t really care about that. What’s suprising to me is that non other IDers could point out how wrong you were, and the many problems in the press release and this post.
I find it wonderful to see an effort like this that will leave no stone unturned, sort of speak. And check out the terabytes of data the paper links to!
Data access Sequence alignments and haplotypes for all molecularly phased genomes are available from the website http://www.molgen.mpg.de/~genetic-variation/ngs_data/ . In addition, haplotypes for all molecularly phased genomes can be viewed in a UCSC browser session at http://www.molgen.mpg.de/~genetic-variation/UCSC_12phasedgenomes . Data files related to gene categories, the ‘CDP’ and ‘phase-alternate’ genes can be downloaded from http://www.molgen.mpg.de/~genetic-variation/diploid_landscape/ .
You can't model that using Darwinian theory. But you can with the ID theory that I'm willing to defend. Are you willing to help? What language(s) do you prefer to code in?Gary S. Gaulin
November 30, 2014
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why of course wd400, no empirical finding is ever a problem for Darwinism, just like nothing is ever a problem for the 'science' of crystal ball reading: :) And you think we aren't as smart as you because we just don't understand that nothing can ever be a problem for Darwinism! “Being an evolutionist means there is no bad news. If new species appear abruptly in the fossil record, that just means evolution operates in spurts. If species then persist for eons with little modification, that just means evolution takes long breaks. If clever mechanisms are discovered in biology, that just means evolution is smarter than we imagined. If strikingly similar designs are found in distant species, that just means evolution repeats itself. If significant differences are found in allied species, that just means evolution sometimes introduces new designs rapidly. If no likely mechanism can be found for the large-scale change evolution requires, that just means evolution is mysterious. If adaptation responds to environmental signals, that just means evolution has more foresight than was thought. If major predictions of evolution are found to be false, that just means evolution is more complex than we thought.” ~ Cornelius Hunter "In other words, we do not fully understand how evolution works at the molecular level." Philip Ball http://www.evolutionnews.org/2013/04/genetics_is_too071621.html http://www.nature.com/nature/journal/v496/n7446/full/496419a.htmlbornagain77
November 30, 2014
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PaV You summarised the press release about the paper because you thought it presented a problem for "Darwinism". In fact, it doesn't, and it's not even about what you thought was about. Given that, I think it's probably not a good idea to go casting aspersions on other people. But I don't really care about that. What's suprising to me is that non other IDers could point out how wrong you were, and the many problems in the press release and this post.wd400
November 30, 2014
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as to wd400: "That y’all could be so excited by such a confused write up of such an appalling press release about such an average paper speaks volumes about where ID stands." Translation 1 "Nothing to see here" :) https://www.youtube.com/watch?v=rSjK2Oqrgic Translation 2 "You just don't understand evolution" :) Reminder to wd400, Darwinism does not even qualify as a proper science in the first place but is instead a pseudo-science! This pseudo-scientific description includes your own field of population genetics wd400!: Lynn Margulis Criticizes Neo-Darwinism in Discover Magazine (Updated) - Casey Luskin April 12, 2011 Excerpt: Population geneticist Richard Lewontin gave a talk here at UMass Amherst about six years ago, and he mathemetized all of it--changes in the population, random mutation, sexual selection, cost and benefit. At the end of his talk he said, "You know, we've tried to test these ideas in the field and the lab, and there are really no measurements that match the quantities I've told you about." This just appalled me. So I said, "Richard Lewontin, you are a great lecturer to have the courage to say it's gotten you nowhere. But then why do you continue to do this work?" And he looked around and said, "It's the only thing I know how to do, and if I don't do it I won't get grant money." - Lynn Margulis - biologist http://www.evolutionnews.org/2011/04/lynn_margulis_criticizes_neo-d045691.html The main reason why Darwinian evolution is more properly thought of as