Evolution

Darwin’s peppered myth: Turns out, peppered moths take care to protect themselves

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A Darwin cult (the peppered myth) developed during the twentieth century around the peppered moths, with the recent “resounding triumph” that it turns out that pollution effects do favour dark coloured moths over light coloured ones in the same species, with no important changes.

Whoop whoop. That is all Darwinism can come up with, in real life, after all this time.

But so? Snowbelt effects explain why the Canadian Groundhog Day groundhog is white and the American one is brown. No evolution was ever harmed in the making of the diverting nonsense.

In “Peppered Moths Without Evolution” (July 31, 2012), Creation-Evolution Headlines comments , noting a recent, more detailed study,

Kettlewell and Majerus didn’t take into account the moths’ behavior. They treated moths as passive creatures that would alight on tree trunks at random. They placed the selective power in the environment, with lower contrast producing greater camouflage, leaving the high-contrast moths vulnerable to birds.

The South Korean researchers found, instead, that moth behavior plays a vital role in the camouflage. They “found out that moths are walking on the tree bark until they settle down for resting; the insects seem to actively search for a place and a body position that makes them practically invisible.” A video clip embedded in the article shows the moths doing this.

The article avoids superstitious homage to Darwin as well, apparently. That’s a start  in the right direction.

We always thought that the moth had more interest in protecting its hide than the researchers did, and guess what? But how do the moths know if, when they feel invisible, they really are invisible?

See also: US Darwinists (US ranked 14th) wail over South Korea (ranked 1st), supposedly “not able to compete”

212 Replies to “Darwin’s peppered myth: Turns out, peppered moths take care to protect themselves

  1. 1
    PaV says:

    In the video (at PhysOrg), it looks like the moths are flapping their wings up and down so as to match the light intensity of their wings to that of the background, and orient their bodies until that happens.

  2. 2
    bornagain77 says:

    For a twist on this experiment that would really drive Darwinists bonkers, they could artificially darken or lighten some moths and see if their behavior adjusts accordingly. It would certainly raise some interesting issues if they did adjust their behavior, as well as throwing another monkey wrench into the Darwinian Icon of peppered moths

  3. 3
    NickMatzke_UD says:

    Yet another example of why real biologists think creationists/IDists are kooks, and rightly so.

    Amongst the problems with this post and the young-earth creationist one that is referenced:

    1. You creationists screamed for 10 years about how the peppered moth example was a “peppered myth” because allegedly the evidence was against the bird predation/camouflage hypothesis first documented by Kettlewell. But it turned out Kettlewell was right, as was obvious throughout to anyone who carefully read Kettlewell’s research and the half dozen subsequent studies which confirmed Kettlewell’s basic conclusions. You don’t get to call something a myth when the evidence has confirmed it. Your position was the mythical one.

    2. The peppered moth isn’t “all Darwinism can come up with, in real life, after all this time”. That’s just silly taunting, even creationists know there are many other examples of natural selection in the wild, not to mention all of the other evidence for evolution, NS, etc. If there weren’t, you guys wouldn’t spend so much time talking about all of those other pieces of evidence.

    3. You quote Creation-Evolution Headlines saying “Kettlewell and Majerus didn’t take into account the moths’ behavior.” That’s just wrong. Both Kettlewell and Majerus, and other researchers, did work specifically on the resting behavior of peppered moths, and whether or not they sought out matching backgrounds or not. IIRC, Kettlewell thought they did, and proposed the “contrast/conflict” hypothesis as a behavioral explanation for how they might do it (by trying to minimize the contrast between a part of the body their eyes can see, and the surface beneath). However, the experimental tests of these ideas, including by Majerus IIRC, have not found much evidence for peppered moths specifically picking backgrounds matching their white or black body color. It looks like peppered moths, at least, just look for a shady spot on a tree. (And actually, this makes the bird predation/camouflage hypothesis even stronger, since if peppered moths picking matching backgrounds, this would weaken selection against white moths when soot darkened parts of the environment; the white moths would just behaviorally avoid darkened areas).

    4. The study being discussed is on moths in South Korea. These are not the same species as the peppered moth in England, even if the Korean moths are “peppered”. It looks like they’re not even the same genus. Some moths do indeed actively seek out matching backgrounds. This was known before the Korean study — e.g. Ted Sargent documented this in an American moth species in the 1990s IIRC.

    But it looks like, whatever those species do, the British peppered moth species doesn’t have this behavior. So the behavior of these other species is irrelevant to them. There are tens of thousands of moth species on the planet, you can’t just read something about a moth species in Korea and make wild, random claims about the implications for a species of moth on the other side of the planet in England which has been very well studied on its own.

    Short version: you and your YEC source made a complete incompetent hash of this story, if you had any sense of scientific propriety or care for truth you would issue a retraction, recommend that Creation-Evolution Headlines did the same, and write them off as anti-scientific yammerers who don’t care about research or accuracy if they don’t. This kind of thing is the *primary* reason creationists don’t get no respect from scientists. They don’t deserve it. They don’t earn it. In fact, what creationists earn is just pity and scorn, through confident-but-poorly-researched-and-inaccurate screeds like this one.

  4. 4
    Maus says:

    Correct me if I’m wrong, but I could swear I saw this previously on this site. Is this a repeat or a replication?

  5. 5
    bornagain77 says:

    I’m with you Nick, it really is kind of kooky to try to prove anything conclusive about Darwinism with peppered moths. Perhaps we can get down to some real biology with winged insects?

    Bernard d’Abrera on Butterfly Mimicry and the Faith of the Evolutionist – October 5, 2011
    Excerpt: For it to happen in a single species once through chance, is mathematically highly improbable. But when it occurs so often, in so many species, and we are expected to apply mathematical probability yet again, then either mathematics is a useless tool, or we are being criminally blind.,,, Evolutionism (with its two eldest daughters, phylogenetics and cladistics) is the only systematic synthesis in the history of the universe that proposes an Effect without a Final Cause. It is a great fraud, and cannot be taken seriously because it outrageously attempts to defend the philosophically indefensible.
    http://www.evolutionnews.org/2.....51571.html

    Well that’s not good for your Darwinism Nick! Hey Nick I have another question for you, why do you still believe neo-Darwiniism to be true when, even if we had all the scientists and all the supercomputers in the world, you still cannot make even a single ‘simple’ insect wing from scratch?

  6. 6
    sergiomendes says:

    bornagain77,

    “For a twist on this experiment that would really drive Darwinists bonkers, they could artificially darken or lighten some moths and see if their behavior adjusts accordingly.”

    most insightful point. i myself would volunteer to assist in this excellent effort to advance science and intelligent design.

    sergio

  7. 7
    sergiomendes says:

    bornagain77,

    “you still cannot make even a single ‘simple’ insect wing from scratch?”

    impossible to humanly copy what God has already perfected, no?

    sergio

  8. 8
    Joe says:

    Hey Nick, how can one tell natural selection from genetic drift, in the wild?

    And how can we test that either natural selection or genetic drift produced moths from non-moths? THAT is the myth Nick, that natural selction has anything to do with the arrival of moths.

    IOW what is the evidence that natural selection or genetic drift can do anything?

    Ya see Nick that is why the vast majority of people think that evolutionary biologists are kooks and liars- and rightly so.

  9. 9
    Joe says:

    Ken Miller on the peppered moth:

    What we do know is that the rise and fall of dark-colored moths, a phenomenon known as “industrial melanism,” remains a striking and persuasive example of natural selection in action. What we have to be cautious about is attributing 100% of the work of natural selection in this case to the camouflage of the moths and their direct visibility to birds.

    That’s it? REALLY? If that is all natural selection can “do” then it is obvious that the theory of evolution is in deep poo….

  10. 10
    A Gene says:

    Hey Nick, how can one tell natural selection from genetic drift, in the wild?

    One could calculate the probabilistic resources needed to get the observed changes: the increase and subsequent decrease in melanism. Here’s a chance to throw some ID theory at a problem.

  11. 11
    PaV says:

    Nick:

    You creationists screamed for 10 years about how the peppered moth example was a “peppered myth” because allegedly the evidence was against the bird predation/camouflage hypothesis first documented by Kettlewell. But it turned out Kettlewell was right, as was obvious throughout to anyone who carefully read Kettlewell’s research and the half dozen subsequent studies which confirmed Kettlewell’s basic conclusions.

    Judith Hooper, in her “Of Moths and Men”, raises substantial issues with Kettlewell’s study. She is neither a “creationist”, nor an ID adherent. So why go blaming IDists?

    And, there’s your mention of Ted Sargent. He is mentioned quite often in Hooper’s book. Here’s what he says about melanism:

    In this same way, I have suggested that melanic polymorphisms may actually be polyphenisms, with the gene (or genes) for melanism being expressed under some conditions, and not expressed under others. The fact that melanism acts like a Mendelian dominant is irrelevent to my suggestion. I would agree that the gene is a dominant one, and is inherited as such, under conditions where this gene is expressed. And, indeed, selection would act to increase or decrease the incidence of melanism under these conditions, since at least two phenotypes (“typical” and “melanic”) are being produced. But what I am also suggesting is that the gene in question (i.e., the dominant allele for melanism) may not be expressed under some conditions. This could give the impression that the “typical” form is due to a homozygous recessive genotype. But perhaps the moths in question possess the genetic potential to be either typical or melanic – and the dominant allele (for melanism) is not being expressed (just as the alleles for a “spring” form are not being expressed in the “fall” brood of species with seasonal forms). Thus, I am suggesting that gene (or allele) frequencies may not be changing in nature, at least to the extent suggested by the changing frequencies of the two forms that are seen in species exhibiting industrial melanism. Putting it another way, phenoypes may change without changes in the underlying genotypes. Or, at least there need not be a simple relationship between the two.

