Evolutionary biology Genetics Genomics Intelligent Design

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. . . . .

135 Replies to “Another Day; Another Bad Day for Darwinism: Pt. 43

  1. 1
    PaV says:

    There is also this statement at the end:

    So far, researchers have estimated the risk of disease only by the presence or absence of mutations. 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. The location of mutations therefore needs to be considered in the diagnosis, prediction and prevention of diseases in future.

    If, indeed, the “location” of a mutation is determinative of “fitness,” then the discussion that took place on this board years ago regarding the ill use of a UPD for the genome is in many ways undermined—something to be added to the weaknesses that have already been pointed out.

  2. 2
    PaV says:

    And this:

    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. If the duality of genes goes awry and the wrong protein form is used, this can trigger pathogenic mechanisms. This is probably why those 4,000 genes include many disease genes.

    So much for RV+NS. This describes a more Lamarckian form of inheritance, and an adaptive process that can take place epigenetically—————and quickly!

  3. 3
    bornagain77 says:

    I actually was going to use your line for this paper PaV when I listed it earlier,,, glad you did it instead,,,, so much better to hear it from the horses mouth!

    I’ve already had two atheists on FB saying that this supports evolution,,, 🙂 ,,, just blocked them instead of arguing,,, I figured anyone who would claim that was not worth the trouble of correcting,,

  4. 4
    Dionisio says:

    They ain’t seen nothing yet.

    The party is just starting, the funniest part is still ahead.

    🙂

  5. 5
    bornagain77 says:

    OT: podcast – “The Universe Next Door: Dr. Paul Nelson”
    http://intelligentdesign.podom.....7_19-08_00
    hear Dr. Paul Nelson’s latest discussion with Tom Woodward on The Universe Next Door. Nelson and Woodward talk about what can be conceptualized about the origin of life from the story of Humpty Dumpty; Dr. Nelson’s experience in graduate school, and his recent visit to the intelligent design community in Brazil; and finally, current research around self-replicating RNA and the origin of life.

  6. 6
    Querius says:

    Absolutely fascinating!

    Thank you.

    -Q

  7. 7

    Another prediction of the ID theory (and Genesis) is proving to be true! This is fantastic news!!

  8. 8
    Mapou says:

    So mutations are not random after all? NS + RM is a big lie? Our kids were forced for decades, under penalty of law, to be indoctrinated in the state religion only to discover that the state religion was a pile of BS. I say it’s time we ejected the science deniers from our schools.

  9. 9
    Andre says:

    Unguided evolution is the best explanation for the diversity of life…..

    Keith S debunked by scientific observation amongst other refutations….

    Hehehe

  10. 10
    ringo says:

    Born Again, Barry or anyone else – could you explain the implications of this paper in laymen terms? Thank you

  11. 11
    Andre says:

    Ringo

    There is no such thing as random mutations or natural selection, Alfred Wallace is right that it is a guided process.

  12. 12

    Dionisio:

    They ain’t seen nothing yet.

    The party is just starting, the funniest part is still ahead.

    Bidirectional associative memory?

    http://en.wikipedia.org/wiki/B.....ive_memory

  13. 13
    gpuccio says:

    PaV:

    Extremely interesting. Thank you! 🙂

  14. 14
    bornagain77 says:

    ringo

    “could you explain the implications of this paper in laymen terms? Thank you”

    OK I’ll try, let’s see,, how to put this simply??,,, MMMM, how about this short video?

    https://www.youtube.com/watch?v=rSjK2Oqrgic

    The bomb is this evidence. The blown up building is Darwin’s theory. The man denying the destruction of the building is a Darwinist! 🙂

  15. 15
    gpuccio says:

    ringo:

    It’s not really simple. I am trying to analyze the paper in depth.

    In brief, as a very quick summary, I would tentatively point to at least two important aspects:

    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.

  16. 16
    ppolish says:

    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

  17. 17
    Dionisio says:

    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!

  18. 18
    ppolish says:

    “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.

  19. 19
    Dionisio says:

    The original paper in Nature Communications:

    http://www.nature.com/ncomms/2.....s6569.html

  20. 20
    Dionisio says:

    #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?

    🙂

  21. 21
    bornagain77 says:

    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/2.....s6569.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/multi.....-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/j.....11233.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/.....07245.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.or.....iology/184

  22. 22
    bornagain77 says:

    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.....4/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.
    http://www.uncommondescent.com.....-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.

  23. 23

    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.

  24. 24
    gpuccio says:

    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! 🙂

  25. 25
    gpuccio says:

    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.

  26. 26
    wd400 says:

    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 mechanism

  27. 27

    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.

  28. 28
    PaV says:

    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.”

  29. 29
    PaV says:

    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.

  30. 30
    PaV says:

    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!!! 🙂

  31. 31
    bornagain77 says:

    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/2.....45691.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/2.....90231.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/.....O-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/techn.....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/a704d.....fa9c20.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=T8CLgiYZyZE

  32. 32
    wd400 says:

    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.

  33. 33
    bornagain77 says:

    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/2.....71621.html
    http://www.nature.com/nature/j.....6419a.html

  34. 34

    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/~gene...../ngs_data/ . In addition, haplotypes for all molecularly phased genomes can be viewed in a UCSC browser session at http://www.molgen.mpg.de/~gene.....sedgenomes . Data files related to gene categories, the ‘CDP’ and ‘phase-alternate’ genes can be downloaded from http://www.molgen.mpg.de/~gene.....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?

  35. 35
    gpuccio says:

    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?

  36. 36
    Dionisio says:

    @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.]

    🙂

  37. 37
    Dionisio says:

    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.

    🙂

  38. 38
    Dionisio says:

    Please, let’s read carefully gpuccio’s post #35, so we all, specially onlookers/lurkers can see clearly what is discussed here. Thank you.

  39. 39
    Dionisio says:

    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.

    🙂

  40. 40
    Dionisio says:

    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.

    🙂

  41. 41
    bornagain77 says:

    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?

    http://www.uncommondescent.com.....ent-533308

  42. 42
    Zachriel says:

    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.

  43. 43
    Joe says:

    So something that doesn’t have a function isn’t subject to natural selection? Really?

  44. 44
    gpuccio says:

    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.

  45. 45
    gpuccio says:

    Dionisio:

    Your “intrusions” are always appreciated! 🙂

  46. 46
    gpuccio says:

    BA:

    “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?”

    You are probably right. However, I would advice to take some time to reflect on this paper and its implications. The concept is rather new, and it deserves careful evaluation.

  47. 47
    gpuccio says:

    BA:

    However, I am a medical doctor, but not a surgeon! 🙂

  48. 48
    Zachriel says:

    gpuccio: I think you have not taken the time to read my post carefully.

    Er … well, um.

    gpuccio: I think that you would have more chances if you tried to attribute the observed pattern to positive selection.

    Stabilizing selection, which tends towards an equilibrium state, and encompasses purifying selection against the extremes.

    gpuccio: I don’t think that we have an immediate explanation for those findings.

    No, but there are immediate avenues for investigation by looking for evidence of evolutionary processes.

    bornagain77: 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?

    Good question. Evolutionary biologists would hypothesize stabilizing selection, meaning it is at a functional fitness peak, and that there may be evidence that this came about through evolutionary processes.

  49. 49
    wd400 says:

    Gpuccio, you seem almost as confused as PaV,

    From the top,

    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)

    Indeed. Isn’t it remarkable, then, that almost all coverage on new science here is a rehash or a press release collected by PhysOrg, ScienceDaily on some other PR aggregator?

    But the most interesting part of the paper is exactly the connection of the differential distribution of variation with function.

    I don’t think they show this. Even if they did, Pav was wrong to think this paper was about the randomness of mutation, and wrong to thing non-random distribution among parental chromosomes was a problem for “Darwinism”.

    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.

    As you say, I was commenting on the 85% figure, which arises from that basic understanting of probability, and thus is not at all intestig (you do realise the 85% figure if for diplotypes, not unique genetic sequences?)

    The 60:40 ratio is probably another simple artifact, be we’ll get to that.

    “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…

    Pav (and apprently you) thought the high diversity meant purifying selection could be ruled out. In fact if (a) read the paper and (b) no even the first thing about population genetics you’d see they find evidence for purifying selection on proteins (though they don’t explictly say this). The number of protein diplotypes is vastly lower than the number of DNA diplotypes. Given that ~75% of nucleotide changes result in amino acid changes, we wouldn’t expect to see that under neutrality, so, indeed, protein-changing mutations are being kept out of the genome and other regions are acquiring diversity near the neutral expectation.

    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).

    No, it did not. It found some protein haplotypes with substantially different amino acid substitutions relative to the reference genome come in pairs (i.e. two ahaplotypes with similarly different variants), others usually come packed up with something more like the wildtype. You need not invent any magic regulatory process for this — it’s almost certainly a result of the frequency distribution of haplotypes and the (exceedingly small effect sized) differences in broad functional classifications likely relate to the same.

    The 60:40 ratio is within genomes, and again requires no magic. If you take 12 different samples, each with thousands of replicates, you expect the each sample to converge on the population-wide expectation. That’s all this paper found.

    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?

    Of course I am quite capable of rethinking postions in the light of substantial evidence that such a rethink is required. There’s just nothing very surprising in this paper.

  50. 50
    wd400 says:

    Dionisio, if a post of mine has a typo that makes extracting its meaning difficult then by all means ask for a clarification. But I’m not interested in the school master act, calling up typos while ignoring the many substantial faults in the OP.

  51. 51
    bornagain77 says:

    Zach, you state:

    “Good question. Evolutionary biologists would hypothesize stabilizing selection, meaning it is at a functional fitness peak, and that there may be evidence that this came about through evolutionary processes.”

    After the fact story telling by Darwinists of a non-predicted, contrary, finding to their theory is part and parcel to Darwinism,,,

    EVOLUTIONARY JUST-SO STORIES
    Excerpt: ,,,The term “just-so story” was popularized by Rudyard Kipling’s 1902 book by that title which contained fictional stories for children. Kipling says the camel got his hump as a punishment for refusing to work, the leopard’s spots were painted on him by an Ethiopian, and the kangaroo got its powerful hind legs after being chased all day by a dingo.
    Kipling’s just-so stories are as scientific as the Darwinian accounts of how the amoeba became a man.
    Lacking real scientific evidence for their theory, evolutionists have used the just-so story to great effect. Backed by impressive scientific credentials, the Darwinian just-so story has the aura of respectability.
    Biologist Michael Behe observes:
    “Some evolutionary biologists–like Richard Dawkins–have fertile imaginations. Given a starting point, they almost always can spin a story to get to any biological structure you wish” (Darwin’s Black Box).,,,
    http://www.wayoflife.org/datab.....ories.html

    “Grand Darwinian claims rest on undisciplined imagination”
    Dr. Michael Behe – 29:24 mark of following video
    http://www.youtube.com/watch?f.....fM#t=1762s

  52. 52
    PaV says:

    wd400:

    Indeed. Isn’t it remarkable, then, that almost all coverage on new science here is a rehash or a press release collected by PhysOrg, ScienceDaily on some other PR aggregator?