a pseudo-science instead of a proper science is because Darwinian evolution has no rigid mathematical basis, like other overarching physical theories of science do. A rigid mathematical basis in order to potentially falsify it (in fact, in so far as math can be applied to Darwinian claims, mathematics constantly shows us that Darwinian evolution is astronomically unlikely),, “On the other hand, I disagree that Darwin’s theory is as `solid as any explanation in science.; Disagree? I regard the claim as preposterous. Quantum electrodynamics is accurate to thirteen or so decimal places; so, too, general relativity. A leaf trembling in the wrong way would suffice to shatter either theory. What can Darwinian theory offer in comparison?” - Berlinski, D., “A Scientific Scandal?: David Berlinski & Critics,” Commentary, July 8, 2003 WHAT SCIENTIFIC IDEA IS READY FOR RETIREMENT? Evolution is True - Roger Highfield - January 2014 Excerpt:,,, Whatever the case, those universal truths—'laws'—that physicists and chemists all rely upon appear relatively absent from biology. Little seems to have changed from a decade ago when the late and great John Maynard Smith wrote a chapter on evolutionary game theory for a book on the most powerful equations of science: his contribution did not include a single equation. http://www.edge.org/response-detail/25468 Darwinians Try to Usurp Biomimetics Popularity - October 9, 2014 Excerpt: "it is remarkable, therefore, that formal mathematical, rather than verbal, proof of the fact that natural selection has an optimizing tendency was still lacking after a century and a half later.",,, More importantly, its proponents are still struggling, a century and a half after Darwin, to provide evidence and the mathematical formalism to demonstrate that random natural processes have the creative power that Darwin, Dawkins, and others claim it has. Everyone already knows that intelligent causes have such creative power. http://www.evolutionnews.org/2014/10/darwinians_try090231.html Active Information in Metabiology – Winston Ewert, William A. Dembski, Robert J. Marks II – 2013 Except page 9: Chaitin states [3], “For many years I have thought that it is a mathematical scandal that we do not have proof that Darwinian evolution works.” In fact, mathematics has consistently demonstrated that undirected Darwinian evolution does not work.,, Consistent with the laws of conservation of information, natural selection can only work using the guidance of active information, which can be provided only by a designer. http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2013.4/BIO-C.2013.4 Chaitin is quoted at 10:00 minute mark of following video in regards to Darwinism lack of a mathematical proof - Dr. Marks also comments on the honesty of Chaitin in personally admitting that his long sought after mathematical proof for Darwinian evolution failed to deliver the goods. https://www.youtube.com/watch?v=No3LZmPcwyg&feature=player_detailpage#t=600 As mentioned in the preceding paper, not only does Darwinism fail to have a mathematical proof that can be tested against, to the extent that math can be applied to Darwinian claims, mathematics has consistently demonstrated that undirected Darwinian evolution does not work Using Numerical Simulation to Test the Validity of Neo-Darwinian Theory - 2008 Abstract: Evolutionary genetic theory has a series of apparent “fatal flaws” which are well known to population geneticists, but which have not been effectively communicated to other scientists or the public. These fatal flaws have been recognized by leaders in the field for many decades—based upon logic and mathematical formulations. However population geneticists have generally been very reluctant to openly acknowledge these theoretical problems, and a cloud of confusion has come to surround each issue. Numerical simulation provides a definitive tool for empirically testing the reality of these fatal flaws and can resolve the confusion. The program Mendel’s Accountant (Mendel) was developed for this purpose, and it is the first biologically-realistic forward-time population genetics numerical simulation program. This new program is a powerful research and teaching tool. When any reasonable set of biological parameters are used, Mendel provides overwhelming empirical evidence that all of the “fatal flaws” inherent in evolutionary genetic theory are real. This leaves evolutionary genetic theory effectively falsified—with a degree of certainty which should satisfy any reasonable and open-minded person. http://www.icr.org/i/pdf/technical/Using-Numerical-Simulation-to-Test-the-Validity-of-Neo-Darwinian-Theory.pdf