    Well, Nick, if Ted Sargent–an established scientist, not a Creationist, not an IDist–is correct, then “melanism” as an example of neo-Darwinian mechanisms looks like it might be completely wrongheaded.

    So, who’s guilty then of making “a complete incompetent hash of this story”, the IDists, or the evolutionists?

  12. 12
    Starbuck says:

    When the changes were first noted the genetic basis was unknown, and one idea tried out was simply that the
    pollution on food plants caused the insects to become darker. However, the melanics are genetic (usually simple Mendelian dominants) and pollution has not been shown to change the color of adults, so the most likely selective agent is (visual) predation.

  13. 13
    NickMatzke_UD says:

    Hey Nick, how can one tell natural selection from genetic drift, in the wild?

    This is easy, do you really not know this? We teach it to undergrads in genetics class.

  14. 14
    NickMatzke_UD says:

    When the changes were first noted the genetic basis was unknown, and one idea tried out was simply that the
    pollution on food plants caused the insects to become darker. However, the melanics are genetic (usually simple Mendelian dominants) and pollution has not been shown to change the color of adults, so the most likely selective agent is (visual) predation.

    Yep.

  15. 15
    NickMatzke_UD says:

    Wow, you IDists are so incredibly desperate to take down the peppered moth example, you will say almost anything, no matter if it contradicts even your own previous criticisms. Here’s the Discovery Institute Anony-News person:

    http://www.evolutionnews.org/2.....62781.html

    So, Kang et al. decided to go back to the original plan and let the moths do what they do naturally without investigators interfering. They let the moths choose the trees to land on, and they photographed what they did after they landed. It changed the picture entirely.

    Into the forest they went, releasing their captive moths (two native species), and watching them with Canon cameras in hand. They photographed the initial landing spot and orientation, then watched them come to a final resting spot and orientation — often some centimeters from where they initially landed. Calibrating their photographs carefully with controls, they brought these photographs into the lab, cropped them to remove extraneous cues, and showed them to human subjects as “experimental predators.”

    Using software that flashed the images on a screen, they asked the human predators to hunt for the moths in the photographs within a reasonable time limit. A major discovery followed. The moths were much harder to spot after they moved from their initial landing spot to the final resting spot. You can see this for yourself in some of the photographs they published. The moths moved around, some of them rotating, till they became almost invisible. You can also watch the moth behavior in movie clips from the Supporting Information page. Sure enough; those clever insects demonstrated an uncanny ability to blend perfectly into the bark by moving around. If you had photographed only their initial landing spot (or had glued them to the tree trunk), you wouldn’t know this.

    It’s astonishing (and deplorable) that during the 57 years that the peppered moth has been promoted as a stellar case of evolution in action, nobody performed this experiment until now: “… no direct test of adaptive role of this behavior has been conducted,” the team says on page 2, and again on page 5, “This is the first study that directly measures the detection of moths by visual predators before and after a moth performed the body positioning behavior.”

    Yet the behavior of the moth is key to the story. In the real world, as opposed to the staged peppered-moth photos we have all seen in textbooks, the moths would not have stood out like sore thumbs on the tree trunks. They would have wandered about for a place to blend in; most likely, they would not have landed in such conspicuous spots in the first place (Wells, p. 148). Letting the moths do what comes naturally is what the experimenters should have done. The old peppered moth experiments, consequently, have been invalidated (again).

    Over here in real life:

    1. Kettlewell and Majerus both *did do* bird predation experiments where the moths were allowed to find their own resting spots. The new study didn’t even do anything with bird predation.

    2. Wells himself, copying the critiques by Majerus and others of peppered moth work, claimed that it was a problem when (in some experiments) human vision was used to judge hiddenness, rather than bird vision. Some peppered moth work was also criticizied for artificiality, yet when the Korean study flashes images to humans on a dang computer screen, no such complaint is raised, even though this is far more artificial than anything done in the various classic peppered moth studies.

    When these sorts of points can be used against peppered moth work, it’s a huge crashing problem for peppered moth work! But when these Korean researchers ignored this and used human vision, oh that was just fine, and revolutionary work debunking the peppered moth example, somehow-or-other-we-wont-say. Get your dang story straight, guys.

    3. The DI post neglects to note that Kettlewell and Majerus did both explicitly study peppered moth resting and positioning behavior, and were well aware of its potential importance.

    4. It also failed to mention that the background-matching behavior observed in the Korea moths has been explicitly sought in the peppered moth, but the behavior isn’t really found in that species.

    Incompetence, thy name is creationism/ID.

  16. 16
    bornagain77 says:

    Starbuck, this is not a paper directly challenging natural selection per se in the shifts of light colored to dark colored moths. To be sure, Kang et al. do not deny that natural selection might be at work. This paper primarily points out how weak the experimental setup was in the first place. Moreover the paper reveals a highly sophisticated behavior in moths for searching out the best camouflage. Indeed I do not doubt that populations of moths have shifted in proportions to dark and light colors, but what I want to know is where did the moths get the genetic information for light and dark colors, and where did they get this highly sophisticated camouflaging behavior in the first place? Darwinists simply never address these important issues!

    ENV has weighed in:

    Journal of Evolutionary Biology Confirms Jonathan Wells (by Name) on Peppered Moth Myth – August 2012
    Excerpt: It’s astonishing (and deplorable) that during the 57 years that the peppered moth has been promoted as a stellar case of evolution in action, nobody performed this experiment until now: “… no direct test of adaptive role of this behavior has been conducted,” the team says on page 2, and again on page 5, “This is the first study that directly measures the detection of moths by visual predators before and after a moth performed the body positioning behavior.” ,,,
    Yet the behavior of the moth is key to the story. In the real world, as opposed to the staged peppered-moth photos we have all seen in textbooks, the moths would not have stood out like sore thumbs on the tree trunks. They would have wandered about for a place to blend in; most likely, they would not have landed in such conspicuous spots in the first place (Wells, p. 148). Letting the moths do what comes naturally is what the experimenters should have done. The old peppered moth experiments, consequently, have been invalidated (again).
    In summary, by using one of the iconic examples of evolution, we showed how a morphological adaptation cannot be fully understood without taking into account a full behavioural phenotype responsible in natural situations for increasing the adaptive function of the morphological trait.
    http://www.evolutionnews.org/2.....62781.html

  17. 17
    bornagain77 says:

    Nick states:

    Wow, you IDists are so incredibly desperate to take down the peppered moth example,

    I not desperate at all Nick. Indeed you scientifically inept Darwinists have taught me patience well. Please show me the exact experimental work that shows the origination of the light and dark colored gene(s), as well as the exact experimental work showing me exactly how this highly sophisticated camouflaging behavior arose?!?

  18. 18
    NickMatzke_UD says:

    I not desperate at all Nick. Indeed you scientifically inept Darwinists have taught me patience well. Please show me the exact experimental work that shows the origination of the light and dark colored gene(s), as well as the exact experimental work showing me exactly how this highly sophisticated camouflaging behavior arose?!?

    Peppered moths don’t have highly sophisticated camouflaging behavior. They don’t look around for a matching spot. The junk you are reading on UD and the DI website is talking about a paper about moth species in Korea which are not the same species or even the same genus as the peppered moth. For some bizarre reason they are conflating these different species, even though it is easy to see that this is a huge, basic, mistake.

    As for the mutational change from light to dark in the peppered moth, we don’t quite know the exact mutational change yet, but it could well be just a point mutation. It’s not exactly hard for a mutation to push up the amount of melanin in an organism.

  19. 19
    Joe says:


    Hey Nick, how can one tell natural selection from genetic drift, in the wild?

    This is easy, do you really not know this? We teach it to undergrads in genetics class.

    I don’t think it is possible, Nick. So it would be interesting to know exactly what is taught and exactly how it is verified- that natural selection, a result, didit.

    And what this new study demonstrates is that behavioural changes are the way to go as opposed to waiting for the right mutation to come along and change your color.

  20. 20
    PeterJ says:

    http://www.evolutionnews.org/2.....62781.html

    Something for Nick to look at. All his arguments have aleady been considered, and in my view simply show him up.

  21. 21
    bornagain77 says:

    As typical Nick, instead of actual experimental evidence showing the origination of anything of significance by neo-Darwinian processes, as requested from you, I get excuses from you. Excuse making is NOT EMPIRICAL SCIENCE Nick!

    Nothing In Molecular Biology Is Gradual – Doug Axe PhD. – video
    http://www.metacafe.com/watch/5347797/

    “Charles Darwin said (paraphrase), ‘If anyone could find anything that could not be had through a number of slight, successive, modifications, my theory would absolutely break down.’ Well that condition has been met time and time again. Basically every gene, every protein fold. There is nothing of significance that we can show that can be had in a gradualist way. It’s a mirage. None of it happens that way. – Doug Axe PhD.