    Wouldn’t it be nice if we were professors at some university where we had access to the actual papers? But we aren’t. And I’m certainly not going to subscribe to all kinds of magazines.

    A little bit of perspective is needed here.

    I don’t think they show this. Even if they did, Pav was wrong to think this paper was about the randomness of mutation, and wrong to thing non-random distribution among parental chromosomes was a problem for “Darwinism”.

    So, apparently it was “wrong” to set off in ‘bold-face’ the quote from the actual article. Could you explain, please?

    Pav (and apprently you) thought the high diversity meant purifying selection could be ruled out. In fact if (a) read the paper and (b) no even the first thing about population genetics you’d see they find evidence for purifying selection on proteins (though they don’t explictly say this). The number of protein diplotypes is vastly lower than the number of DNA diplotypes. Given that ~75% of nucleotide changes result in amino acid changes, we wouldn’t expect to see that under neutrality, so, indeed, protein-changing mutations are being kept out of the genome and other regions are acquiring diversity near the neutral expectation.

    Purifying selection is meant to “eliminate” alleles that are deleterious, and, hence, a check on diversity. But that’s not what we see going on here. Yes, there is a difference between which ‘genes’ (DNA) are being expressed and which are not, resulting in the distinction between the “protein” and “gene” diplotypes you point to. You choose to call this “purifying selection.” Yet, the diverse “gene” forms remain.

    IOW, what is preventing the genome from changing its expression away from the “current” DNA being expressed and having the genome now express one of these alternative haplotypes or diplotypes? In fact, in terms of “adaptability” of an organism, one would surely suspect that upstream initiation sites would, if you will, turn “on” and turn “off” in response to environmental stimuli.

    In the author’s minds, this possibility throws the whole idea of a “wild-type” allele into question. That’s why they say that everything we’ve been taught about Mendelian genetics may have to now be re-taught. The same goes, obviously, for population genetics.

    Another Day; Another Bad Day for Darwinism.

  53. 53
    wd400 says:

    Wouldn’t it be nice if we were professors at some university where we had access to the actual papers? But we aren’t. And I’m certainly not going to subscribe to all kinds of magazines.

    It’s an open access paper. In general, it is a bad idea to presume a research institute’s press office (a) knows what the hell their scientists paper is about and (b) wants to give an even-handed account of the research’s import. If you are stuck with secondary sources then it’s better to reply on a good science writer, if you can’t find one of those you ought to be skeptical.

    (How likely is it that the paper that overturned Mendel was published in an open access fall-back journal, then not covered by any reputable science writers?)

    So, apparently it was “wrong” to set off in ‘bold-face’ the quote from the actual article. Could you explain, please?

    It’s perfectly evident that you thought that quote made for a “bad day for Darwinism”, and that it showed mutation was not random in the way modern evolutionary biology holds mutations are. That was wrong, both in the context of the quote and due to the fact the study wasn’t about de novo mutation so couldn’t possibly done what you thought it did.

    Purifying selection is meant to “eliminate” alleles that are deleterious, and, hence, a check on diversity. But that’s not what we see going on here.

    That’s exactly what we see.

    Yes, there is a difference between which ‘genes’ (DNA) are being expressed and which are not, resulting in the distinction between the “protein” and “gene” diplotypes you point to.

    No. The difference is not in expression, it’s in what sorts of variatns are present. Synonynous and non-coding variants are more common than non-synonymous ones. So, when DNA haplotypes get translated to proteins you get substantially fewer distinct proteins than distinct DNA types. The fact there are markedly fewer protein-types, despite the fact most exonic mutations would be non-synonymous, tells you those non-synonymous mutations are being eliminated. That’s purifying selection. Hardly a new finding, but evidence that even in the face of the (not at all suprising) diversity in “diplotypes”, puridying selection is well attested in our genome.

    The rest of your comment appears to be based on your misunderstanding of the above.

  54. 54
    PaV says:

    From the paper:

    Exorbitant diversity at the gene level was found to converge upon a common diplotypic proteome, a subset of genes preferentially encoding two different proteins, allowing gene functions to be differentially exerted and/or diversified. Thus, the CDP [common diplotypic proteome] may represent a ‘major modulating principle’ generating diverse cellular and physiological outcomes in individual organisms, and a the population level giving rise to phenotypic diversity, adaptive and evolutionary processes.”

    Now, in their view, this might mean that the CDP “isolates” the organism from “purifying selection”, and so “duplicated genes” are free to mutate, resulting in a richer diversity of possible expression in haplotype and diplotype forms, and, so, would be consistent with current evolutionary thought; however, how does this comport with the modern view of population genetics and its reliance on the “infinite allele” model when, for the most part, there is no “wild-type” allele?

    Or, from the OP:

    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.

    This kind of diversity would have thrown Kimura into conniption fits.

  55. 55
    PaV says:

    wd400:

    It’s an open access paper.

    Yes, this one. Is the “exception” the “rule” now?

    (How likely is it that the paper that overturned Mendel was published in an open access fall-back journal, then not covered by any reputable science writers?

    How likely is it that a paper that “overturns Mendel” would be welcomed at a “reputable” journal?

    PaV: Purifying selection is meant to “eliminate” alleles that are deleterious, and, hence, a check on diversity. But that’s not what we see going on here.

    wd400: That’s exactly what we see.

    What “check on diversity” do we really see? There is extravagant diversity within the genome. It’s the proteome that is not displaying this diversity; but, again, this can all be attributed to how the “alleles” are being regulated.

    No. The difference is not in expression, it’s in what sorts of variations are present. Synonynous and non-coding variants are more common than non-synonymous ones. So, when DNA haplotypes get translated to proteins you get substantially fewer distinct proteins than distinct DNA types.

    From what I’ve read, they have concerned themselves ONLY with non-synonymous mutations. So, if you’re correct in your take on this paper, these variant protein forms should have been seen. But they’re not. So, OTOH, we have genomic evidence of the various ‘forms’ of alleles, but, OTOH, the expression of the various ‘forms’ of alleles are not seen. The logical conclusion is either: (1) these other ‘forms’ are NOT being expressed (my position), or (2) they are being expressed and then the organism dies (purifying selection—your position).

    I prefer my take on the paper. Why? Because if they were being “eliminated,” then these diverse molecular forms of the ‘gene’ would disappear.

  56. 56
    wd400 says:

    but, again, this can all be attributed to how the “alleles” are being regulated.

    Not. It can’t. Because this study looks only a genomic DNA. No expression, no proteomics.

    You “prefer your take on the paper” only because you don’t understand the paper.

    As I said earlier, it is interesting that none of your fellow travelers are able to set you straight on this.

  57. 57
    Dionisio says:

    @50 wd400

    I’m not interested in the school master act, calling up typos while ignoring the many substantial faults in the OP.

    Do you really believe that your personal interest can determine what others write about in this blog?

    If you’re not interested in something written here, just ignore it, skip it, move on. Remember some comments here are written for the onlookers/lurkers, whose motivations are unknown to us. Not for you and your comrades. You and your fellow travelers have revealed your motivations already. They are obvious to any observer. 😉

  58. 58
    wd400 says:

    Well, I’m sure onlookers will learn a great deal from the way you focus on typos and ignore the substantial errors of fact in the original post and subsequent comments, Dionisio.

  59. 59
    bornagain77 says:

    wd400, since you are the one defending a unsubstantiated pseudo-science, i.e. defending neo-Darwinism, and apparently don’t even realize it, do you think you should really be lecturing anybody on anything as to what you think is factually in error or not? ,,,

    http://www.uncommondescent.com.....ent-533577

    I seem to recall a scripture of pulling a beam out of your own eye before attempting to pull a splinter out of someone else’s,,,

  60. 60
    fifthmonarchyman says:

    hey all.

    Allow me to make a few observations. I hope all this makes sense to someone

    1) The set of all the variants to a particular gene is irreducibly complex. ie it contains all the variants and nothing else.

    2) ‘wild-type’forms of genes do not exist in the physical world they are Platonic Ideals existing only outside the cave

    3) If we wanted to calculate the Kolmogorov complexity for producing a given genetic variant in the set with out the “key” we would need to add (Phi to the Nth power)to the raw K Complexity of the variant taken individually.

    Where Phi is the golden ratio and N is the total number of variants in the set.

    4) On the other hand once we had a variant the computational power necessary to move to an adjacent variant in the set is trivial.

    That in a nut shell is the difference between Mico and Macro evolution.

    peace

  61. 61
    fifthmonarchyman says:

    I think the golden ratio is telling us something here.

    The ratio is exactly what you would expect if a particular variant represented one part of an irreducibly Complex set.

    Think about a golden rectangle.. The shorter square side is the variant and the longer side of the rectangle is the rest of the variants taken as a whole.

    Together they make up one complete IC set.

    At least that is what it looks like to me

    Peace

  62. 62
    wd400 says:

    … another chance to test the rigour of the ID movement…

  63. 63
    keith s says:

    fifthmonarchyman:

    Allow me to make a few observations. I hope all this makes sense to someone

    🙂

  64. 64
    bornagain77 says:

    wd400, can you please point me to the empirical tests that have been conducted that have established the rigor of Darwinism? or is the beam of hypocrisy in your eye too blinding for that task?

    “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

  65. 65
    Dionisio says:

    @58 wd400

    Well, I’m sure onlookers will learn a great deal from the way you focus on typos and ignore the substantial errors of fact in the original post and subsequent comments

    I pay attention to grammatical and syntactical issues because English is not my first language and I’m still learning it. Almost everything I read in English I treat it as a reading comprehension test.

    If you read my post #36 in this thread, you will notice that I request that others call my attention to any grammatical or syntactical mistakes in my own posts. Apparently you did not read carefully what I wrote in that post?

    Also, in my post #37 I clearly wrote that my grammar/syntax observations were less important than the actual discussion on the OP subject. Apparently you did not read carefully that post either?

    Onlookers/lurkers reading this post may verify what I’m saying here.