Using Numerical Simulation to Better Understand Fixation Rates, and Establishment of a New Principle - "Haldane's Ratchet" - Christopher L. Rupe and John C. Sanford - 2013 Excerpt: We then perform large-scale experiments to examine the feasibility of the ape-to-man scenario over a six million year period. We analyze neutral and beneficial fixations separately (realistic rates of deleterious mutations could not be studied in deep time due to extinction). Using realistic parameter settings we only observe a few hundred selection-induced beneficial fixations after 300,000 generations (6 million years). Even when using highly optimal parameter settings (i.e., favorable for fixation of beneficials), we only see a few thousand selection-induced fixations. This is significant because the ape-to-man scenario requires tens of millions of selective nucleotide substitutions in the human lineage. Our empirically-determined rates of beneficial fixation are in general agreement with the fixation rate estimates derived by Haldane and ReMine using their mathematical analyses. We have therefore independently demonstrated that the findings of Haldane and ReMine are for the most part correct, and that the fundamental evolutionary problem historically known as "Haldane's Dilemma" is very real. Previous analyses have focused exclusively on beneficial mutations. When deleterious mutations were included in our simulations, using a realistic ratio of beneficial to deleterious mutation rate, deleterious fixations vastly outnumbered beneficial fixations. Because of this, the net effect of mutation fixation should clearly create a ratchet-type mechanism which should cause continuous loss of information and decline in the size of the functional genome. We name this phenomenon "Haldane's Ratchet". http://media.wix.com/ugd/a704d4_47bcf08eda0e4926a44a8ac9cbfa9c20.pdf ============= Verse and Music: Romans 8:20-21 For the creation was subjected to futility, not willingly, but because of him who subjected it, in hope that the creation itself will be set free from its bondage to corruption and obtain the freedom of the glory of the children of God. 7eventh Time Down "Just Say Jesus" https://www.youtube.com/watch?v=T8CLgiYZyZEbornagain77
November 30, 2014
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wd400:
That y’all could be so excited by such a confused write up of such an appalling press release about such an average paper speaks volumes about where ID stands.
Yes. You're right. We're ahead of the curve!!! :)PaV
November 30, 2014
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From the paper:
Our global view of haplotype/diplotype diversity in relation to population size suggests that current efforts are still far from capturing the majority of gene forms and that saturation may not even be achievable. The concept of a predominant, ‘wild-type’form of ‘the’ gene appears obsolete for over 85% of genes,challenging traditional ‘Mendelian’ views. This highlights the need for an expansion of current concepts of ‘the’ gene,along with the development of appropriate documentation and language
wd400: If "wild-type" forms of genes seem obsolete, then population genetics, built upon such an analysis, seems, to a "85% degree, also to be "obsolete." I did not find any references to either "purifying selection" or "negative selection" when I searched the paper.PaV
November 30, 2014
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wd400: Your response tells us a lot about Darwinists. The theory is never wrong. The theory is never in doubt. There's nothing new here; we've known this for years. Etc. The same reaction with "junk-DNA." No one ever called it that!! we're told. Yet, where did the name come from? And now study after study confirms the ID prediction that "genes" are but a tool set, and it is the regulatory mechanisms that control the use of these genes that is primary, much of this located in so-called "junk-DNA." Retrotransposons. Same thing. This is proof that random processes are at work and confirmation of "common descent." And, now, studies hint at a very critical role for these structures, and that perhaps they are the cause of "uncommon descent"; i.e., the source of regulatory mechanisms that make species what they are. The intellectual structure of Darwinism is collapsing, beam by beam. Another Day; Another Bad Day for Darwinism. This has now reached the status of "Moore's Law."PaV
November 30, 2014
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gpuccio:
The importance of polarization in biology, be it male-female or of other kinds, cannot be denied.