    Nick you can’t even demonstrate the fixation of a single beneficial mutation in a metazoan much less a gene/protein:

    Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) – October 2010
    Excerpt: “Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, “This research really upends the dominant paradigm about how species evolve,” said ecology and evolutionary biology professor Anthony Long, the primary investigator.
    http://www.arn.org/blogs/index.....ruit_flies

    And Nick the fixation of advantageous mutations in bacteria are found to produce negative epistasis when combined:

    Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations)
    Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
    http://www2.cnrs.fr/en/1867.htm?theme1=7

    You simply Nick, no matter how ‘desperate’ you are to deny it to the contrary, have no empirical evidence to support your ‘bottom up’ neo-Darwinian worldview!

    This ‘problem’ is even admitted in peer-review

    The Fate of Darwinism: Evolution After the Modern Synthesis – January 2012
    Excerpt: We trace the history of the Modern Evolutionary Synthesis, and of genetic Darwinism generally, with a view to showing why, even in its current versions, it can no longer serve as a general framework for evolutionary theory. The main reason is empirical. Genetical Darwinism cannot accommodate the role of development (and of genes in development) in many evolutionary processes.
    http://www.springerlink.com/co.....03g3t7002/

    Peer-Reviewed Paper Concludes that Darwinism “Has Pretty Much Reached the End of Its Rope” – Jonathan M. – February , 2012
    Excerpt: Contrary to the Darwin lobby’s oft-repeated assertion that there are absolutely no weaknesses in Darwinian theory, the paper offers the concession that the modern synthesis has never provided an account of “how major forms of life evolved” — an omission that is not unsubstantial, to put it mildly.
    http://www.evolutionnews.org/2.....55941.html

    further notes on the bankruptcy of Nick’s ‘bottom up’ neo-Darwinian worldview:

    More from Ann Gauger on why humans didn’t happen the way Darwin said – July 2012
    Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population.
    You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect.
    Facing Facts
    But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes.
    http://www.uncommondescent.com.....rwin-said/

    Science & Human Origins: Interview With Dr. Douglas Axe (podcast on the strict limits found for changing proteins to other very similar proteins) – July 2012
    http://intelligentdesign.podom.....3_53-07_00

    Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video with references
    http://www.vimeo.com/17135166

    Nick if you want to know where the massive amounts of complex functional information came from in life, indeed if you want to know where life itself came from, I will give you a huge hint:

    Verse and Music

    John 1:1-5
    In the beginning was the Word, and the Word was with God, and the Word was God. He was with God in the beginning. Through him all things were made; without him nothing was made that has been made. In him was life, and that life was the light of all mankind. The light shines in the darkness, and the darkness has not overcome it.

    Newsboys – God’s Not Dead
    http://www.godtube.com/watch/?v=FMF12FNU

  22. 22
    Maus says:

    ” You don’t get to call something a myth when the evidence has confirmed it.” — Nick Matzke.

    You can of course, but you’ll rightly be called a blistering moron. And this is just how it should be. And just the same the you don’t get to call something a not-myth when the only evidence is mythology. Or, again, you can if you wish to be rightly called a blistering moron.

    “Wow, you IDists are so incredibly desperate to take down the peppered moth example, you will say almost anything, no matter if it contradicts even your own previous criticisms.”

    I thought this was known as ‘self-correcting’ rather than ‘desperation’. If there’s a difference between the two terms then I should sorely like to know what it is.

    “1. Kettlewell and Majerus both *did do* …”

    Truth in advertising is such a difficult thing. Kettlewell did not control for this appropriately and there were proper criticisms raised. However, Majerus did control for such things. And, if Wiki is to be considered faithful on the subject then indeed the peppered moth in question did prefer shaded areas. Which, really, isn’t terribly surprising at all.

    But if this is just a replication of the notion that moths prefer shady areas then there can hardly be an objection to it on that basis. And it’s hardly germane as to whether its the same or differing genus.

    Of course, the problem with experimental validation is never the experimental set up itself. It is always and only the conclusions that we draw from the experiment. And if the set up doesn’t permit us to draw the conclusions that we wish to draw then: Put a sock in it.

    I can’t fathom you disagreeing with any of these points, but if you do, then feel free to raise your objections.

    “2. Wells himself, copying the critiques by Majerus and others …”

    I agree. If one is to be speaking of bird vision in conclusion then one needs to include a tetrachromatic or pentachromatic model. Or show that the difference in cones are irrelevant for the given subject. Neither makes an issue for speaking of moth behaviour and camouflage with respect to the human visible spectra.

    “Peppered moths don’t have highly sophisticated camouflaging behavior.”

    That’s irrelevant. If they preferentially seek shaded areas then it is immaterial as to whether it is simple phototaxi behaviour or if it is predicated on the ability of moths to solve differntial equations with a slide rule.

    “As for the mutational change from light to dark in the peppered moth, we don’t quite know the exact mutational change yet, but it could well be just a point mutation.”

    Which is a fancy way to state “We don’t know. Full stop.”

    The problem here is that we are speaking only of the notion that predators can only predate what they can find and that predators are preferentially lazy. That predate first what’s easiest to go after. But that’s trivially observable without respect to any theory at all.

    And certainly if evolution were not consistent with such pedestrian notions then it would be a great charade. But of course, this is not the case. But what this doesn’t do is establish empirical evidence for evolution itself.

    It is, again, a problem of drawing conclusions that are supported by the experimental set up.

  23. 23
    A Gene says:

    I don’t think it is possible, Nick. So it would be interesting to know exactly what is taught and exactly how it is verified- that natural selection, a result, didit.

    Oh dear – there’s a whole book about it. There’s even papers specifically comparing drift and selection. How about pulling your head out of the sand and doing some research?

  24. 24
    bornagain77 says:

    Thou Shalt Not Put Evolutionary Theory to a Test – Douglas Axe – July 18, 2012
    Excerpt: “For example, McBride criticizes me for not mentioning genetic drift in my discussion of human origins, apparently without realizing that the result of Durrett and Schmidt rules drift out. Each and every specific genetic change needed to produce humans from apes would have to have conferred a significant selective advantage in order for humans to have appeared in the available time (i.e. the mutations cannot be ‘neutral’). Any aspect of the transition that requires two or more mutations to act in combination in order to increase fitness would take way too long (>100 million years).
    My challenge to McBride, and everyone else who believes the evolutionary story of human origins, is not to provide the list of mutations that did the trick, but rather a list of mutations that can do it. Otherwise they’re in the position of insisting that something is a scientific fact without having the faintest idea how it even could be.” Doug Axe PhD.
    http://www.evolutionnews.org/2.....62351.html

    Here is a Completely Different Way of Doing Science – Cornelius Hunter PhD. – April 2012
    Excerpt: But how then could evolution proceed if mutations were just neutral? The idea was that neutral mutations would accrue until finally an earthquake, comet, volcano or some such would cause a major environmental shift which suddenly could make use of all those neutral mutations. Suddenly, those old mutations went from goat-to-hero, providing just the designs that were needed to cope with the new environmental challenge. It was another example of the incredible serendipity that evolutionists call upon.
    Too good to be true? Not for evolutionists. The neutral theory became quite popular in the literature. The idea that mutations were not brimming with cool innovations but were mostly bad or at best neutral, for some, went from an anathema to orthodoxy. And the idea that those neutral mutations would later magically provide the needed innovations became another evolutionary just-so story, told with conviction as though it was a scientific finding.
    Another problem with the theory of neutral molecular evolution is that it made even more obvious the awkward question of where these genes came from in the first place.
    http://darwins-god.blogspot.co.....ay-of.html

    Majestic Ascent: Berlinski on Darwin on Trial – David Berlinski – November 2011
    Excerpt: The publication in 1983 of Motoo Kimura’s The Neutral Theory of Molecular Evolution consolidated ideas that Kimura had introduced in the late 1960s. On the molecular level, evolution is entirely stochastic, and if it proceeds at all, it proceeds by drift along a leaves-and-current model. Kimura’s theories left the emergence of complex biological structures an enigma, but they played an important role in the local economy of belief. They allowed biologists to affirm that they welcomed responsible criticism. “A critique of neo-Darwinism,” the Dutch biologist Gert Korthof boasted, “can be incorporated into neo-Darwinism if there is evidence and a good theory, which contributes to the progress of science.”
    By this standard, if the Archangel Gabriel were to accept personal responsibility for the Cambrian explosion, his views would be widely described as neo-Darwinian.
    http://www.evolutionnews.org/2.....53171.html

  25. 25
    Joe says:

    A Gene- as I thought, post hoc and ad hoc speculations are nice but they do not amount to much scientifically.

    Ya see there is no way to predict what will be slected for at any point in time and there is no way to predict what variation will arise at any point in time, so all one can do is post hoc and ad hoc speculations.

    And none of that deals with the arrival of the organism in the forst place.

  26. 26
    wd400 says:

    Joe,

    Didn’t you want to know how you tell the difference between drift and selection in the wild? And didn’t you get told?

    What has any of that got to do with “speculation” or the predictions you’re going on about?

  27. 27
    Joe says:

    wd400-

    The only way to tell the difference between genetic drift and natural selection in the wild is post hoc/ ad hoc speculation.