    🙂

  66. 66
    bornagain77 says:

    of note to wd400 dissing ID, it interesting to note the beam in his eye,,,

    Science owes nothing to Darwinism – Jonathan Wells
    http://www.uncommondescent.com.....ent-531669

    Of related interest to Darwinism failing to provide a fruitful heuristic for science, (ignoring the many blind alleys Darwinism has led science down), Intelligent Design does not suffer from such an embarrassment:

    “It has become clear in the past ten years that the concept of design is not merely an add-on meta-description of biological systems, of no scientific consequence, but is in fact a driver of science. A whole cohort of young scientists is being trained to “think like engineers” when looking at biological systems, using terms explicitly related to engineering design concepts: design, purpose, optimal tradeoffs for multiple goals, information, control, decision making, etc. This approach is widely seen as a successful, predictive, quantitative theory of biology.”
    David Snoke*, Systems Biology as a Research Program for Intelligent Design

    podcast: “David Snoke: Systems Biology and Intelligent Design, pt. 1”
    http://intelligentdesign.podom.....9_09-07_00
    podcast: David Snoke: Systems Biology and Intelligent Design, pt. 2
    http://intelligentdesign.podom.....0_01-07_00

    How the Burgeoning Field of Systems Biology Supports Intelligent Design – July 2014
    Excerpt: Snoke lists various features in biology that have been found to function like goal-directed, top-down engineered systems:
    *”Negative feedback for stable operation.”
    *”Frequency filtering” for extracting a signal from a noisy system.
    *Control and signaling to induce a response.
    *”Information storage” where information is stored for later use. In fact, Snoke observes:
    “This paradigm [of systems biology] is advancing the view that biology is essentially an information science with information operating on multiple hierarchical levels and in complex networks [13]. ”
    *”Timing and synchronization,” where organisms maintain clocks to ensure that different processes and events happen in the right order.
    *”Addressing,” where signaling molecules are tagged with an address to help them arrive at their intended target.
    *”Hierarchies of function,” where organisms maintain clocks to ensure that cellular processes and events happen at the right times and in the right order.
    *”Redundancy,” as organisms contain backup systems or “fail-safes” if primary essential systems fail.
    *”Adaptation,” where organisms are pre-engineered to be able to undergo small-scale adaptations to their environments. As Snoke explains, “These systems use randomization controlled by supersystems, just as the immune system uses randomization in a very controlled way,” and “Only part of the system is allowed to vary randomly, while the rest is highly conserved.”,,,
    Snoke observes that systems biology assumes that biological features are optimized, meaning, in part, that “just about everything in the cell does indeed have a role, i.e., that there is very little ‘junk.'” He explains, “Some systems biologists go further than just assuming that every little thing has a purpose. Some argue that each item is fulfilling its purpose as well as is physically possible,” and quotes additional authorities who assume that biological systems are optimized.,,,
    http://www.evolutionnews.org/2.....87871.html

    Systems Biology as a Research Program for Intelligent Design – David Snoke – 2014
    http://bio-complexity.org/ojs/.....O-C.2014.3

    A Response to Questions from a Biology Teacher: How Do We Test Intelligent Design? – March 2010
    Excerpt: Regarding testability, ID (Intelligent Design) makes the following testable predictions:
    (1) Natural structures will be found that contain many parts arranged in intricate patterns that perform a specific function (e.g. complex and specified information).
    (2) Forms containing large amounts of novel information will appear in the fossil record suddenly and without similar precursors.
    (3) Convergence will occur routinely. That is, genes and other functional parts will be re-used in different and unrelated organisms.
    (4) Much so-called “junk DNA” will turn out to perform valuable functions.
    http://www.evolutionnews.org/2.....rom_a.html

    A Positive, Testable Case for Intelligent Design – Casey Luskin – March 2011 – several examples of cited research
    http://www.evolutionnews.org/2.....45311.html

    podcast – “How the Latest Findings in Molecular Biology Support Intelligent Design, pt. 1” – Oct. 2014
    http://intelligentdesign.podom.....0_39-07_00
    “How the Latest Findings in Molecular Biology Support Intelligent Design, pt. 2”
    http://intelligentdesign.podom.....1_17-07_00

  67. 67
    Dionisio says:

    @60 fifthmonarchyman

    That in a nut shell is the difference between Mico and Macro evolution.

    Micro?

    🙂

  68. 68
    fifthmonarchyman says:

    Dionisio.

    I meant Micro probably the only thing WD400 and I share is a tendency to misspell and TYPO. He is a light weight compared to me in that regard 😉

  69. 69
    Dionisio says:

    @66 bornagain77

    of note to wd400 dissing ID, it interesting to note the beam in his eye,,,

    Just to show wd400 that my treatment is fair and balanced, I wrote post #67 in reference to post #60 by fifthmonarchyman and now let’s point to this one too:

    it’s interesting

    🙂

  70. 70
    bornagain77 says:

    Dionisio, I probably am worse than
    fifthmonarchyman and wd400 put together on typos!

  71. 71
    fifthmonarchyman says:

    Dionisio,

    We also have something in common English is a second language to me as well.

    I grew up speaking Southern backwoods a merkin.

    😉

    Peace

  72. 72
    Dionisio says:

    @68 fifthmonarchyman

    I meant Micro probably the only thing WD400 and I share is a tendency to misspell and TYPO. He is a light weight compared to me in that regard 😉

    We all misspell and typo, but probably no one does it more often than I do it. Y’all are lightweights compared to me in that regard. 🙂

    Now, one thing that clearly distinguishes you from your interlocutor is your humility to graciously accept a correction. That’s quite a difference. 🙂

    May God bless you.

  73. 73
    Dionisio says:

    @70 bornagain77

    I probably am worse than
    fifthmonarchyman and wd400 put together on typos!

    Please, allow me to disagree on that. Given the relatively large amount of text you usually post in most threads within this blog almost daily, probably your typo average is quite low. 🙂

    However, your humility to graciously admit that you have made mistakes, sets you apart from your interlocutor, who didn’t like my pointing to his error.

    Onlookers/lurkers can notice this difference in reactions and take it into account when arriving at their own conclusions after reading the different posts in this blog. 🙂

  74. 74
    Dionisio says:

    @71 fifthmonarchyman

    We also have something in common English is a second language to me as well.
    I grew up speaking Southern backwoods a merkin.

    That’s funny! Thank you!

  75. 75
    PaV says:

    wd400:

    You “prefer your take on the paper” only because you don’t understand the paper.

    I’m having difficulty understanding your take on the paper.

    It is you, not the authors, who is positing “purifying selection.” It is you, not the authors, who is saying that the 60:40 ratio is a residue of recombination.

    I think I understand the paper. They’re using methods to analyze both strands of DNA for a select number of genomes, and then comparing them, statistically, to a large collection of genomes. From their analysis, which is apparently more accurate that diploid studies, they’ve found “exorbitant diversity.” They’ve found that a “wild-type” allele happens in less than 15% of the cases. Should I go on?

    It is you who are mucking things up. Where did I ever say that they were doing proteomic investigations? Where? But they did “compare” their results to known proteomic results. Then it was you who asserted that this discrepancy is proof of “purifying selection.” The following discussion was my attempt at saying: ‘I don’t buy your analysis.’ The genetic variance is there. Whether, and how, that is expressed is a story for a different day.

    I honestly don’t understand why you’re making such a big deal of proteomic results. That’s not their focus. Their focus is more along the lines of how these allelic variants might affect the efficacy of drug treatments. By that, I presume that they mean the genome is capable of switching to these other variant alleles, and that a drug schema, built around proteomic expression, might not, in the end, work.

    Here’s how they end the paper:

    Thus, the relationship between the CDP, mono-allelic expression and also allele-specific expression requires clarification. So does the role of the CDP in transcriptome diversity within and between individuals, species, tissues, developmental and physiological stages, health and disease. The CDP represents a new aspect of the highly complex proteome, as such subject to further diversification through alternative splicing and post-translational modifications. The molecular validation of the mutations defining these protein diplotypes will present future challenges.

    You’re take on all of this is: (1) they don’t know what they’re talking about, (2) there’s no problem here at all.

    Meanwhile—I guess because they don’t have anything better to do—they’re saying that Mendelian genetics must be completely rethought. Are they really that wrong? Or, is this just: “Another Day; Another Bad Day for Darwinism”?

  76. 76
    wd400 says:

    Here’s your test ID movement — who can save PaV from him/her self?

  77. 77

    Wd400:

    Here’s your test ID movement — who can save PaV from his/her self?

    We need a new Intelligence Design Lab, or genetics will soon make no sense to almost everyone.

  78. 78
    fifthmonarchyman says:

    Wd400,

    It’s common practice for critics to claim that folks with ID sympathies are stupid and uneducated.

    For all I know this may be a valid critique especially in my case. I am definitely not the brightest bulb in the pack

    But it is a very poor way to win hearts and minds to your cause.

    If you want to change minds I would think a better approach would be to demonstrate where your opponent is mistaken.

    Maybe that’s not your intention here. If not I have no clue what it is.

    I know I’m here to sharpen my own ideas but I can’t believe that is your purpose,

    peace

  79. 79
    wd400 says:

    Fifth,

    I don’t claim IDers are stupid. But most IDers (and most pro-evolutionary biology folks on the internet for that matter) don’t know much about modern biology.

    I think it’s very strange that people who think we should throw out most of modern biology don’t first educate themselves on what biology actually is. This thread started with PaV misunderstanding a press release, and has got worse from there.

    There is no point in my continuing to correct PaV’s errors – he/she is set in their position and no evidence will change it. But if ID has folks they really do know something about biology, shouldn’t they be able to set PaV straight?

    (as to why I’m here — I find it really interesting to know where anti-science ideas come from and how they coalesce into broader movements/belief systems)

  80. 80
    bornagain77 says:

    as to: “I find it really interesting to know where anti-science ideas come from and how they coalesce into broader movements/belief systems”

    Yet, amazingly, you are a dedicated proponent of ‘anti-science’ with your relentless promotion of neo-Darwinism,,,

    For instance of the anti-science inherent in neo-Darwinism, if the atheistic/materialistic version of neo-Darwinism were actually true it would lead to the epistemological failure of science itself,,,

    Evolutionary Argument Against Naturalism (An Introduction) – video
    https://www.youtube.com/watch?v=vpQ1-AGPysM

    Scientific Peer Review is in Trouble: From Medical Science to Darwinism – Mike Keas – October 10, 2012
    Excerpt: Survival is all that matters on evolutionary naturalism. Our evolving brains are more likely to give us useful fictions that promote survival rather than the truth about reality. Thus evolutionary naturalism undermines all rationality (including confidence in science itself). Renown philosopher Alvin Plantinga has argued against naturalism in this way (summary of that argument is linked on the site:).
    Or, if your short on time and patience to grasp Plantinga’s nuanced argument, see if you can digest this thought from evolutionary cognitive psychologist Steve Pinker, who baldly states:
    “Our brains are shaped for fitness, not for truth; sometimes the truth is adaptive, sometimes it is not.”
    Steven Pinker, evolutionary cognitive psychologist, How the Mind Works (W.W. Norton, 1997), p. 305.
    http://blogs.christianpost.com.....ism-12421/

    Quote: “In evolutionary games we put truth (true perception) on the stage and it dies. And in genetic algorithms it (true perception) never gets on the stage”
    Donald Hoffman PhD. – Consciousness and The Interface Theory of Perception – 7:19 to 9:20 minute mark – video
    https://www.youtube.com/watch?feature=player_detailpage&v=dqDP34a-epI#t=439

  81. 81
    fifthmonarchyman says:

    Wd400 says,

    (as to why I’m here — I find it really interesting to know where anti-science ideas come from and how they coalesce into broader movements/belief systems)

    I say,

    I’m not sure where the ideas that you would call “anti-science” come from but when they are flippantly dismissed instead of addressed straightforwardly they tend to coalesce.