I love your optimism but I'm relatively confident that some of the excuse makers will brush-off the importance of male-female polarization with another "Natural selection did it" type answer that explains absolutely nothing about its purpose, or how said phenomenon works. We also have two brain hemispheres instead of one single twice as large system Darwinian theory can be used to predict should have "evolved", which can be denied by resorting to religious philosophy nonscience where the redundant hemisphere (or other polarization) becomes a "bad design", which is in turn used to claim victory for their side. gpuccio:
I have often argued that the most universal property of any living system is probably the ability to generate a difference between what is “out” and what is “in” by an active, intelligently engineered delimitation (a membrane).
I understand what you are saying. This is where we find membrane enclosed chromosome territories that input and output to others through channels where signaling molecules and products flow like through a pipeline or highway (and in the case of signaling molecules flow like through a wire to transmit control signals from place to place). gpuccio:
Asymmetric cell polarization and division is another fundamental example, really essential to the advent of multicellularity.
Yes. The ID theory I'm developing predicts that this male-female based behavior can also be expressed by cell(ular) level intelligence, detectable in cell polarization and division. Although there is some humor in my speculation: maybe the male is the half that goes off to work (differentiates) while the female half takes care of other chores required to keep them both alive. I recall a study that found a 50/50 sharing of workload does not work in a partnership. From my experience around 60/40 is needed or else work and chores take longer to get done or never finished at all. Being too alike can lead to bad marriages. At least one has to like to cook (I don't) or both can end up living on junk food. Where both love cooking it's easy to quickly become overweight. In our case it works out so my thinness from skipping meals rubs off on my wife who would weigh much more where I instead liked to help her overeat. The paper seems to explaining this sort of 60/40 duality in our parental alleles. There is still something "golden ratio" about it, but how that can be and what it all means gets us totally into uncharted scientific territory. But thankfully not all are afraid of such a demanding voyage of discovery, into what makes us intelligent and how intelligent cause works.Gary S. Gaulin
November 30, 2014
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That y'all could be so excited by such a confused write up of such an appalling press release about such an average paper speaks volumes about where ID stands. From the OP.
The results also show that genetic mutations do not occur randomly in the two parental chromosome sets and that they are distributed in the same ratio in everyone.
If you read the paper you'll see they don't actually detect de novomutations, just variants, so there results won't tell us anything about the randomness of mutation. What's more, when evolutionary biologists say mutations are random when mean random with respect to fitness -- not "distributed in the same ration in everyone".
More than 85 percent of all genes have no predominant form which occurs in more than half of all individual
This is not even a little bit suprising. If you take genes that have many variant sites (including synonymous ones), mix those up by recombination then package them into sets of two. Most of the time no single set of two genes is going to occur in 50% of people. The paper found very strong evidence for purifying selection, if you care to read it.
“We need to fundamentally rethink the view of genes that every schoolchild has learned since Gregor Mendel’s time. Moreover, the conventional view of individual mutations is no longer adequate.
Such nonsense is pretty common -- the only question is anyone think these results require such a rethink. All they've shown (as far I can tell, parts of the paper are nearly unparsable) is that for any gene there are more combinations of two variants than there are variants, which is not really groundbreaking... From the comments we have this
However, there is evidence that in cancer, for example, the severity and course of the disease is determined by the wrong distribution of a mutation.
Which doesn't appear to mean anything, and
This dual gene and protein arrangement has the advantage that it allows the activity of genes to be more flexibly adjusted and altered. By using the more favourable variant, the body is better able to adapt to changes in its own processes and to environmental conditions.
Which is purest speculation, based on no finding in the paper and with no plausable mechanismwd400
November 30, 2014
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Gary S. Gaulin: The importance of polarization in biology, be it male-female or of other kinds, cannot be denied. I have often argued that the most universal property of any living system is probably the ability to generate a difference between what is "out" and what is "in" by an active, intelligently engineered delimitation (a membrane). Asymmetric cell polarization and division is another fundamental example, really essential to the advent of multicellularity.gpuccio
November 30, 2014
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ppolish at #18: Prompted by the recent post on the golden ratio, I had noticed that too. If you look at the original paper (table 1), you can see that the ratio, in the most numerous set (372EUR) is 61.7 to 38.3. The difference with the golden ratio is only 0.0071. A very good approximation, I would say! :)gpuccio
November 29, 2014
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The original paper in Nature Communications: http://www.nature.com/ncomms/2.....s6569.html
And it's open access too. That's sure a plus. What most scientifically matters to the ID movement is to further explain how intelligent cause works, which requires knowing more about the importance of diploidy. From abstract:
This work identifies key features characterizing the diplotypic nature of human genomes and provides a conceptual and analytical framework, rich resources and novel hypotheses on the functional importance of diploidy.