  28. 28
    sergiomendes says:

    Joe,

    “Ya see there is no way to predict what will be slected for at any point in time and there is no way to predict what variation will arise at any point in time, so all one can do is post hoc and ad hoc speculations.”

    I D most certainly against evolution, yes? I D acts to explain not needing “speculation”, yes? [“speculation” used in proper form, no? please correct if no]

    sergio

  29. 29
    wd400 says:

    You keep saying “speculation” – I don’t think you know what it means.

  30. 30
    A Gene says:

    The only way to tell the difference between genetic drift and natural selection in the wild is post hoc/ ad hoc speculation.

    Care to explain what you mean? Could you explain, precisely, the “post hoc/ ad hoc speculation” in this paper, for example?

    Or are you going to stick to your usual strategy of making general accusations, and avoiding backing them up?

  31. 31
    Starbuck says:

    You might find this one interesting as well.

  32. 32
    kairosfocus says:

    F/N: Worth looking from ENV:

    Kang et al. do not deny that natural selection might be at work. They propose that morphological and behavioral adaptations might “co-evolve” to produce the moths’ highly effective camouflage. Some might criticize their methods on various grounds.

    Possible criticisms include: (1) “Human predators” are a poor substitute for the moths’ natural bird predators. The authors acknowledge this, but explain that both birds and humans rely on visual cues to first locate the moths; besides, previous investigators also used humans to test camouflage effectiveness. (2) UV light, to which some birds are sensitive, might affect the visibility of the moths on the trees. The authors took this into account, but from their measurements of the UV spectrum of tree trunks and moths, they believe it would be a minor factor, at most, for UV-sensing birds. (3) They only studied two Korean moth species, and not peppered moths. The authors realize this; they were not making a global generalization. They were just cautioning investigators to be aware that behavioral phenotypes must be considered in all future studies of adaptive camouflage; and, thereby, they invalidated all previous work that had ignored this factor . . .

    KF

  33. 33
    Joe says:

    From A Gene’s link:

    The main result is that both drift and selection are significant factors affecting changes in the allele frequency of the medionigra gene.

    If one reads the paper they explain the difficulties in picking one gene. The other difficulty is the species you are going to study and the data you need. Then there is population size- the bigger the population the less effect natural selection will have- never mind changing environments shifting the selection pressures.

    Evolution cannot be plugged into any equation and have its history unfold. That is a fool’s errand.

  34. 34
    Joe says:

    Starbuck- what about by design?

  35. 35
    PaV says:

    Nick Matzke:

    Wow, you IDists are so incredibly desperate to take down the peppered moth example, you will say almost anything, no matter if it contradicts even your own previous criticisms.

    I think the real ‘desperation’ is on the part of the Darwinists. In fact, that is the whole undercurrent of Hooper’s book: that Ford, desperate to find evidence in nature for Darwinian mechanisms, pushed Kettlewell to come up with the ‘right’ statistical numbers for his experiment.

    Then there’s Ted Sargeant: his phenotypic induction hypothesis makes a lot of sense, has substantial evidence in its favor, and could even possibly, if not likely, apply to B. Betularia (that’s his opinion).

    It is Darwinists who want to insist that allelic frequencies changed in the B. Betularia population—something that is improbable on its surface. But, if they want to prove this to be the case, it is really quite simple to do: obviously the melanic form and dark form should have different allelic characters. So why not just sequence their genomes? What’s so hard about that?

    But, guess what, it hasn’t been done. Or, at least, it hadn’t been done when Majerus was writing this in 2004:

    So, what is needed to prove whether changes in
    frequencies of the peppered moth are indeed the result of differential bird predation?

    Two evidences for proof

    In my view, two pieces of evidence are critical (PP37). The first is that birds eliminate a greater proportion of one form than the other to an extent consistent with monitored
    changes in the frequencies of the forms. The second is that a connection should be made between the genotype and phenotype.

    The genotype – phenotype link

    Taking the second point first, it is an unfortunate omission that the multiple allelic gene that controls melanism in the peppered moth in Britain has not been identified and sequenced. The critical step of connecting genotype with phenotype has thus not been accomplished in this classical case of Darwinian evolution in action.

    However, this step has recently been accomplished in another case of adaptive melanism involving crypsis (Nachman et al., 2003) (PP38). The rock pocket mouse, Chaetodipus intermedius, varies in coat colour.

    I guess it’s still “unfortunate” that Darwinist haven’t bothered to check gene sequences and confirm changing alleles. Too bad. Maybe they’d find that the alleles are all there in each of the forms per Sargeant’s view. But, of course, that would ‘overturn’ an “icon of evolution”, and why take the risk. So, we’ll just push that down the road. (Who’s desperate here?)

    And then, to want to compare moths to mammals, and wing coloration to coat coloration? Isn’t this a bit of a stretch?

    So, here’s this real good scientist (we know this because he’s a Darwinist) who compares mammals to moths—and that’s OK. But we terrible “creationists” want to compare a moth in N. Korea to a moth in England. What’s the matter with us? What kind of scientific illiterates are we?

    Sorry for all the sarcasm, but I just can’t see what your ranting is all about. Industrial melanism, if conceded, is terribly inadequate to explain anything of importance in the progressive development of forms. The problem here is that it’s possible, almost likely, that it represents bad science. Why shouldn’t it be questioned? Or, IOW, why haven’t they sequenced B. Betularia yet?

    P.S.

    Just to cover myself, I did a Google search for sequencing. Here’s what I found:

    Industrial melanism in the peppered moth (Biston betularia) is an iconic case study of ecological genetics but the molecular identity of the gene determining the difference between the typical and melanic (carbonaria) morphs is entirely unknown. We applied the candidate gene approach to look for associations between genetic polymorphisms within sixteen a priori melanisation gene candidates and the carbonaria morph. The genes were isolated and sequence characterised in B. betularia using degenerate PCR and from whole-transcriptome sequence. The list of candidates contains all the genes previously implicated in melanisation pattern differences in other insects, including aaNAT, DOPA-decarboxylase, ebony, tan, tyrosine hydroxylase, yellow and yellow2 (yellow-fa). Co-segregation of candidate gene alleles and carbonaria morph was tested in 73 offspring of a carbonaria male-typical female backcross. Surprisingly, none of the sixteen candidate genes was in close linkage with the locus controlling the carbonaria-typical polymorphism. Our study demonstrates that the ‘carbonaria gene’ is not a structural variant of a canonical melanisation pathway gene, neither is it a cis-regulatory element of these enzyme-coding genes. The implication is either that we have failed to characterize an unknown enzyme-coding gene in the melanisation pathway, or more likely, that the ‘carbonaria gene’ is a higher level trans-acting factor which regulates the spatial expression of one or more of the melanisation candidates in this study to alter the pattern of melanin production.

    As to my comment about Majerus—this really good scientist—comparing mammals to insects, here’s a quote from the paper:

    In contrast to the success of the candidate gene approach applied to melanism in vertebrates, particularly through Mc1r [4], [5] but also tyrosinase-related protein 1 [41], Agouti [42], and K locus [43], the same strategy has been far less useful as a means to identifying polymorphisms controlling melanism in insects.

    Other than ruling out specific candidate genes, the present study does not bring us any closer to finding the ‘carbonaria gene’. Having effectively exhausted the a priori list of promising melanisation candidates, we are currently in the process of constructing a linkage map of B. betularia to identify the region that controls this famous polymorphism.

    Maybe it’s chemicals that control this putative ‘control region’, such as factory emissions, or tree bark chemicals themselves. This is the more likely explanation of “industrial melanization.” So, what, then, becomes of this “icon of evolution.”

    Read it and weep, Nick.

  36. 36
    wd400 says:

    Maybe it’s chemicals that control this putative ‘control region’, such as factory emissions, or tree bark chemicals themselves

    Nope, people tried that line in the 30s, turns out is a simple Mendelian trait, with carbonaria is dominant to the light-bodied form. Moreover, the gene has been mapped to a position homologous to silkworm chromosome 17:

    http://dx.doi.org/10.1126/science.1203043

    Note that study also found genomic evidence for recent rapid selection for the carbonaria allele – of the sort you’d expect if modern dark-bodied moths descend from one (or maybe a few) new mutants rather than from standing variation.

  37. 37
    wd400 says:

    Joe,

    The paper is an example (one of many…) of how to measure selection on an allele in the wild though, right? The thing you said you didn’t think would be possible?

  38. 38
    Joe says:

    wd400-

    Just because someone can say they did it doesn’t mean it actually pertains to natural selection.

  39. 39
    Maus says:

    wd400: From the abstract: “The rapid spread of a novel black form (known as carbonaria) of the peppered moth Biston betularia in 19th-century Britain is a textbook example of how an altered environment may produce morphological adaptation through genetic change.”

    From one of the authors: “‘We didn’t know if industrial melanism in the peppered moth is due to a single recent mutation or several, or if it came from outside Britain,’ explains Saccheri.”

    http://planetearth.nerc.ac.uk/.....spx?id=964

    Two points here: Again, to belabor the obvious, predators are lazy. And this can be verified by spending an afternoon watching any watering hole on the serengeti.