    I’m not saying you need to beat a dead horse but surely you should at least make sure it is not still charging at you.

    From this side it looks like you did a little quick hand waving about the article and then just proceeded to try and belittle the apposition for not acquiescing to you and the powers that be.

    Just my opinion

    peace

  82. 82
    bornagain77 says:

    footnote to 80:

    Sam Harris’s Free Will: The Medial Pre-Frontal Cortex Did It – Martin Cothran – November 9, 2012
    Excerpt: There is something ironic about the position of thinkers like Harris on issues like this: they claim that their position is the result of the irresistible necessity of logic (in fact, they pride themselves on their logic). Their belief is the consequent, in a ground/consequent relation between their evidence and their conclusion. But their very stated position is that any mental state — including their position on this issue — is the effect of a physical, not logical cause.
    By their own logic, it isn’t logic that demands their assent to the claim that free will is an illusion, but the prior chemical state of their brains. The only condition under which we could possibly find their argument convincing is if they are not true. The claim that free will is an illusion requires the possibility that minds have the freedom to assent to a logical argument, a freedom denied by the claim itself. It is an assent that must, in order to remain logical and not physiological, presume a perspective outside the physical order.
    http://www.evolutionnews.org/2.....66221.html

  83. 83
    wd400 says:

    I’m not sure where the ideas that you would call “anti-science” come from but when they are flippantly dismissed instead of addressed straightforwardly they tend to coalesce.

    I don’t know how I can be more straightforward about PaV’s mistakes. The paper doesn’t claim mutations are non-random in the sense evolutionary biology assumes mutations are random. The diversity of diplotyes (combinations of two haplotypes) is no suprising given haplotypes are diverse. The data presented in the paper shows strong evidence for purifying selection, despite the OP’s claim the paper was evidence against the operation of this process in our genome. None of this mystical stuff about regulation of alternative haplotypes has any basis in a result in the paper.

    That’s just the OP. How can I be more straightforward in pointing out the mistakes?

  84. 84
    REC says:

    wd400 is all over this one….but geez the paper and PaV’s hype are 180 degrees away.

    Also, even within the human population, where you might define a narrow tiny bulls-eye of function in sequence space, what do we find? Enormous diversity of functional sequences.

    Remember you’re favoring the tiny side of functional sequence space to get to your big big numbers. So, as you crow about the diversity of functional sequences amounting to no single “wild type” sequence in human genes…..

  85. 85
    bornagain77 says:

    as to:

    “The paper doesn’t claim mutations are non-random in the sense evolutionary biology assumes mutations are random.”

    give me a break, having extremely sophisticated molecular machines direct mutations to DNA in a overarching pattern is completely antithetical to the original Darwinian assumption of ‘random, accidental’ mutations,,, Shapiro created quite a few waves by pointing this now accepted fact out:

    Revisiting the Central Dogma in the 21st Century – James A. Shapiro – 2009
    Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, (Page 14) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112).
    http://shapiro.bsd.uchicago.ed.....0Dogma.pdf

    Also of interest from the preceding paper, on page 22, is a simplified list of the ‘epigenetic’ information flow in the cell that directly contradicts what was expected from the central dogma (Genetic Reductionism/modern synthesis model) of neo-Darwinism.

  86. 86
    Pachyaena says:

    Dionisio said: “You and your fellow travelers have revealed your motivations already. They are obvious to any observer.”

    As are yours. Non-IDers are trying to educate IDers and others and keep religious bunk and other woo out of science, education, and public policies, while you IDers are trying to ‘wedge’ your religious bunk and other woo into science, education, and public policies.

    You and other IDers seem to think that all observers (or “onlookers”) are IDers or are open to ID. Imagining that likely gives you comfort but you might want to look around and see what kind of reputation ID and this blog have before you get too comfy.

  87. 87
    Joe says:

    wd400:

    The paper doesn’t claim mutations are non-random in the sense evolutionary biology assumes mutations are random.

    In what way does evolutionary biology assume mutations are random?

    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”.

    That is incorrect. Random wrt biology means accidental as “random wrt fitness” is nonsense because it doesn’t say if the mutations were directed or not.

  88. 88
    fifthmonarchyman says:

    Rec said,

    Remember you’re favoring the tiny side of functional sequence space to get to your big big numbers. So, as you crow about the diversity of functional sequences amounting to no single “wild type” sequence in human genes…..

    I say,

    This is an interesting comment.

    I wonder about the difference between the narrow side of functionality for proteins verses the apparent diversity in genes.

    Suppose there were only 1 protein that worked for a vital purpose but it could be built by 500 different genetic variants.

    This would seem to be an excellent mechanism for front-loading robustness into a “seed” cell you could pretty much guarantee that a given necessary protein would arise.

    Now imagine the opposite: 1 gene can build 500 different proteins. Now you have just made any kind of phenotypical continuity in a population nonexistent. If life existed at all it would appear random to us.

    Is there any physically necessary reason we should see one scenario and not the other?

    interesting

    peace

  89. 89
    bornagain77 says:

    Pachy, contrary to what you atheists believe, it is impossible to do science in the first place without presupposing ‘purpose’ on some level. Moreover, atheists live in denial of the ‘purpose seeing’ that is built into them:

    Design Thinking Is Hardwired in the Human Brain. How Come? – October 17, 2012
    Excerpt: “Even Professional Scientists Are Compelled to See Purpose in Nature, Psychologists Find.” The article describes a test by Boston University’s psychology department, in which researchers found that “despite years of scientific training, even professional chemists, geologists, and physicists from major universities such as Harvard, MIT, and Yale cannot escape a deep-seated belief that natural phenomena exist for a purpose” ,,,
    Most interesting, though, are the questions begged by this research. One is whether it is even possible to purge teleology from explanation.
    http://www.evolutionnews.org/2.....65381.html

    Children Act Like Scientists – October 1, 2012
    Excerpt: New theoretical ideas and empirical research show that very young children’s learning and thinking are strikingly similar to much learning and thinking in science. Preschoolers test hypotheses against data and make causal inferences; they learn from statistics and informal experimentation, and from watching and listening to others. The mathematical framework of probabilistic models and Bayesian inference can describe this learning in precise ways.
    http://crev.info/2012/10/child.....cientists/

    Children are born believers in God, academic claims – 24 Nov 2008
    Excerpt: “Dr Justin Barrett, a senior researcher at the University of Oxford’s Centre for Anthropology and Mind, claims that young people have a predisposition to believe in a supreme being because they assume that everything in the world was created with a purpose.”
    http://www.telegraph.co.uk/new.....laims.html

    Geometric Principles Appear Universal in Our Minds – May 2011
    Excerpt: Villagers belonging to an Amazonian group called the Mundurucú intuitively grasp abstract geometric principles despite having no formal math education,,, Mundurucú adults and 7- to 13-year-olds demonstrate as firm an understanding of the properties of points, lines and surfaces as adults and school-age children in the United States and France,,,
    http://www.wired.com/wiredscie.....-geometry/

    “Geometry is unique and eternal, a reflection from the mind of God. That mankind shares in it is because man is an image of God.”
    – Johannes Kepler

    As well, biology is replete with teleology, i.e. with purpose. In fact, it is impossible to ‘do biology’ without using words that imply intentionality, functionality, strategy, and design.

    Life, Purpose, Mind: Where the Machine Metaphor Fails – Ann Gauger – June 2011
    Excerpt: I’m a working biologist, on bacterial regulation (transcription and translation and protein stability) through signalling molecules, ,,, I can confirm the following points as realities: we lack adequate conceptual categories for what we are seeing in the biological world; with many additional genomes sequenced annually, we have much more data than we know what to do with (and making sense of it has become the current challenge); cells are staggeringly chock full of sophisticated technologies, which are exquisitely integrated; life is not dominated by a single technology, but rather a composite of many; and yet life is more than the sum of its parts; in our work, we biologists use words that imply intentionality, functionality, strategy, and design in biology–we simply cannot avoid them.
    Furthermore, I suggest that to maintain that all of biology is solely a product of selection and genetic decay and time requires a metaphysical conviction that isn’t troubled by the evidence. Alternatively, it could be the view of someone who is unfamiliar with the evidence, for one reason or another. But for those who will consider the evidence that is so obvious throughout biology, I suggest it’s high time we moved on. – Matthew
    http://www.evolutionnews.org/2.....nt-8858161

    The ‘Mental Cell’: Let’s Loosen Up Biological Thinking! – Stephen L. Talbott – September 9, 2014
    Excerpt: Many biologists are content to dismiss the problem with hand-waving: “When we wield the language of agency, we are speaking metaphorically, and we could just as well, if less conveniently, abandon the metaphors”.
    Yet no scientist or philosopher has shown how this shift of language could be effected. And the fact of the matter is just obvious: the biologist who is not investigating how the organism achieves something in a well-directed way is not yet doing biology, as opposed to physics or chemistry. Is this in turn just hand-waving? Let the reader inclined to think so take up a challenge: pose a single topic for biological research, doing so in language that avoids all implication of agency, cognition, and purposiveness1.
    One reason this cannot be done is clear enough: molecular biology — the discipline that was finally going to reduce life unreservedly to mindless mechanism — is now posing its own severe challenges. In this era of Big Data, the message from every side concerns previously unimagined complexity, incessant cross-talk and intertwining pathways, wildly unexpected genomic performances, dynamic conformational changes involving proteins and their cooperative or antagonistic binding partners, pervasive multifunctionality, intricately directed behavior somehow arising from the interaction of countless players in interpenetrating networks, and opposite effects by the same molecules in slightly different contexts. The picture at the molecular level begins to look as lively and organic — and thoughtful — as life itself.
    http://natureinstitute.org/txt.....ell_23.htm

    Of supplemental note,

    Bruce Charlton’s Miscellany – October 2011
    Excerpt: I had discovered that over the same period of the twentieth century that the US had risen to scientific eminence it had undergone a significant Christian revival. ,,,The point I put to (Richard) Dawkins was that the USA was simultaneously by-far the most dominant scientific nation in the world (I knew this from various scientometic studies I was doing at the time) and by-far the most religious (Christian) nation in the world. How, I asked, could this be – if Christianity was culturally inimical to science?
    http://charltonteaching.blogsp.....-wife.html

    Jerry Coyne on the Scientific Method and Religion – Michael Egnor – June 2011
    Excerpt: The scientific method — the empirical systematic theory-based study of nature — has nothing to so with some religious inspirations — Animism, Paganism, Buddhism, Hinduism, Shintoism, Islam, and, well, atheism. The scientific method has everything to do with Christian (and Jewish) inspiration. Judeo-Christian culture is the only culture that has given rise to organized theoretical science. Many cultures (e.g. China) have produced excellent technology and engineering, but only Christian culture has given rise to a conceptual understanding of nature.
    http://www.evolutionnews.org/2.....47431.html

    The truth about science and religion By Terry Scambray – August 14, 2014
    Excerpt: In 1925 the renowned philosopher and mathematician, Alfred North Whitehead speaking to scholars at Harvard said that science originated in Christian Europe in the 13th century. Whitehead pointed out that science arose from “the medieval insistence on the rationality of God, conceived as with the personal energy of Jehovah and with the rationality of a Greek philosopher”, from which it follows that human minds created in that image are capable of understanding nature.
    The audience, assuming that science and Christianity are enemies, was astonished.
    http://www.americanthinker.com.....igion.html

  90. 90
    Silver Asiatic says:

    Pachyaena 86

    Non-IDers are trying to … keep religious bunk and other woo out of science, …while you IDers are trying to ‘wedge’ your religious bunk and other woo into science …

    Who owns science?