The ID theory I'm developing suggests that evidence is leading to a (earlier mentioned in comment #12) bidirectional associative memory type system. Or in other words: inside our cell nuclei, man and woman (2 parental alleles of 23 chromosomes each) are intelligently working together as one to keep all of mankind going. This new insight also has a way of adding new meaning to Genesis:
New International Version So God created mankind in his own image, in the image of God he created them; male and female he created them.
A scientific theory that's able to do all this is most empowering to Biblical "creationism" and "creationist". This way ID theory meets expectations as something truly different that makes exciting predictions.Gary S. Gaulin
November 29, 2014
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Further notes along that line
Physiology is rocking the foundations of evolutionary biology - Denis Noble - 17 MAY 2013 Excerpt: The ‘Modern Synthesis’ (Neo-Darwinism) is a mid-20th century gene-centric view of evolution, based on random mutations accumulating to produce gradual change through natural selection.,,, We now know that genetic change is far from random and often not gradual.,,, http://onlinelibrary.wiley.com/doi/10.1113/expphysiol.2012.071134/abstract “The genome is an ‘organ of the cell’, not its dictator” - Denis Nobel – President of the International Union of Physiological Sciences Die, selfish gene, die - The selfish gene is one of the most successful science metaphors ever invented. Unfortunately, it’s wrong - Dec. 2013 Excerpt: But 15 years after Hamilton and Williams kited [introduced] this idea, it was embraced and polished into gleaming form by one of the best communicators science has ever produced: the biologist Richard Dawkins. In his magnificent book The Selfish Gene (1976), Dawkins gathered all the threads of the modern synthesis — Mendel, Fisher, Haldane, Wright, Watson, Crick, Hamilton, and Williams — into a single shimmering magic carpet (called the selfish gene). Unfortunately, say Wray, West-Eberhard and others, it’s wrong. https://uncommondescent.com/darwinism/epigenetics-dawkins-selfish-gene-discredited-by-still-more-scientists-you-should-have-heard-of/
And for cherry on the cake, not only is 'the selfish gene' wrong, Dr. Trifonov states that the concept of the selfish gene 'inflicted an immense damage to biological sciences', for over 30 years:
Second, third, fourth… genetic codes - One spectacular case of code crowding - Edward N. Trifonov - video (quoted at the 10:30 minute mark of the video) https://vimeo.com/81930637
ringo, of course there is much more than can be brought out of this paper as gpuccio and others will probably do, but I hope that this helps clarify why this paper is so damaging to neo-Darwinism.bornagain77
November 29, 2014
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Ringo, to put the problem for the modern synthesis of neo-Darwinism more simply, (and far less flippantly than I did before), it is good to look at this excerpt from the discussion portion of the paper:
Multiple haplotype-resolved genomes reveal population patterns of gene and protein diplotypes - 26 November 2014 Excerpt Discussion: Our global view of haplotype/diplotype diversity in relation to population size suggests that current efforts are still far from capturing the majority of gene forms and that saturation may not even be achievable. The concept of a predominant, ‘wild-type’ form of ‘the’ gene appears obsolete for over 85% of genes, challenging traditional ‘Mendelian’ views. This highlights the need for an expansion of current concepts of ‘the’ gene^29, along with the development of appropriate documentation and language. The enormous diversity of haploid and diploid gene forms raises fundamental questions concerning the relationships between sequence(s), structure(s) and function(s)^21 http://www.nature.com/ncomms/2014/141126/ncomms6569/full/ncomms6569.html
Towards the latter half of the following podcast, Dr Sternberg, who has a PhD in evolutionary biology, elucidates how the overturning/loss of the 'gene' as the central unit of inheritance turns the modern synthesis of neo-Darwinism from a science into no better than the disgarded alchemy or Ptolemy astronomy of yesteryear.