    And again, to belabor the obvious, this is not empirical evidence of where the mutation came from, or that the non-carbonaria morph has, will, or can be extinguished from the population. Yes, differing allele frequencies are one crucial component to things. But showing that allele frequencies can change is not the same showing from how and where they arise.

    Lastly, this distinguishes Evo from ID not a whit. Both make the statement that if *there already exist* given variants then the one that is most disadvantageous will be predated more.

  40. 40
    wd400 says:

    Joe,

    OK, so tell us where O’hara went wrong in that paper.

    Maus,

    This doesn’t seem to be related to the paper, which shows that the black moths likely descend form a single mutant. If you are squeezing your skepticism down to that mutation being somehow directed then you seem to be reaching beyond the testable?

  41. 41
    Maus says:

    wd400: “This doesn’t seem to be related to the paper, which shows that the black moths likely descend form a single mutant.”

    How does one empirically demonstrate a ‘maybe’?

    ” If you are squeezing your skepticism down to that mutation being somehow directed then you seem to be reaching beyond the testable?”

    Allow me the cheek to quote myself from the post you’re responding to: “…this is not empirical evidence of where the mutation came from …” This applies to every theory at all. Or none if you prefer to go Hypothesis non fingo.

    But I am curious as to your standpoint. Do you believe that the inaccessible past is ‘testable’ in the absence of time machines?

  42. 42
    wd400 says:

    “How does one empirically demonstrate a ‘maybe’?”

    You calculate how likely that maybe is given the evidence that you see, obviously.

    Past events are testable, in the sense you calculate the probability of present-day items with or without those past events.

  43. 43
    Maus says:

    wd400: “You calculate how likely that maybe is given the evidence that you see, obviously.”

    Sure, that’s statistics. You take a population and you study the present day frequency of the occurrence that you are interested in.

    “Past events are testable, in the sense you calculate the probability of present-day items with or without those past events.”

    Well, quite obviously we cannot count past events we do not have access to. But we can count the current ones. But in this case it would not then be a question of: ““‘We didn’t know if industrial melanism in the peppered moth is due to a single recent mutation or several, or if it came from outside Britain,’ explains Saccheri.”

    It would be the empirically derived statement that: “We have observed this mutation occur with x percent chance in y sized population over z time period.”

    But this has not been done.

  44. 44

    The whole peppered moth example of “evolution” is pretty amusing. If we carefully examine the storyline — indeed, if we even accept it hook-line-and-sinker as fact — what does it really show? That populations fluctuate around a norm without any meaningful evolutionary change occurring over time.

    As Philip Johnson has aptly noted, the peppered moth story has been trumpeted around the world to generations of unsuspecting students as a critical proof of Darwin’s theory. Yet nothing new emerged. The population essentially returned to a stable norm.

    Does it show natural selection making a difference? There can be some reasoned disagreement about this, but even if we grant it for sake of argument, it teaches us exactly zero about the larger evolutionary story. There is simply no rational reason to assume that the kinds of processes that led to a change in the ratio of light to dark moths had anything to do with bringing about moths in the first place.

    It is great fun, however, to see it still being upheld as one of the prime examples of “evolution” in action.

  45. 45
    wd400 says:

    Maus,

    Did you miss the tense of the statement you are quoting. “We didn’t…” now we do, because of statistics.

  46. 46
    A Gene says:

    Evolution cannot be plugged into any equation and have its history unfold. That is a fool’s errand.

    Err, but that’s what was done on the paper. I’ll second wd400’s question – what’s wrong with the paper? Please, give specific criticisms, not general denial or dismissal.

  47. 47
    Maus says:

    wd400: “Did you miss the tense of the statement you are quoting. “We didn’t…” now we do, because of statistics.”

    Heh, I did miss that, my English teacher looks smug right now. But it simply emphasizes my point. Regardless, your answer is non responsive. If ‘now we do’ then what observations were we counting?

    A Gene: “Please, give specific criticisms, not general denial or dismissal.”

    For starters its a purely correlative issue, as all such genomic studies are; but it wishes to assign a causation. This is simply a Post Hoc Ergo Propter Hoc fallacy. If one states that this then confirms a prior statement then its Affirming the Consequent. Note, this is a formal fallacy.

    But as a larger problem, as I’ve been discussing with wd400, we can fudge these issues a bit by stating that ‘In 80% of the cases that we observed what caused x, y was the cause. Therefore, for any x there is an 80% change y was the cause’. However, we have not of course observed the carboneria mutation occur at all, let alone coincident with a demonstrable cause. So there is simply no ability to bean-count, collect up frequencies, and attempt this anyways.

    It is still either Post Hoc or Affirming the Consequent, but it is now mathematically illiterate as well. Which is not to state that the manner in which they isolated the locus was invalid or anything less than interesting. I assume good faith and accuracy in their work in such.

    The problem is that they’re preaching far in excess of what the empirical results allow.

  48. 48
    Joe says:


    Evolution cannot be plugged into any equation and have its history unfold. That is a fool’s errand.

    Err, but that’s what was done on the paper.

    Errrrrr, that does not make it correct. And I gave specific criticisms.

  49. 49
    Joe says:

    OK, so tell us where O’hara went wrong in that paper.

    For starters, attempting to do something that cannot be done.

  50. 50
    bornagain77 says:

    Evolution cannot be plugged into any equation and have its history unfold.

    Indeed math is not kind to Evolution in the least:

    Haldane’s Dilemma
    Haldane was the first to recognize there was a cost to selection which limited what it realistically could be expected to do. He did not fully realize that his thinking would create major problems for evolutionary theory. He calculated that in man it would take 6 million years to fix just 1,000 mutations (assuming 20 years per generation).,,, Man and chimp differ by at least 150 million nucleotides representing at least 40 million hypothetical mutations (Britten, 2002). So if man evolved from a chimp-like creature, then during that process there were at least 20 million mutations fixed within the human lineage (40 million divided by 2), yet natural selection could only have selected for 1,000 of those. All the rest would have had to been fixed by random drift – creating millions of nearly-neutral deleterious mutations. This would not just have made us inferior to our chimp-like ancestors – it surely would have killed us. Since Haldane’s dilemma there have been a number of efforts to sweep the problem under the rug, but the problem is still exactly the same. ReMine (1993, 2005) has extensively reviewed the problem, and has analyzed it using an entirely different mathematical formulation – but has obtained identical results.
    John Sanford PhD. – “Genetic Entropy and The Mystery of the Genome” – pg. 159-160

    Kimura’s Quandary
    Kimura realized that Haldane was correct,,, He developed his neutral theory in responce to this overwhelming evolutionary problem. Paradoxically, his theory led him to believe that most mutations are unselectable, and therefore,,, most ‘evolution’ must be independent of selection! Because he was totally committed to the primary axiom (neo-Darwinism), Kimura apparently never considered his cost arguments could most rationally be used to argue against the Axiom’s (neo-Darwinism’s) very validity.
    John Sanford PhD. – “Genetic Entropy and The Mystery of the Genome” – pg. 161 – 162

    In Barrow and Tippler’s book The Anthropic Cosmological Principle, they list ten steps necessary in the course of human evolution, each of which, is so improbable that if left to happen by chance alone, the sun would have ceased to be a main sequence star and would have incinerated the earth. They estimate that the odds of the evolution (by chance) of the human genome is somewhere between 4 to the negative 180th power, to the 110,000th power, and 4 to the negative 360th power, to the 110,000th power. Therefore, if evolution did occur, it literally would have been a miracle and evidence for the existence of God. William Lane Craig

    William Lane Craig – If Human Evolution Did Occur It Was A Miracle – video
    http://www.youtube.com/watch?v=GUxm8dXLRpA

    Darwin and the Mathematicians – David Berlinski
    “The formation within geological time of a human body by the laws of physics (or any other laws of similar nature), starting from a random distribution of elementary particles and the field, is as unlikely as the separation by chance of the atmosphere into its components.”
    Kurt Gödel, was a preeminent mathematician/logician who is considered one of the greatest to have ever lived. Of Note: Godel was a Christian Theist!
    http://www.evolutionnews.org/2.....cians.html

    “Darwin’s theory is easily the dumbest idea ever taken seriously by science.”
    Granville Sewell – Professor Of Mathematics – University Of Texas – El Paso

  51. 51
    wd400 says:

    >> OK, so tell us where O’hara went wrong in that paper.?

    > For starters, attempting to do something that cannot be done.

    Ha! The paper didn’t measure selection because Joe knows it’s not possible to measure selection. That’s beautiful.

  52. 52
    bornagain77 says:

    I like how Berlinski sums up the mathematical predicament that neo-Darwinism finds itself in:

    Majestic Ascent: Berlinski on Darwin on Trial – David Berlinski – November 2011
    Excerpt: The publication in 1983 of Motoo Kimura’s The Neutral Theory of Molecular Evolution consolidated ideas that Kimura had introduced in the late 1960s. On the molecular level, evolution is entirely stochastic, and if it proceeds at all, it proceeds by drift along a leaves-and-current model. Kimura’s theories left the emergence of complex biological structures an enigma, but they played an important role in the local economy of belief. They allowed biologists to affirm that they welcomed responsible criticism. “A critique of neo-Darwinism,” the Dutch biologist Gert Korthof boasted, “can be incorporated into neo-Darwinism if there is evidence and a good theory, which contributes to the progress of science.”
    By this standard, if the Archangel Gabriel were to accept personal responsibility for the Cambrian explosion, his views would be widely described as neo-Darwinian.
    http://www.evolutionnews.org/2.....53171.html

  53. 53
    wd400 says:

    Maus,

    Read the paper, it explains how you can use pattern of heterozygosity around an allele to infer a “selective sweep” in which an allele enters the population an becomes common more quickly than recombination can break it up from surrounding sequences.