  91. 91
    PaV says:

    wd400:

    There is no point in my continuing to correct PaV’s errors – he/she is set in their position and no evidence will change it. But if ID has folks they really do know something about biology, shouldn’t they be able to set PaV straight?

    Thank you for your opinion. But opinion is just that: opinion. You say I don’t understand the paper. But as I’ve said already, it is you who is coming along and “interpreting” the paper. You say there is “evidence” for “purifying selection,” when there is no mention of this in the entire paper, and you base your ‘evidence’ on a Figure on the paper that basically proves the opposite: viz., that there are two ‘forms’ of the allele that are expressed as proteins.

    The fact that the cis:trans ratio is constant, you say is simply an artifact of the method they employ. But they say that it is a ‘constant’ ratio which indicates that “mutations” are NOT ‘random.’ You simply pooh-pooh this.

    So, this is not about understanding the paper. This is about wd400 saying: (1) you can’t believe what’s put out in the press release (although in the paper they make this exact same claim), and (2) you should look to learned scientists to determine a paper’s worth, and (3) then you should follow their interpretation.

    Well, I don’t care to follow your suggestion.

    Whatever your opinion of the paper, the authors have found that in only 15% of the genes is there something like what population geneticists would call a “wild-type” allele. The majority of the time there are AT LEAST two or more forms of the allele.

    This is molecular data. Say what you want, the data remains. And the data is a great big blow to neo-Darwinism/population genetics since many assumptions made since the discovery of Mendel’s paper now need to be revisited and thought through again.

    Kimura found way, way more diversity within genes to continue with standard PG analyses, so he switched to his “neutral theory,” and moving neutral drift to the forefront. Now, with this study, we’re seeing a tremendous number of non-synonymous differences between alleles, alleles that are supposed to be “wild-type.”

    This cannot be good news for PG since it becomes hard to explain the presence of this diversity, and because it indicates a more secondary role for genes.

    If you have problems with the paper, then write to Nature Communications and tell them about your concerns. When Nature Communications addresses those concerns, should they do that, then your opinion will have been validated, and I will then be happy to grapple with your understanding of the paper. Until such time, let’s not waste any more of our valuable time discussing this.

  92. 92
    wd400 says:

    There is certainly no value in correcting all of your errors, PaV. But, since no IDers seems to want to, I’ll correct the most glaring ones.

    It’s simply not possible that the reduction in diverity of protein-types can be “attributed to how the alleles are being regulated”, because this paper is about genomic DNA, and does nothing to measure the results of the regulation of that DNA. You are wrong that is only considers nsSNPS, you are wrong in claiming there are a “tremendous number of non-synonymous differences between alleles” (among those that vary at all they report 1.3–1.7 nsSNPs!), and you are wrong that it compares genomic results to proteomic ones. I’m not sure how more wrong you can be.

    You don’t seem to understand what the 60:40 ratio is. It’s whether chemically altering (or just non-syn.) variant are present in both chromosomes, or only on one. The ratio is only “stable” when aggregated across whole genomes – i.e when you take thousands of draws from underlying distribution. Just like the mean of series of dice throws will converge on 3.5, the mean of this ratio will converge on the population-mean when you takes thousands of draws, so the spread (60–64% single-chromosomes) is not a surprise. There’s actually at least some suggestion of purifying selection in these results too, since the chemically altering variants have a high “single chromosome” frequency than normal nsSNPS (presumably because chemically altering variants are rarer than nsSNPs at large, which in turn are rarer than syn. SNPs).

    Finally, I don’t what you are on about with this fixation with wild types (for large genes made mostly of introns…). The paper finds something we’ve already known, and which is fairly obvious. If you take haplotypes that contain many variable sites then eventually no single haplotype will have a frequency > 0.5. Why do you think this is a problem. There is no “wild type genome”, or “wild type chromosome 12”, that there is no haplotype for some 20 kb gene with frequency > 0.5 hardly seems to matter.

    So, I’m afraid it’s a matter of fact that you don’t understand the paper. As I’ve said from the start, that’s not really news, though it is still interesting that no one could pull you up on all these mistakes.

  93. 93
    wd400 says:

    Oh, on this

    So, this is not about understanding the paper. This is about wd400 saying: (1) you can’t believe what’s put out in the press release (although in the paper they make this exact same claim), and (2) you should look to learned scientists to determine a paper’s worth, and (3) then you should follow their interpretation.

    Nah. Here’s the thing. You shouldn’t believe what gets put in press releases, because the job of press officers is to promote their university, not communicate science. You don’t have to trust other scientists on a papers worth, but, and this should hardly need saying, you should be skeptical of all results.

    Instead of credulously copy-paste-bolding sentences that you thought supported your own position, you should’ve read the paper, understood what they mean by “mutations” and the manner in which they were claiming they were non-random.

  94. 94
    ppolish says:

    Wd400, I don’t think “press officers promoting their University” is applicable here.. Max Planck Institute is not a University. They don’t need promo like maybe your University does lol. A member there won this years Nobel though:

    http://www.mpg.de/8688233/nobel-prize-hell-2014

  95. 95
    wd400 says:

    Max Planck institutes need promotion just like everyone else, why else would they have a PR office? Or create such a ludicrous release for that matter?

  96. 96
    ppolish says:

    What was ludicrous WD? Please cite a specific ludicrous sentence or two in the press release if you want. Maybe the German language statement is ludicrous, but the English version seems well written. World Class outfit over there at Max Planck.

  97. 97
    wd400 says:

    Well, starting from the start, the opening paragraph doesn’t describe the paper. Even gpuccio agress the press release doesn’t describe the paper very well.

    (By the way, there isn’t a single Max Planck institute to call a world class outfit — there are many across Germany and a few elsewhere, each with there own area of focus, including one of the leading centres for evolutionary anthropology).

  98. 98
    ppolish says:

    The opening paragraph does not meet the definition of ludicrous sorry. And you now realize the Max Planck Institute is not a University as you earlier assumed. Margret Hoehe is also one sharp cookie. Fighting disease instead of wasting time fighting “creationists”. Guys like Dawkins & Coyne & PZMyers are such lightweights.

  99. 99
    wd400 says:

    Well, I don’t know what’ more ludicruous than a press release that doesn’t describe the paper, and claims that paper is the end of Mendel. So I guess we just differ.

    I don’t what the point of the rest of your comment is (some folks that spend their time defending evolutionary biology don’t work on diseases so they are lightweights?), so let’s call that an end.

  100. 100
    bornagain77 says:

    wd400, so you consider Dawkins & Coyne & PZMyers (throw Tyson in there) to be heavyweights in science? 🙂

    Thanks for the laugh, I consider them to be nothing more than dogmatic atheists who have wrapped themselves in the cloak of science so as to promote their religion,,,, all the while ignoring, explaining away, and/or obfuscating (as you also do wd400), any and all contrary evidence that does not fit their preferred materialistic worldview,,, The only one who did anything of note in science was Dawkins with the ‘polished’ selfish gene, and even that idea is now considered bunk, even harmful to science, by many people in the field,, people like Shapiro, Sternberg, Nobel, Koonin, Trivonov etc.. etc..

    No those atheists are certainly not heavyweights in science, not even close,,, they will soon quickly be forgotten when science moves on, perhaps a footnote for how Dawkins and Tyson misled science with false ideas, but that’s about it.

  101. 101
    PaV says:

    wd400:

    It’s simply not possible that the reduction in diverity of protein-types can be “attributed to how the alleles are being regulated”, because this paper is about genomic DNA, and does nothing to measure the results of the regulation of that DNA.

    The only reason that I was speaking of “regulation” in the first place was because of your claim that there was “purifying selection.” I couldn’t begin to understand why you were making such a claim.

    You are wrong that is only considers nsSNPS, you are wrong in claiming there are a “tremendous number of non-synonymous differences between alleles” (among those that vary at all they report 1.3–1.7 nsSNPs!), and you are wrong that it compares genomic results to proteomic ones. I’m not sure how more wrong you can be.

    I still haven’t read the entire paper. Nor do I intend to.
    I was referring to the cumulative number of nsSNPs they found. It was in the millions across the genome. But, your numbers are right, and, yes, at the protein level, less variation is expressed.
    Yet, here is what they write:

    Taken together, the diversity of haploid and diploid protein forms was much lower than their counterparts at the DNA sequence level. The absolute numbers were, however, still considerable, particularly of the protein diplotypes, up to 90% of which encoded two different proteins in the population. These can allow huge functional versatility of diploid genomes as an inherent key feature of diploidy and play an important role in biological variation within and between cells and organisms.

    You’ve called this a form of “purifying selection.” I don’t agree. It’s just the difference between non-synonymous and synonymous substitutions. Differences at the molecular level don’t always show up as differences at the amino acid level. We all know this. And the fact that for 90% of ‘genes’ “two different proteins” are encoded seems like someone turned off the purifying selection. “Purifying selection” is meant to reduce deleterious alleles. But we find lots of allelic forms. That is the origin of my comment about “purifying selection.” I don’t see why you can’t acknowledge this.