Podcast - Richard Sternberg PhD - On Human Origins: Is Our Genome Full of Junk DNA? Part 5 (emphasis on ENCODE and the loss of the term 'gene' as a accurate description in biology and how that loss undermines the modern synthesis of neo-Darwinism) http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna-pt-5/
This paper is not the first to call for a redefinition of the concept of the gene. ENCODE called for a redefinition as well:
Landscape of transcription in human cells – Sept. 6, 2012 Excerpt: Here we report evidence that three-quarters of the human genome is capable of being transcribed, as well as observations about the range and levels of expression, localization, processing fates, regulatory regions and modifications of almost all currently annotated and thousands of previously unannotated RNAs. These observations, taken together, prompt a redefinition of the concept of a gene.,,, Isoform expression by a gene does not follow a minimalistic expression strategy, resulting in a tendency for genes to express many isoforms simultaneously, with a plateau at about 10–12 expressed isoforms per gene per cell line. http://www.nature.com/nature/journal/v489/n7414/full/nature11233.html Time to Redefine the Concept of a Gene? - Sept. 10, 2012 Excerpt: As detailed in my second post on alternative splicing, there is one human gene that codes for 576 different proteins, and there is one fruit fly gene that codes for 38,016 different proteins! While the fact that a single gene can code for so many proteins is truly astounding, we didn’t really know how prevalent alternative splicing is. Are there only a few genes that participate in it, or do most genes engage in it? The ENCODE data presented in reference 2 indicates that at least 75% of all genes participate in alternative splicing. They also indicate that the number of different proteins each gene makes varies significantly, with most genes producing somewhere between 2 and 25. Based on these results, it seems clear that the RNA transcripts are the real carriers of genetic information. This is why some members of the ENCODE team are arguing that an RNA transcript, not a gene, should be considered the fundamental unit of inheritance. http://networkedblogs.com/BYdo8
As Dr. Bohlin points out in the following video, this ain't your Grandaddy's gene anymore,,,
The Extreme Complexity Of Genes - Dr. Raymond G. Bohlin https://vimeo.com/106012299
James Shapiro echos much the same sentiment as Dr. Sternberg did in the podcast
Why the 'Gene' Concept Holds Back Evolutionary Thinking - James Shapiro - 11/30/2012 Excerpt: The Century of the Gene. In a 1948 Scientific American article, soon-to-be Nobel Laureate George Beadle wrote: "genes are the basic units of all living things.",,, This notion of the genome as a collection of discrete gene units prevailed when the neo-Darwinian "Modern Synthesis" emerged in the pre-DNA 1940s. Some prominent theorists even proposed that evolution could be defined simply as a change over time in the frequencies of different gene forms in a population.,,, The basic issue is that molecular genetics has made it impossible to provide a consistent, or even useful, definition of the term "gene." In March 2009, I attended a workshop at the Santa Fe Institute entitled "Complexity of the Gene Concept." Although we had a lot of smart people around the table, we failed as a group to agree on a clear meaning for the term. The modern concept of the genome has no basic units. It has literally become "systems all the way down." There are piecemeal coding sequences, expression signals, splicing signals, regulatory signals, epigenetic formatting signals, and many other "DNA elements" (to use the neutral ENCODE terminology) that participate in the multiple functions involved in genome expression, replication, transmission, repair and evolution.,,, Conventional thinkers may claim that molecular data only add details to a well-established evolutionary paradigm. But the diehard defenders of orthodoxy in evolutionary biology are grievously mistaken in their stubbornness. DNA and molecular genetics have brought us to a fundamentally new conceptual understanding of genomes, how they are organized and how they function. http://www.huffingtonpost.com/james-a-shapiro/why-the-gene-concept-hold_b_2207245.html
The loss of the gene as a unifying concept for neo-Darwinism is of no small importance. The entire edifice of the modern synthesis of neo-Darwinism is built upon the idea of the 'gene' as the central unit of inheritance, i.e. is built upon the idea of 'the selfish gene'.