  54. 54
    bornagain77 says:

    Hmm randomness assumed instead of proven?,,

    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

  55. 55
    PaV says:

    wd400:

    Nope, people tried that line in the 30s, turns out is a simple Mendelian trait, with carbonaria is dominant to the light-bodied form. Moreover, the gene has been mapped to a position homologous to silkworm chromosome 17:

    If you took the time to read the paper I linked to, you’d see that there’s no question that the gene is ‘dominant’ in the Mendelian sense, i.e., in terms of inheritance. But the question is: what’s triggering the expression. So we’re talking about epigenetics. And that, clearly, can, and does, involve environmental factors.

  56. 56
    Joe says:

    OK, so tell us where O’hara went wrong in that paper.?

    For starters, attempting to do something that cannot be done.

    Ha! The paper didn’t measure selection because Joe knows it’s not possible to measure selection. That’s beautiful

    LoL! Nice non-sequitur. You asked where the paper went wrong, not whether or not they measured, or said they did, selection.

    But now that you mention it, saying you are doing something is not the same as actually doing it. No one can verify it. They can only nod or mumble. I would rather stand up and state the obvious.

  57. 57
    Maus says:

    wd400: “Read the paper, it explains how you can use pattern …”

    This is strictly incorrect. It can indicate recent fitness differences, but it cannot tell you when and were it came from. But this is again non responsive to the basic topic at hand. Again, count what?

  58. 58
    A Gene says:

    Joe @ 48 –

    Errrrrr, that does not make it correct. And I gave specific criticisms.

    Where? Comment 33? That raises a couple or irrelevant points (choosing the gene & species, well that was done by E.B. Ford), and the comment about selection being less effective when the population size is larger is just wrong: it’s the other way around (which is one of the points of the paper): the smaller the population size, the stronger the effect of drift.

    Try again?

  59. 59
    bornagain77 says:

    OT: New video uploads:

    Multidimensional Genome – Dr. Robert Carter – video (Notes in video description)
    http://www.metacafe.com/w/8905048

    What Is The Genome? It’s Not Junk! – Dr. Robert Carter – video – (Notes in video description)
    http://www.metacafe.com/w/8905583

  60. 60
    wd400 says:

    Maus,

    No, you just don’t understand the paper.

    Joe,

    Let’s try again: tell us why O’Hara failed to measure selection in a natural population.

  61. 61
    wd400 says:

    PaV,

    You’re going to have to explain to me how a trait can be Mendelian dominant in breeding experiments and “epigenetically” controlled.

    Well, actually, I wouldn’t bother. Even if the was some weird epigenetic thing going on, the evidence for strong selection on a newly arising mutant would still stand.

  62. 62
    Maus says:

    wd400: “No, you just don’t understand the paper.”

    Then since you do we know you are perfectly capable of explaining it. You may begin by answering the continued question: What was counted?

  63. 63
    carlg says:

    I am addressing only Nick’s first post and the first few responces. As a proponent of ID I read Nick’s post with interest and thought he made a few good points. In reading the responces I thought maybe I was on the Richard Dawkins site. His specific points went unanswered as only antidarwinian arguments were made. This long non sequiter approach was continued with a piling on effect. If consensus is of limited value among scientists, it has no value on web site for advocates. When you fall while water sking, let go of the rope. Admit his good points and move on. As for Nick’s name calling, please don’t emulate it. Never get in your opponents way when they are self destructing.

  64. 64
    PeterJ says:

    Hi Carlg,

    I think you will find most of Nicks points are in some ways answered here.

    http://www.evolutionnews.org/2.....62781.html

    I think it may be why he hasn’t been back to this thread?

  65. 65
    kairosfocus says:

    CG: That first few responses thing is key, cf say 32 above (and there are others), which clips a key part of the just linked by PJ. Note for instance PaV at 11 and BA 77 at 16, which also points to and clips the ENV article. In short, the evidence is that NM was responded to fairly promptly and on the merits. KF

  66. 66
    Starbuck says:

    Maybe it’s chemicals that control this putative ‘control region’, such as factory emissions, or tree bark chemicals themselves. This is the more likely explanation of “industrial melanization.” So, what, then, becomes of this “icon of evolution.”

    I don’t think you understood the use of the word ‘control’. They are talking about the genetic and developmental mechanism that underlies (‘controls’) the difference between the black (carbonaria) and peppered (typical) forms, which is ultimately determined by a difference in DNA base sequence (that we haven’t quite pinpointed yet). This difference is fixed within individuals irrespective of the environmental conditions the caterpillars grow up in. The
    relative survival of the dark and light forms is influenced by their visibility on different coloured resting surfaces, to bird predators.

    You should read a recent article, published in Biology Letters, dealing with the bird predation side of the story:

    http://rsbl.royalsocietypublis.....hort?rss=1

  67. 67
    bornagain77 says:

    Of related interest:

    The Mysterious Epigenome. What lies beyond DNA – video
    http://www.youtube.com/watch?v=RpXs8uShFMo

    Epigenetic changes don’t last – September 2011
    Excerpt: They found that epigenetic changes are many orders of magnitude more frequent than conventional DNA mutations, but also often short lived. They are therefore probably much less important for long-term evolution than previously thought.
    http://www.physorg.com/news/20.....-dont.html

  68. 68
    NickMatzke_UD says:

    Ugh, this “discussion” thread just further illustrates the complete intellectual bankruptcy of the creo/ID side.

    1. There’s absolutely no evidence for environmental/epigenetic factors control whether a peppered moth is light or dark. This was suggested decades ago, looked for and not found. On the contrary, when scientists looked for Mendelian inheritance, the trait was found to be Mendelian. I.e., it’s genetic, like many other thousands of inherited traits in other species (e.g., flower color, eye color, hair color, etc.)

    Furthermore, recent studies in the last few years have narrowed down the region of the genome that controls melanism. As was mentioned, they also found classic genomic signatures of a selective sweep there (reduced diversity in that region). And this is exactly what you would expect if Majerus’s suggestion — that a point mutation swept through the population — is correct.

    You can’t just sit around and make half-baked comments suggesting that some already-refuted explanation is more plausible and expect to be taken seriously.

    And other creationists can’t just sit around and let junk like this get said by their side without correction. It completely discredits your claims to intellectual credibility.

    2. A similar attempt at distraction is the failure to admit that the DI/UD posts tried to use the Korean study to cast doubt on the British peppered moth studies, even though it is *already tested and known* that peppered moths don’t have the actively-search-for-matching-background behavior which was the major point of the Korean study. #1 and the points below have been raised just to avoid admitting the mistakes made by DI/UD.

    3. Another attempt at evasion/distraction is to pretend that the peppered moth study, by itself, is supposed to be some kind of universal proof of every piece of evolution. That’s just crazy. The peppered moth work does demonstrate several things: (1) NS is real; (2) it occurs in the wild, sometimes at rates that humans can observe over a few years; (3) selection can spread mutations from miniscule frequencies (the first dark moth was only observed in the 1800s IIRC) to very high frequencies (it was 99% in highly polluted regions); (4) the result of this process is a specific functional adaptation to the environment, i.e. camouflage, which “looks designed”.

    None of (1)-(4) should be controversial, even to IDists/creationists who usually say that they accept that at least natural selection at least exists, and it’s all just a product of demographics and differential survival rates over the course of a few decades. It’s not “mysterious”. But for some reason, probably just blind instinctive antievolutionism and hatred for evolution, you guys feel the need to dispute these.

    4. An even stranger claim some creationists/IDists have been making recently is something about how selection can’t fix mutations. In the peppered moth, we’ve observed melanism go from basically 0% frequency to 99% frequency in polluted regions. But you’re seriously going to try to make some kind of argument that getting from 99% to 100% is impossible? Why? Any change in allele frequency is just demographics. If you assert that fixation is impossible for some bizarre reason, you are asserting that it’s impossible for the 1% or 0.1% or whatever of a population to die off. Why, oh why, would this be impossible?

    5. Yet another bizarre claim is the idea that you can’t distinguish selection from drift. But it’s trivial to do so in a case like the peppered moth, where you have measurements of allele frequency for many years. Genetic drift is random. Allele frequencies randomly move up and down each generation. Natural selection is nonrandom. Allele frequencies move in whatever direction selection is pushing.

    When you graph these two options, they are totally different. In any large population, drift means the allele frequency exhibits brownian motion, i.e. “drifts” up and down, back and forth, etc. But selection means the allele frequency moves smoothly in one direction, in a smooth sigmoidal curve, until it hits fixation.