    Here’s what they write:

    The average number of haplotypes ‘per gene’ was between 3 and 22, much lower than the global averages described above (Supplementary Table 10c). These results demonstrate that the vast majority of genes, over 85%, do not encode one predominant haplotype. ‘Therefore, the concept
    that there is one predominant or ‘wild-type’ form of a gene and few rare or ‘mutant’ forms is overly simplistic and misleading’(quote from the study by Stephens et al.24).

    wd400:

    You don’t seem to understand what the 60:40 ratio is. It’s whether chemically altering (or just non-syn.) variant are present in both chromosomes, or only on one. The ratio is only “stable” when aggregated across whole genomes – i.e when you take thousands of draws from underlying distribution. Just like the mean of series of dice throws will converge on 3.5, the mean of this ratio will converge on the population-mean when you takes thousands of draws, so the spread (60–64% single-chromosomes) is not a surprise.

    Here’s what the authors write:

    Overall, cis configurations, leaving one form of the gene unperturbed, would be expected to occur more frequently in an individual genome to preserve organismal function. Thus, we determined the ratio of cis to trans configurations across all autosomal protein-coding genes for each individual genome in all sample sets (Methods). In fact, a striking phase imbalance was observed: without any exception, in each of the 14 molecularly phased genomes (Supplementary Table 16), 57CEU (Supplementary Table 14) and 372EUR statistically phased genomes, cis configurations of potentially perturbing mutations occurred significantly more frequently than trans configurations (Po7.68 10 8–
    2.11 10 3), resulting in an overall ratio of about 60:40
    (Table 1; Supplementary Note 4).

    This is not what they were expecting. Under random variation and negative selection, if anything, the ratio would be expected to be the reverse: trans:cis of 60:40. But, as usual, this doesn’t surprise you.

    Finally, I don’t what you are on about with this fixation with wild types (for large genes made mostly of introns…). The paper finds something we’ve already known, and which is fairly obvious. If you take haplotypes that contain many variable sites then eventually no single haplotype will have a frequency > 0.5. Why do you think this is a problem. There is no “wild type genome”, or “wild type chromosome 12?, that there is no haplotype for some 20 kb gene with frequency > 0.5 hardly seems to matter.

    Well, why don’t we listen to the authors. Perhaps you should write and inform them of the insignificance of their results. Here’s what they say (I’ve already quoted this, so, it apparently means little to you)

    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. The enormous diversity of haploid and diploid gene forms raises fundamental questions concerning the relationships between sequence(s), structure(s) and function(s).

    It is obvious to the authors, and was obvious to me, that this ‘diversity’ of forms undermines conventional neo-darwinian presumptions. I take their statement about “saturation may not even be achievable” to mean that there are so many “forms” floating around in the genome that they might not ever be able to identify them all.

    This has to be a nightmare** [see the paper cited in my comment below]** for a traditionally-trained population geneticist. You fall in that camp. And yet you just wave away problem after problem. It reminds me of the string quartet playing away atop the Titanic.

    So, I’m afraid it’s a matter of fact that you don’t understand the paper. As I’ve said from the start, that’s not really news, though it is still interesting that no one could pull you up on all these mistakes.

    You might have just as well added this: “As I’ve said from the start, that’s not really news, though it is still interesting that no one could pull ‘the authors’ up on all these mistakes.” IOW, do you want to claim that the authors have no knowledge of modern evolutionary biology? It is them, and their results, that you protest, not mine.
    End of discussion.

  102. 102
    PaV says:

    wd400:

    You’re a handful! 🙂

  103. 103
    PaV says:

    BTW, while I was looking around, I found this paper.

    The Abstract:

    Some species exhibit very high levels of DNA sequence variability; there is also evidence for the existence of heritable epigenetic variants that experience state changes at a much higher rate than sequence variants. In both cases, the resulting high diversity levels within a population (hyperdiversity) mean that standard population genetics methods are not trustworthy. We analyze a population genetics model that incorporates purifying selection, reversible mutations and genetic drift, assuming a stationary population size. We derive analytical results for both population parameters and sample statistics, and discuss their implications for studies of natural genetic and epigenetic variation. In particular, we find that (1) many more intermediate frequency variants are expected than under standard models, even with moderately strong purifying selection (2) rates of evolution under purifying selection may be close to, or even exceed, neutral rates. These findings are related to empirical studies of sequence and epigenetic variation.

    Author:
    Brian Charlesworth——Institute of Evolutionary Biology, School of Biological Sciences, University of
    Edinburgh, Edinburgh EH9 3JT, United Kingdom

    Submitted July 2014

    Does this man know nothing of modern evolutionary biology either?

    Yet, he’s saying exactly what I’m saying, isn’t he?

  104. 104
    PaV says:

    wd400:

    I wouldn’t bad-mouth Max Planck Institute too much.

    Here’s their “About Us” from the homepage:

    he Max Planck Society is Germany’s most successful research organization. Since its establishment in 1948, no fewer than 18 Nobel laureates have emerged from the ranks of its scientists, putting it on a par with the best and most prestigious research institutions worldwide. The more than 15,000 publications each year in internationally renowned scientific journals are proof of the outstanding research work conducted at Max Planck Institutes – and many of those articles are among the most-cited publications in the relevant field.

    What is the basis of this success? The scientific attractiveness of the Max Planck Society is based on its understanding of research: Max Planck Institutes are built up solely around the world’s leading researchers. They themselves define their research subjects and are given the best working conditions, as well as free reign in selecting their staff. This is the core of the Harnack principle, which dates back to Adolph von Harnack, the first president of the Kaiser Wilhelm Society, which was established in 1911. This principle has been successfully applied for nearly one hundred years. The Max Planck Society continues the tradition of its predecessor institution with this structural principle of the person-centered research organization.

    The currently 82 Max Planck Institutes conduct basic research in the service of the general public in the natural sciences, life sciences, social sciences, and the humanities. Max Planck Institutes focus on research fields that are particularly innovative, or that are especially demanding in terms of funding or time requirements. And their research spectrum is continually evolving: new institutes are established to find answers to seminal, forward-looking scientific questions, while others are closed when, for example, their research field has been widely established at universities. This continuous renewal preserves the scope the Max Planck Society needs to react quickly to pioneering scientific developments.

  105. 105
    wd400 says:

    YOu forget that most mutations in exons are non-synonymous, for the difference in DNA-diversity and protein-diversity o occur you need (a) magic stopping non-synonymous mutations happening or (b) selection keeping them at low frequency.

    Charlesworth is talking about a different problem. When the population-mutation rate per site is high, the infinite allele model breaks down because the “same allele” can be created mulitple times. So, some nice pop gen results don’t work anymore. The same problem doesn’t arise when you define variants over long stretches of variable sites, because new mutations are making new alleles in those cases. Papers like Charlesworth’s update our models, and make them applicable to cases they previously weren’t. They don’t require us to back up, burn The Origin and start again…

  106. 106
    fifthmonarchyman says:

    WD400 says,

    Papers like Charlesworth’s update our models, and make them applicable to cases they previously weren’t. They don’t require us to back up, burn The Origin and start again…

    I say,

    If you wonder why folks seem to be willfully ignorant of evolutionary biology this probably is a big part of the reason.

    To the interested inquirer other scientific fields always seem to be on the cusp of discovering something exciting and revolutionary. There is always something going on be it fusion or the holographic principle or quantum computing or who knows what.

    Meanwhile the Darwinist is forever updating his models.

    Talk about boring. There is more excitement in the average scrabble tournament than that.

    If the ID movement did not exist it would be in the best interest of the Darwinist camp to invent something like it just to liven the place up a little bit.

    peace

  107. 107
    wd400 says:

    Everyone wants a (scientific) revolution, no one wants to show one is required…

  108. 108
    fifthmonarchyman says:

    A little revolution never hurt anybody.

    This should be obvious to someone studying living things.

    Without an occasional scary upheaval there is only debilitating stagnation and eventual death.

    peace

  109. 109
    fifthmonarchyman says:

    WD400 said

    Everyone wants a (scientific) revolution, no one wants to show one is required

    I say,

    It must be terribly sad to be committed to a field of study where all the exciting stuff happened more than a hundred years ago

    peace

  110. 110
    Zachriel says:

    fifthmonarchyman: It must be terribly sad to be committed to a field of study where all the exciting stuff happened more than a hundred years ago

    The last century has seen the discovery of the DNA helix, not to mention feathered dinosaurs, and the 99 Lives Cat Whole Genome Sequencing Initiative. These discoveries aren’t as scientifically momentous as “Origin of Species”, of course, but they are certainly exciting to biologists, and to many non-scientists too.


    Edited to reduce snark quotient.

  111. 111
    fifthmonarchyman says:

    Of course the Darwinist response to those developments is to “update the models”.

    what Fun

    peace

  112. 112
    Zachriel says:

    fifthmonarchyman: Of course the Darwinist response to those developments is to “update the models”.

    The discovery of the DNA double-helix was reasonably consistent with genetic theory of the time, but it certainly established genetics as a central concern of evolutionary biology. Feathered dinosaurs have resulted in a somewhat different branching order for birds. And the 99 Lives Cat Whole Genome Sequencing Initiative is important to the health of kitties around the world!

    Only the feathered dinosaurs represents a change to the Theory of Evolution, and then, only to the precise genealogical relationships, not to the underlying mechanics involved.

  113. 113
    fifthmonarchyman says:

    Zac said,

    Only the feathered dinosaurs represents a change to the Theory of Evolution, and then, only to the precise genealogical relationships, not to the underlying mechanics involved.

    I say,

    Like I said evolutionary biology is the only scientific endeavor I know of where nothing ever changes.

    No matter what the discovery everything just stays the same talk about snooze-ville.

    According to Zac in a hundred years all that has changed is a few tweaks to “precise genealogical relationships”

    No wonder folks don’t care about learning this stuff.

    boring

    peace

  114. 114
    fifthmonarchyman says:

    I’m telling you guys if I was just starting out and I had the choice of endlessly “updating the models” or looking into this 60:40 ratio thing to see if there was something there.

    I’d explore the ratio in a heartbeat. It might be totally wrong but at least it’s exciting.

    check this out

    http://www.scielo.org.za/pdf/s.....210312.pdf

    peace

  115. 115
    Me_Think says:

    PaV @ 104

    It is obvious to the authors, and was obvious to me, that this ‘diversity’ of forms undermines conventional neo-darwinian presumptions. I take their statement about “saturation may not even be achievable” to mean that there are so many “forms” floating around in the genome that they might not ever be able to identify them all.

    Just search for ‘Wild type gene’ you will find articles as far back as 1998 which says exactly what this paper says.
    Eg: Jones, Elizabeth; Hartl, Daniel L. (1998). Genetics: principles and analysis.

    It is now appreciated that most or all gene loci exist in a variety of allelic forms, which vary in frequency throughout the geographic range of a species, and that a uniform wild type does not exist.

    Now you decide if the Max Planck paper has something that was not already know.
    Isn’t diversity of form exactly what evolution needs ? How is this a detriment to the process of evolution ?

  116. 116
    fifthmonarchyman says:

    Wow so apparently the ‘Wild type gene’ is known to be non-existent for 15 years and it caused no change at all to TOE.