Modern Synthesis Of Neo-Darwinism Is False – Denis Nobel – video http://www.metacafe.com/w/10395212 ,, In the preceding video, Dr Nobel states that around 1900 there was the integration of Mendelian (discrete) inheritance with evolutionary theory, and about the same time Weismann established what was called the Weismann barrier, which is the idea that germ cells and their genetic materials are not in anyway influenced by the organism itself or by the environment. And then about 40 years later, circa 1940, a variety of people, Julian Huxley, R.A. Fisher, J.B.S. Haldane, and Sewell Wright, put things together to call it ‘The Modern Synthesis’. So what exactly is the ‘The Modern Synthesis’? It is sometimes called neo-Darwinism, and it was popularized in the book by Richard Dawkins, ‘The Selfish Gene’ in 1976. It’s main assumptions are, first of all, is that it is a gene centered view of natural selection. The process of evolution can therefore be characterized entirely by what is happening to the genome. It would be a process in which there would be accumulation of random mutations, followed by selection. (Now an important point to make here is that if that process is genuinely random, then there is nothing that physiology, or physiologists, can say about that process. That is a very important point.) The second aspect of neo-Darwinism was the impossibility of acquired characteristics (mis-called “Larmarckism”). And there is a very important distinction in Dawkins’ book ‘The Selfish Gene’ between the replicator, that is the genes, and the vehicle that carries the replicator, that is the organism or phenotype. And of course that idea was not only buttressed and supported by the Weissman barrier idea, but later on by the ‘Central Dogma’ of molecular biology. Then Dr. Nobel pauses to emphasize his point and states “All these rules have been broken!”. Professor Denis Noble is President of the International Union of Physiological Sciences.
,,You can pick up the rest of the high points of Dr. Nobel's talk at the two minute mark of the preceding video I referenced, or you can watch the entire video here:
Rocking the foundations of biology - video http://www.voicesfromoxford.org/video/physiology-and-the-revolution-in-evolutionary-biology/184
bornagain77
November 29, 2014
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#16 ppolish
The German Lab that did this study has shown up before on “bad day for Darwin” posts I believe. Sharp group. http://www.molgen.mpg.de/2168/en
That's kind of suspicious, isn't it? They don't seem to understand 'n-D e' at all. Are they just ID proponents pretending to be objective impartial scientists? :) Or maybe that's a fake report that did not come from that institution, but was published by ID folks pretending to be part of that lab? :)Dionisio
November 29, 2014
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The original paper in Nature Communications: http://www.nature.com/ncomms/2014/141126/ncomms6569/full/ncomms6569.htmlDionisio
November 29, 2014
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“It’s amazing how precisely the 60:40 ratio is maintained. It occurs in the genome of every individual – almost like a magic formula,” Ratio probably more precisely 62:38 not 60:40. The "Golden Ratio" would predict closer to the 62:38:) Almost like a magic formula. But not magic, it is by chance. Just kidding, it's Design.ppolish
November 29, 2014
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gpuccio wrote:
a) The genome and proteome exhibit important variations in a normal, rather homogeneous population. That is not really news, but it is very important to have quantitative data about that point. b) The distribution of that variation between the two alleles of each gene seems to be non random, and to have functional importance. That adds a new layer of complexity to the big problem of biological individuality and of functional regulation.
Interesting observations. Thank you!Dionisio
November 29, 2014
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The German Lab that did this study has shown up before on "bad day for Darwin" posts I believe. Sharp group. http://www.molgen.mpg.de/2168/enppolish
November 29, 2014
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