    In other words, for the love of God, look stuff up. Google is your friend. E.g.:

    http://www.nature.com/scitable.....w-15186648

    6. Lastly, yet one more bit of bizarre weirdness put forth in this thread is that the peppered moth example is irrelevant because the moths are going back to the light “peppered” form. But we know the cause of that — the cause is the Clean Air Act that England passed in the 1950s. Up until the 1950s, large parts of England were polluted by black soot “fallout” from the smokestacks of factories. Photos show soot coating buildings and trees. The peppered moth populations in polluted areas gradually turned melanic during this period. After the Clean Air Act, the environment became cleaner, and the lighter moths were favored again. Natural selection means that populations track the environment. If an environmental change is permanent, then the adaptive change will be also. But if it’s not, it’s not.

    When you make the “it’s irrelevant because the moths went back to light” argument, you are effectively saying “it’s irrelevant because the Brits passed the Clean Air Act, but if they had let the environment remain polluted, it would be relevant”. It’s a bizarre argument you are making. No well-informed scientist will ever take ID/creationism seriously when you make these sorts of arbitrary and confused claims, or leave them standing without rebuttal. The point of the peppered moth story is that natural selection changes allele frequencies in an adaptive direction. The fact that this happened both to make the species darker (in a polluted environment) and lighter (in a clean environment) makes the example stronger, not weaker.

    Short version: you’re not going to get any respect from the scientific community, nor deserve it, until you can eliminate your basic, crashingly basic, mistakes, and correct the mistakes from others on your side, and only criticize the science when you actually know what you are talking about and actually take the actual published data seriously.

  69. 69
    NickMatzke_UD says:

    Oh yeah, I forgot to add:

    7. Bornagain77’s posts — what the heck? I mean, really, do you guys like having him/her on your side? That person specializes in thread derailment and in not engaging the actual topic under discussion. Are they just congenitally unable to focus on a topic and engage in actual discussion, rather than spamming with irrelevant, thrown-together links and quotes?

  70. 70
    bornagain77 says:

    NickMatzke_UD

    you state:

    Are they just congenitally unable to focus on a topic and engage in actual discussion, rather than spamming with irrelevant, thrown-together links and quotes

    Funny that when you make unsubstantiated claims that the cyclical variation within peppered moths is proof that all life arose by neo-Darwinian processes you do not consider this unmitigated hogwash, but when I pointed out that you can’t even establish the fixation of single random beneficial mutation in a fruit fly in 35 years of trying,,,

    http://www.uncommondescent.com.....ent-429167

    then you consider this ‘spam’? MMM Hmm, and exactly why is very speculative supporting evidence given such bias over direct empirical evidence in your ‘impartial’ view of science? Have you somehow been fiat right to dictate what evoidence we are allowed to consider and what evidence we are not allowed to consider. Sorry Nick, I’m not nearly as impressed with you hot air as you are!

  71. 71
    bornagain77 says:

    correction: Have you somehow been given fiat right to dictate evidence we are allowed to consider

  72. 72
    bornagain77 says:

    Funny also Nick that it still is commonly, and falsely, automatically assumed in the prevailing neo-Darwinian mindset that any mutations that generate any variations in any particular kind of species, such as the peppered moth variation, are completely random. Yet Shapiro, who is certainly not a IDists, has been creating quite a stir in recent years by pointing out that the vast majority of mutations that generate variations are NOT completely random as is required by within the modern synthesis of neo-Darwinism:

    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

    This, Nick, is not comforting in the least to your basic neo-Darwinian presuppositions that all life arose by purely random, unguided, processes! In fact when we test the central claim of neo-Darwinism, the claim that purely random variations can create novel beneficial features that can then be selected, we find, ‘surprisingly’, that neo-Darwinism’s central claim comes up woefully inadequate!

    Response to John Wise – October 2010
    Excerpt: But there are solid empirical grounds for arguing that changes in DNA alone cannot produce new organs or body plans. A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.
    http://www.evolutionnews.org/2.....38811.html

    Moreover, we now have solid evidence that your not even in the right ballpark with the reductive materialistic neo-Darwinian framework Nick!

    The Origin of Biological Information and the Higher Taxonomic Categories – Stephen Meyer
    “Neo-Darwinism seeks to explain the origin of new information, form, and structure as a result of selection acting on randomly arising variation at a very low level within the biological hierarchy, mainly, within the genetic text. Yet the major morphological innovations depend on a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. Yet if DNA is not wholly responsible for body plan morphogenesis, then DNA sequences can mutate indefinitely, without regard to realistic probabilistic limits, and still not produce a new body plan. Thus, the mechanism of natural selection acting on random mutations in DNA cannot in principle generate novel body plans, including those that first arose in the Cambrian explosion.”
    http://eyedesignbook.com/ch6/eyech6-append-d.html

    supplemental notes:

    The Fate of Darwinism: Evolution After the Modern Synthesis – David J. Depew and Bruce H. Weber – 2011
    Excerpt: We trace the history of the Modern Evolutionary Synthesis, and of genetic Darwinism generally, with a view to showing why, even in its current versions, it can no longer serve as a general framework for evolutionary theory. The main reason is empirical. Genetical Darwinism cannot accommodate the role of development (and of genes in development) in many evolutionary processes.,,,
    http://www.springerlink.com/co.....03g3t7002/

    The Rapid Origin of Domesticated Chicken – Cornelius Hunter – March 2012
    Excerpt: The research finds that epigenetic mechanisms may be the cause of the rapid origin of domesticated chickens brought about by breeding, and that these epigenetic changes are reliably and stably inherited, resulting in lasting change in a population.
    http://darwins-god.blogspot.co.....icken.html

  73. 73
    Axel says:

    He worships a nasty God, too, Nick. Not good medicine.

  74. 74
    bornagain77 says:

    Of related interest, here are a few comments from the ‘non-Darwinian’ evolutionist, James A. Shapiro – PhD. Genetics

    Shapiro on Random Mutation:
    “What I ask others interested in evolution to give up is the notion of random accidental mutation.”
    http://www.huffingtonpost.com/.....11144.html
    -Comment section

    Shapiro on Natural Selection:
    “My argument remains that the innovative process in evolution is rapid natural genetic engineering rather than gradual selection of small changes over long periods of time. This argument does not deny a role for selection. I simply assert that it is unrealistic to ascribe a creative (virtually deus ex machina) role to natural selection.”
    http://www.huffingtonpost.com/.....94315.html

    Shapiro on Cell cognition:
    “Recent postings have provoked numerous questions about my application of the term “cognitive” to cell regulatory processes. I base this usage on the notion that cognitive actions are knowledge-based and involve decisions appropriate to acquired information. It is common today for molecular, cell and developmental biologists to speak of cells “knowing” and “choosing” what to do under various conditions. While most scientists using these terms would insist they are just handy metaphors, I argue here that we should take these instinctive words more literally. Cell cognition may well prove itself a fruitful scientific concept.”
    http://www.huffingtonpost.com/.....54889.html

    Of note: As with neo-Darwinists Shapiro admits he has no ‘real time’ empirical experiments for the origin of novel protein domains/genes by Darwinian processes (so as to be able to have the ‘protein domains’ to shuffle around in the first place) but must rely, as do neo-Darwinists, on the DNA/protein sequence similarity data to try to make his case that ‘natural genetic engineering’ occurred in the distant past so as to create the diversity we see in life on earth. Yet, just as with neo-Darwinists, Shapiro relying on sequence similarity Data to try to make his case for ‘natural genetic engineering’ has the very same ‘unscientific’ problem that neo-Darwinism has of assuming the conclusion beforehand to try to prove very question being asked. i.e. Can novel functional information be generated ‘bottom up’ by the material processes of neo-Darwinism?:

    Here is Shapiro admitting he must rely on sequence similarity data to try to make his case:

    How Natural Genetic Engineering Solves Problems in Protein Evolution – James Shapiro – May 2012
    Excerpt: When I pointed out the potential of domain shuffling by natural genetic engineering to Intelligent Design advocates who claimed protein evolution by natural mechanisms was impossible, they refused to recognize genomic data as irrefutable evidence and insisted on real-time experiments. I disagree with them strongly on the DNA sequence data.
    http://www.huffingtonpost.com/.....41180.html

    This elephant in the living room problem that Shapiro, and neo-Darwinists is exactly the question that needs to be asked! Doug Axe’s work on the rarity of proteins is focused exactly on the rarity of individual protein domains/folds themselves. Doug Axe addresses James Shapiro’s mistaken disagreement with Intelligent Design here:

    On Protein Origins, Getting to the Root of Our Disagreement with James Shapiro – Doug Axe – January 2012
    Excerpt: I know of many processes that people talk about as though they can do the job of inventing new proteins (and of many papers that have resulted from such talk), but when these ideas are pushed to the point of demonstration, they all seem to retreat into the realm of the theoretical.
    http://www.evolutionnews.org/2.....55471.html

    supplemental notes:

    Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe:
    Excerpt: The prevalence of low-level function in four such experiments indicates that roughly one in 10^64 signature-consistent sequences forms a working domain. Combined with the estimated prevalence of plausible hydropathic patterns (for any fold) and of relevant folds for particular functions, this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences.
    http://www.ncbi.nlm.nih.gov/pubmed/15321723