    Talk about rigamortis.

    If the Higgs boson was shown to be merely a statistical construct rather than an actual particle I’ll bet that the change to the standard model would go beyond “updating the models”

    peace

  117. 117
    wd400 says:

    Fifth,

    Evolutionary biology has changed a lot since Darwin’s (and Fisher, and Haldane’s and Maynard Smiths’, and Kimura’s and Allan Wilson’s) time. It’s just that the theory has always advanced when scientists have provided better explanation, usually based on an expansion of the existing framework, or incorporating a new data source in our existing models.

    If that bores you then by all means carry on with the numerology.

  118. 118
    Me_Think says:

    fifthmonarchyman @ 114

    I’d explore the ratio in a heartbeat. It might be totally wrong but at least it’s exciting.

    check this out

    http://www.scielo.org.za/pdf/s…..210312.pdf

    Well, any cranial measurements can be approximated with icosahedron corners, so it can be expressed as Golden ratio.You can have corners like these

    {{0, -GoldenRatio, -1}, {-1, 0, -GoldenRatio}, {-GoldenRatio, -1,0}, {0, -GoldenRatio, -1}, {0,-GoldenRatio, 1}, {1, 0, -GoldenRatio}, {-GoldenRatio, 1, 0}, {0, -GoldenRatio, 1}, {0, GoldenRatio, -1}, {-1, 0, GoldenRatio}, {GoldenRatio, -1, 0}, {0,GoldenRatio, -1}, {0, GoldenRatio, 1}, {1, 0, GoldenRatio}, {GoldenRatio, 1, 0}, {0, GoldenRatio, 1}}

  119. 119

    wd400:

    Evolutionary biology has changed a lot since Darwin’s (and Fisher, and Haldane’s and Maynard Smiths’, and Kimura’s and Allan Wilson’s) time. It’s just that the theory has always advanced when scientists have provided better explanation, usually based on an expansion of the existing framework, or incorporating a new data source in our existing models.

    Could you please in around one paragraph explain the premise, systematics, requirements and necessary variables in “the theory” that “has changed a lot since Darwin’s” time, and without confusing it with other theories such as Cell Theory, Gene Theory and all others?

  120. 120
    Joe says:

    Why do evos keep talking about the “theory of evolution” as if it is something real?

  121. 121
    fifthmonarchyman says:

    wd400 says.

    Evolutionary biology has changed a lot since Darwin’s (and Fisher, and Haldane’s and Maynard Smiths’, and Kimura’s and Allan Wilson’s) time.

    I say

    You guys need to have a meeting or something.

    Zac says the only the feathered dinosaurs represents a change to the Theory of Evolution and this was simply a minor tweak to “precise genealogical relationships”

    Now you say that there was a lot of change but nothing changed in the existing framework. that is a little bit better than tweaking genealogical relationships and adjusting models I suppose but you will have to admit it’s not very sexy.

    I’m sorry but redecorating a living room now and then is just not as much fun as a good old fashioned major remodel.

    As far as exploring the notion that the ratio is an indicator of Irreducible Complexity being merely numerology goes.

    Well it’s that sort of quick dismissal of radical ideas that makes Evolutionary biology sound so boring in the first place compared to fields like cosmology.

    peace

  122. 122
    bornagain77 says:

    PaV, the sun has not even risen yet and it is already another bad day for Darwinists:

    150,000 quadruplex DNA sequence motifs found to be ‘non-randomly’ distributed throughout the genetic material of maize:

    Scientists uncover four-stranded elements of maize DNA – Dec. 3, 2014
    Excerpt: A team led by Florida State University researchers has identified DNA elements in maize that could affect the expression of hundreds or thousands of genes.
    “Maybe they are part of the machinery that allows an organism to turn hundreds of genes off or on,”,,,
    Bass and Carson Andorf,,, began this exploration of the maize genome sequence along with colleagues from FSU, Iowa State and the University of Florida. They wanted to know if certain DNA structures such as the four-strand G-quadruplex (G4) DNA might exist throughout the genetic material of maize.
    G4 structures are present in genes that regulate cancer and cell division in humans, making it an important focus in scientific research. But, not much is known about them.,,,
    The general public thinks of DNA as two connected strands known as the double helix. But scientists also discovered over the years that those strands regularly separate so they can replicate the genetic material. That material can also twist into different shapes such as a G-quadruplex.
    Bass and his colleagues found 150,000 sequence motifs that could theoretically adopt the G4 DNA structure, and they were distributed all over the chromosomes. Further examination showed that they were present in very specific places, as opposed to a random distribution.
    Given the strategic placement, the G4 is likely to perform some sort of function. Preliminary work showed that many of the genes identified were implicated in responses to energy crises within plant cells.,,,
    “It’s a very interesting aspect of DNA,” Bass said. “And people in the genetics field are very excited about it.”
    http://phys.org/news/2014-12-s.....maize.html

    Moreover, G-quadruplexes are found to be ‘conserved’ from bacteria to humans. Which opens the tantalizing possibility that a species specific ‘non-random’ distribution of quadruplex DNA sequence motifs may be found throughout all of biological life:

    Another Remarkable DNA Rescuing Machine (Elucidated) -June 4, 2013
    Excerpt: Some of these are composed of four strands that form stable structures called G-quadruplexes or G4s, so named because they tend to be rich in guanine. They are not uncommon,,,,
    ,,there is a machine that can unwind these G4s quickly and efficiently. Called Pif1 helicase, it is conserved from bacteria to humans.,,,
    Pif1 is “highly conserved, from bacteria to humans,”
    http://www.evolutionnews.org/2.....72811.html

  123. 123
    Zachriel says:

    fifthmonarchyman: Like I said evolutionary biology is the only scientific endeavor I know of where nothing ever changes.

    Seriously? The current Theory of Evolution is substantially changed from the Theory of Evolution of a century ago. Gee whiz, the double-helix wasn’t even discovered until the 1950s, or endosymbiosis in the 1960s. It’s the history of life that entices most of us. And that history is full of surprising twists and turns.

    fifthmonarchyman: in a hundred years all that has changed is a few tweaks to “precise genealogical relationships”

    Sorry that you’re not interested in science. You must be getting old. The kids love the warm-blooded, feathered dinosaurs.

  124. 124
    fifthmonarchyman says:

    Well bornagain77,

    I suppose we might need to adjust the models ZZZZZZZZZZZZZZ

    😉

  125. 125
    Joe says:

    The current Theory of Evolution is substantially changed from the Theory of Evolution of a century ago.

    So you say yet cannot support.

    Sorry that you’re not interested in science.

    Nice projection.

  126. 126
    PaV says:

    Me_Think:

    I did the search. Nothing there of any importance. And you give a citation for a book on population genetics found within a Wikipedia section on wild-type alleles.

    You should have noted that you were quoting Wikipedia and not Hartl’s book.

    Wikipedia articles are constantly being updated. There is no reason to believe that what is there has been known since 1998.

    It’s still the same problem: is using the infinite allele model applicable to what is now known about the diversity found within the genome?

  127. 127
    PaV says:

    BA77:

    PaV, the sun has not even risen yet and it is already another bad day for Darwinists:

    150,000 quadruplex DNA sequence motifs found to be ‘non-randomly’ distributed throughout the genetic material of maize:

    You’ll probably remember that years ago, probably early on, like in 2005-2006, I made the comment numerous times that with “whole genome analysis” either ID or Darwinism would be proved correct.

    And, of course I had in the back of my mind the degree of variation, and the number of actual alternate alleles that exist within the genome. To me, the story has been written. Darwinism cannot possibly survive what WGA provides day-in and day-out. It gave rise, as you know, to my: “Another Day; Another Bad Day for Darwinism.” It was exactly these kinds of results that I was refering to.

    Thanks for the ‘find.’ I’ll take a quick look.

  128. 128
    wd400 says:

    It’s still the same problem: is using the infinite allele model applicable to what is now known about the diversity found within the genome?

    THe human genome? Sure. The infinite allele model only assumes each mutation creates a new allele (i.e. is not a back mutation or a mutation to an existing allele). You only get these “no wild type” genes when you define haplotypes over long runs of chromosomes. But, of course, of all the possible haplotypes over a long run of a chromosome only a few exist, so a new mutation will likely create a new allele.

    As I said above, it works less well well when effective population sizes are very large or the mutation rate per site is very high. Neither of those apply to the resent history of humanity.

  129. 129
    Me_Think says:

    PaV @ 126

    I did the search. Nothing there of any importance. And you give a citation for a book on population genetics found within a Wikipedia section on wild-type alleles.

    If only the concept was confined to wiki pages, but no it is a standard concept. Here are links to Google books:
    iGenetics: A Molecular Approach

    Introduction to Genetic Analysis by Anthony J.F


    Molecular Biology: Concepts and Experiments

    Biological Science, Volume 1 by Scott
    Essentials of Genetics by William S. Klug
    and so on and on…

  130. 130
    fifthmonarchyman says:

    Hey ME_Thinks,

    I have a hypothesis and I need your help to test it.

    Remember the set of strings of coded words that contained one sonnet you provided to me back in the other thread?

    Could you provide me another coded set of the same size this time containing only Shakespearean sonnets?

    If my speculation about the ratio being an indicator of IC is correct then I should be able to measure different random variables in the two sets and the variance ratio should approach 60:40. thus confirming my hypothesis

    Additionally I might be able to look at each string in your original set and find one that fits better in the “all sonnet set”

    All of this will only work if both sets are coded the same way and if I don’t not know which string in your original set is the real one

    What do you say Can you help a brother out?

    Peace

  131. 131
    Me_Think says:

    I no longer have the original cipher, though if you manage to ferret out which of the strings given in the ‘dFSCI thread’ is a sonnet, I can tell you if you are correct.
    In any case, I have another set of encoded strings (with a fresh cipher) which also has Shakespeare sonnet(s). You can try with these strings :

    1. Ad itdk td klxr dltbk vtfp, dx itdk klxr qwxv’dk, If xfp xi klcfp, iwxh kltk vlcyl klxr upstwkpdk; Afu kltk iwpdl jbxxu vlcyl axrfqba klxr jpdkxv’dk, Tlxr htadk ytbb klcfp vlpf klxr iwxh axrkl yxfnpwkpdk, Hpwpcf bcnpd vcduxh, jptrka, tfu cfywptdp; Wcklxrk klcd ixbba, tqp, tfu yxbu upyta: Ii tbb vpwp hcfupu dx, klp kchpd dlxrbu yptdp Afu klwppdyxwp aptw vxrbu htgp klp vxwbu tvta. Lpk klxdp vlxh ftkrwp ltkl fxk htup ixw dkxwp, Htwdl, iptkrwpbpdd, tfu wrup, jtwwpfba spwcdl: Lxxg, vlxh dlp jpdk pfuxv’u, dlp qtnp klpp hxwp; Wlcyl jxrfkpxrd qcik klxr dlxrbudk cf jxrfka ylpwcdl: Slp ytwn’u klpp ixw lpw dptb, tfu hptfk klpwpja, Tlxr dlxrbudk swcfk hxwp, fxk bpk kltk yxsa ucp

    2. Cb xnp klpp cf dryl dxwk, Ad, klxr jpcfq hcfp, hcfp cd kla qxxu wpsxwk; Brk fxv cd jbtyg jptrka’d dryypddcnp lpcw, Afu jptrka dbtfupw’u vckl t jtdktwu dlthp.OK, kvx hcfrkpd cf tfu kltk ycslpw’d chsbphpfkpu. Nxv bpk’d vwckp klp iwpzrpfya tkktyg yxup. Fcwdk vp fppu kx dxwk klp bpkkpwd cf t kpmk cfkx iwpzrpfya xwupw.Ad klxr qxpdk xfvtwud, dkcbb vcbb sbryg klpp jtyg, Slp gppsd klpp kx klcd srwsxdp, kltk lpw dgcbb Mta kchp ucdqwtyp tfu vwpkylpu hcfrkpd gcbb jrk fxk dkcbb gpps, lpw kwptdrwp

    3. Hxv bcgp t vcfkpw ltkl ha tjdpfyp jppf Fwxh klpp, klp sbptdrwp xi klp ibppkcfq aptw! Wltk iwppocfqd ltnp I ipbk, vltk utwg utad dppf! Wltk xbu Dpyphjpw’d jtwpfpdd pnpwavlpwp! Afu apk klcd kchp wphxnpu vtd drhhpw’d kchp; Tlp kpphcfq trkrhf, jcq vckl wcyl cfywptdp, Bptwcfq klp vtfkxf jrwupf xi klp swchp, Lcgp vcuxv’u vxhjd tikpw klpcw bxwud’ upyptdp: Ypk klcd tjrfutfk cddrp dpph’u kx hp Brk lxsp xi xwsltfd, tfu rfitklpw’u iwrck; Fxw drhhpw tfu lcd sbptdrwpd vtck xf klpp, Afu, klxr tvta, klp npwa jcwud twp hrkp: Ow, ci klpa dcfq, ‘kcd vckl dx urbb t ylppw, Tltk bptnpd bxxg stbp, uwptucfq klp vcfkpw’d fptw

    4. Sx xik ltnp I cfnxgpu klpp ixw ha Mrdp, Afu ixrfu dryl itcw tddcdktfyp cf ha npwdp Ad pnpwa tbcpf spf ltkl qxk ha rdp Afu rfupw klpp klpcw sxpda ucdspwdp. Tlcfp papd, kltk ktrqlk klp urhj xf lcql kx dcfq Afu lptna cqfxwtfyp tbxik kx iba, Htnp tuupu iptklpwd kx klp bptwfpu’d vcfq Afu qcnpf qwtyp t uxrjbp htepdka. Ypk jp hxdk swxru xi kltk vlcyl I yxhscbp, Wlxdp cfibrpfyp cd klcfp, tfu jxwf xi klpp: If xklpwd’ vxwgd klxr uxdk jrk hpfu klp dkabp, Afu twkd vckl kla dvppk qwtypd qwtypu jp; Brk klxr twk tbb ha twk, tfu uxdk tuntfyp Ad lcql td bptwfcfq, ha wrup cqfxwtfyp

  132. 132
    fifthmonarchyman says:

    Hey Me_think,

    I must have been unclear.

    You have given me only half of what I need.

    I can use the 4 mixed strings but now I need a set of 4 strings with only Sonnets coded exactly the same way as the first set.

    I’m looking to compare the variation in the set of mixed strings with the variation in the set of only Shakespearean Sonnets. That is why I need two sets.

    peace

  133. 133
    Me_Think says:

    fifthmonarchyman @ 132
    Ok. Here:

    Two sonnets encoded in cipher
    =========================================================
    td itdk td klxr dltbk vtfp, dx itdk klxr qwxv’dk, cf xfp xi klcfp, iwxh kltk vlcyl klxr upstwkpdk; tfu kltk iwpdl jbxxu vlcyl axrfqba klxr jpdkxv’dk, klxr htadk ytbb klcfp vlpf klxr iwxh axrkl yxfnpwkpdk, lpwpcf bcnpd vcduxh, jptrka, tfu cfywptdp; vcklxrk klcd ixbba, tqp, tfu yxbu upyta: ci tbb vpwp hcfupu dx, klp kchpd dlxrbu yptdp tfu klwppdyxwp aptw vxrbu htgp klp vxwbu tvta. bpk klxdp vlxh ftkrwp ltkl fxk htup ixw dkxwp, ltwdl, iptkrwpbpdd, tfu wrup, jtwwpfba spwcdl: bxxg, vlxh dlp jpdk pfuxv’u, dlp qtnp klpp hxwp; vlcyl jxrfkpxrd qcik klxr dlxrbudk cf jxrfka ylpwcdl: dlp ytwn’u klpp ixw lpw dptb, tfu hptfk klpwpja, klxr dlxrbudk swcfk hxwp, fxk bpk kltk yxsa ucp

    dta kltk klxr ucudk ixwdtgp hp ixw dxhp itrbk, tfu c vcbb yxhhpfk rsxf kltk xiipfyp: dsptg xi ha bthpfpdd, tfu c dkwtcqlk vcbb ltbk, tqtcfdk kla wptdxfd htgcfq fx upipfyp. klxr ytfdk fxk bxnp ucdqwtyp hp ltbi dx cbb, kx dpk t ixwh rsxf updcwpu yltfqp, td c’bb hadpbi ucdqwtyp; gfxvcfq kla vcbb, c vcbb tyzrtcfktfyp dkwtfqbp, tfu bxxg dkwtfqp; jp tjdpfk iwxh kla vtbgd; tfu cf ha kxfqrp kla dvppk jpbxnpu fthp fx hxwp dltbb uvpbb, bpdk c, kxx hryl swxitfp, dlxrbu ux ck vwxfq, tfu ltsba xi xrw xbu tyzrtcfktfyp kpbb. ixw klpp, tqtcfdk ha dpbi c’bb nxv upjtkp, ixw c hrdk fp’pw bxnp lch vlxh klxr uxdk ltkp

    Test Strings:
    ===========================================================
    1. dx xik ltnp c cfnxgpu klpp ixw ha hrdp, tfu ixrfu dryl itcw tddcdktfyp cf ha npwdp td pnpwa tbcpf spf ltkl qxk ha rdp tfu rfupw klpp klpcw sxpda ucdspwdp. klcfp papd, kltk ktrqlk klp urhj xf lcql kx dcfq tfu lptna cqfxwtfyp tbxik kx iba, ltnp tuupu iptklpwd kx klp bptwfpu’d vcfq tfu qcnpf qwtyp t uxrjbp htepdka. apk jp hxdk swxru xi kltk vlcyl c yxhscbp, vlxdp cfibrpfyp cd klcfp, tfu jxwf xi klpp: cf xklpwd’ vxwgd klxr uxdk jrk hpfu klp dkabp, tfu twkd vckl kla dvppk qwtypd qwtypu jp; jrk klxr twk tbb ha twk, tfu uxdk tuntfyp td lcql td bptwfcfq, ha wrup cqfxwtfyp

    2. lxv bcgp t vcfkpw ltkl ha tjdpfyp jppf iwxh klpp, klp sbptdrwp xi klp ibppkcfq aptw! vltk iwppocfqd ltnp c ipbk, vltk utwg utad dppf! vltk xbu upyphjpw’d jtwpfpdd pnpwavlpwp! tfu apk klcd kchp wphxnpu vtd drhhpw’d kchp; klp kpphcfq trkrhf, jcq vckl wcyl cfywptdp, jptwcfq klp vtfkxf jrwupf xi klp swchp, bcgp vcuxv’u vxhjd tikpw klpcw bxwud’ upyptdp: apk klcd tjrfutfk cddrp dpph’u kx hp jrk lxsp xi xwsltfd, tfu rfitklpw’u iwrck; ixw drhhpw tfu lcd sbptdrwpd vtck xf klpp, tfu, klxr tvta, klp npwa jcwud twp hrkp: xw, ci klpa dcfq, ‘kcd vckl dx urbb t ylppw, kltk bptnpd bxxg stbp, uwptucfq klp vcfkpw’d fptw

    3. td itw td c th yxfypwfpu klp dltgpdsptwp dxffpk tfu klp yxup cd ltwu kx upycslpw rfbpdd axr gfxv fxk xfba klp dxffpk tfu klp wpbtkp gpa jrk tbdx vltkpnpw cd klp wpsbtyphpfk kpmk. c wptbba uxf’k gfxv vltk kx kasp dx c vcbb dkxs lpwp; tfu fxkp kltk dcfyp ha kaspu kpmk cd ntdkba uciipwpfk iwxh tfa dltgpdsptwp dxffpk, erdk klp stkkpwf dlxrbu jp t uptu qcnptvta ci axr pmthcfp klp bpkkpwd tfu klpcw pfyxucfq ybxdpba. c vcbb bptnp klp wpdk xi klp dxffpk td ck cd:vlxh dlp jpdk pfuxv’u, dlp qtnp klpp hxwp; vlcyl jxrfkpxrd qcik klxr dlxrbudk cf jxrfka ylpwcdl: dlp ytwn’u klpp ixw lpw dptb, tfu hptfk klpwpja, klxr dlxrbudk swcfk hxwp, fxk bpk kltk yxsa ucp

    4. c bxnp klpp cf dryl dxwk, td, klxr jpcfq hcfp, hcfp cd kla qxxu wpsxwk; jrk fxv cd jbtyg jptrka’d dryypddcnp lpcw, tfu jptrka dbtfupw’u vckl t jtdktwu dlthp.xg, kvx: hcfrkpd cf tfu kltk ycslpw’d chsbphpfkpu. fxv bpk’d vwckp klp iwpzrpfya tkktyg yxup. icwdk vp fppu kx dxwk klp bpkkpwd cf t kpmk cfkx iwpzrpfya xwupw.td klxr qxpdk xfvtwud, dkcbb vcbb sbryg klpp jtyg, dlp gppsd klpp kx klcd srwsxdp, kltk; lpw dgcbb hta kchp ucdqwtyp tfu vwpkylpu hcfrkpd gcbb jrk fxk dkcbb gpps, lpw kwptdrwp

  134. 134
    fifthmonarchyman says:

    Me_think

    thank you very much

    I’ll let you know how it turns out I’m really busy so it might take a while

  135. 135
    leebowman says:

    WD400 wrote:

    As I said above, it works less well well when effective population sizes are very large or the mutation rate per site is very high. Neither of those apply to the resent history of humanity.

    Agreed.

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