    The Case Against a Darwinian Origin of Protein Folds – Douglas Axe – 2010
    Excerpt Pg. 11: “Based on analysis of the genomes of 447 bacterial species, the projected number of different domain structures per species averages 991. Comparing this to the number of pathways by which metabolic processes are carried out, which is around 263 for E. coli, provides a rough figure of three or four new domain folds being needed, on average, for every new metabolic pathway. In order to accomplish this successfully, an evolutionary search would need to be capable of locating sequences that amount to anything from one in 10^159 to one in 10^308 possibilities, something the neo-Darwinian model falls short of by a very wide margin.”
    http://bio-complexity.org/ojs/.....O-C.2010.1

    The Case Against a Darwinian Origin of Protein Folds – Douglas Axe, Jay Richards – audio
    http://intelligentdesign.podom.....9_03-07_00

    Seeing Past Darwin II: James A. Shapiro – James Barham – May 2012
    Excerpt: Much in our culture depends upon the public’s being made aware that Darwinian theory as standardly interpreted is intellectually bankrupt.(2) And little that I have encountered communicates this fact so well as the work of James A. Shapiro.
    http://www.thebestschools.org/.....a-shapiro/

  75. 75
    bornagain77 says:

    Axel you state:

    He worships a nasty God, too, Nick.

    actually Axel the new atheists are the ones who worship a ‘nasty’ god. The first part of this video shows what new atheists think of God:

    Ben Stein vs. Richard Dawkins Interview
    http://www.youtube.com/watch?v=GlZtEjtlirc

    Needless to say Dawkins view is NOT my view of God.

  76. 76
    Maus says:

    Matzke:

    I.e., it’s genetic, like many other thousands of inherited traits in other species (e.g., flower color, eye color, hair color, etc.)

    Eye color: http://www.sciencedaily.com/re.....081315.htm

    “The two pictures show the eyes of two genetically identical flies. The difference in eye colour is determined by epigenetic factors.” — from the photo caption.

    Hair color: http://www.ncbi.nlm.nih.gov/pm.....MC2822875/

    “The degree of methylation within the 5? IAP long terminal repeat (LTR) varies dramatically among individual isogenic Avy/a mice, causing a wide variation in coat color ranging from yellow (unmethylated) to pseudoagouti (methylated) (Fig. 1B).” — text immediately preceeding Fig 1B.

    Flower color: http://www.ncbi.nlm.nih.gov/pubmed/15493332

    “The flower variegation patterns can be determined by the frequency and timing of the excision of these transposons, and their stable insertions produce plain color flowers without generating pigmented spots or sectors; furthermore, both genetic and epigenetic regulation appeared to play important roles in determining the frequency and timing of the excision of the transposons.”

    Of particular note with the last: Epigenetic factors plays a role in the transposons directly rather than the ‘pure, simple’ persisted methylation alteration.

    And while all of these notions are Mendelian in nature it is also the case that epigenetics plays a demonstrable role. The Eye and Hair color issues allow you to see that amount of variation of alebdo due epigenetics. Which is, really, the entire point here.

    It’s a safe presumption here that everything is some matter of genetics. But simply tipping your hat to the tautology does not demonstrate cause from correlation. And specifically, if we do not know the specific gene and mechanism at hand then we cannot rule out what sort of effects epigenetics may play. This is especially pertinent in the case I quoted about flower color.

    Strictly, you are speaking beyond what the evidence supports. Don’t do this, it is the sort of ‘intellectual bankruptcy’ that the YEC/ID side engages in, no?

    And this is exactly what you would expect if Majerus’s suggestion — that a point mutation swept through the population — is correct.

    ‘Expect if’ is a weasel word. It either is a valid demonstration or it is not. If you say it is then you have discarded Methodological Naturalism. There simply is no ‘point mutation’ specifically known and in evidence. It is a pure appeal to mythology and has no place in a discussion of the evidence.

    For bonus points: It is never the case that Reality is consistent with a theory. It is always the case that a Theory is consistent with, or refuted by, Reality. The distinction is crucial as the former allows soft-headed individuals to claim that ‘Reality shows x about a theory…’. This is never the case no matter how softly the notion is pedalled.

    You can’t just sit around and make half-baked comments suggesting that some already-refuted explanation is more plausible and expect to be taken seriously.

    See: The above issues on epigenetics.

    … even though it is *already tested and known* that peppered moths don’t have the actively-search-for-matching-background behavior which was the major point of the Korean study.

    And yet Majerus found that Moths preferred to stay in shaded areas. So if you’re stating that Majerus is incompetent and incapable of counting moths in light and shade, then I should sorely like to see a reference as to how he cocked it up and why.

    (1) NS is real; (2) it occurs in the wild, sometimes at rates that humans can observe over a few years; (3) selection can spread mutations from miniscule frequencies (the first dark moth was only observed in the 1800s IIRC) to very high frequencies (it was 99% in highly polluted regions); (4) the result of this process is a specific functional adaptation to the environment, i.e. camouflage, which “looks designed”.

    (1) It shows predation is real. But if NS is synonymous with predation then let us call it that. If it is not then you need to provide a definition for NS to use in this context. (2) Predation does occur in the wild. It’s called the food chain and is obvious. This does not follow from your first point until you can state what NS definitively is and is not. (3) No, it shows that predation can alter allele frequencies. I’m not entirely sure who disagrees with this notion. (4) Differential predation rates over pre-existing morphs does not show ‘specific functional adaptation’ unless you have some truly perverse idea about what a ’cause’ is and what an ‘effect’ is. This goes back to your statements in (1) again.

    I’ll stop here as it is already getting too long in the tooth. But if your statement is that the vocal and self-selected minority that argue for YEC/ID demonstrate that YEC/ID is ‘intellectually bankrupt’ on the basis of their fallacies and sophistries… Then you simply have no argument against me considering the same of not only YEC/ID but of Evo as well. If not based on the majority of argumentation witnessed by Evo proponents, then by your own inability to use any manner of rationality. Unless your argument is to state that ‘But it’s ok when my side does it.’

    But that doesn’t seem to improve things any.

  77. 77
    wd400 says:

    Maus,

    This is ridiculous. The trait acts as dominant in breeding experiments in which pollution or whatever environmental cue you want is taken out of the picture. Why dream up an epigenetic pattern for such a simple trait?

    Moreover, what difference would it make? If the dark-bodied allele is an epiallele that is inherited in such a strict Mendelian fashion, and has been subject to such strong selecton, then it makes no difference if it’s a point mutation or an methyl tag that brought the allele into existence.

  78. 78
    Joe says:

    wd400-

    It is up to you and the author(s) to verify they measured natural selection- that is they measured the differential reproduction based on heritable random variation.

  79. 79
    Joe says:

    And yes evos, TRAITS are genetic. Unfortunately, for you, “being a moth” is NOT a trait.

  80. 80
    A Gene says:

    Joe @78 – I don’t think they looked at differential reproduction, because the suspected mechanism was differential survival. Which Kettlewell did look at.

    BTW, I assume you’ve given up trying to explain what you think is wrong with the O’Hara paper.

  81. 81
    PaV says:

    wd400:

    You’re going to have to explain to me how a trait can be Mendelian dominant in breeding experiments and “epigenetically” controlled.

    Well, actually, I wouldn’t bother. Even if the was some weird epigenetic thing going on, the evidence for strong selection on a newly arising mutant would still stand.

    There is no “carbonaria gene.” So state the authors. The gene pathway that leads to melanism is the same in the typicals and in the ‘carbonaria.’ What changes, apparently, is some kind of molecular ‘factor’. That’s why in the paper I cited they talk about a “control region.” The gene pathway segregates as normal, but it is this control factor that effects the inherited pathway.

    Now, the authors have a subsequent paper that has come out, and they seem to identify the SNP involved in this regulatory factor. Now, this might seem like straightforward “neo-Darwinian” evolution—trivial as it always is; however, can we just simply rule out some environmental factor leading, along its own pathway, to a “directed mutation”? I don’t think so.

    So, what we see is either completely non-neo-Darwinian in character, or, by default, it is a simple SNP, which, given a large population size can be arrived at fairly quickly. But, again, this is a trivial form of so-called “neo-Darwinian” evolution. There’s no new “gene” that has shown up (again, there’s no “carbonaria gene”); it’s a simply SNP—which fits right in with Behe’s conclusions about what so-called “neo-Darwinian” evolution can bring about. (obviously we’re talking about, at most, one, SINGLE, protein-to-protein bond here).

  82. 82
    NickMatzke_UD says:

    And yet Majerus found that Moths preferred to stay in shaded areas.

    Which I’ve already said in this thread. The point is that peppered moths apparently don’t actively match backgrounds to their color, where dark moths rest on dark surfaces and light/peppered moths rest on light surfaces. Yet the DI/UD suggested that the peppered moth work was somehow impeached because some other random species from Korea have this behavior.

    Now, the authors have a subsequent paper that has come out, and they seem to identify the SNP involved in this regulatory factor. Now, this might seem like straightforward “neo-Darwinian” evolution—trivial as it always is; however, can we just simply rule out some environmental factor leading, along its own pathway, to a “directed mutation”? I don’t think so.

    They’ve identified the SNP? Where’s the paper, I haven’t seen it yet I think.

    PS: For all you mutation skeptics, SNP = single nucleotide polymorphism = point mutation.

  83. 83
    bornagain77 says:

    For all you mutation skeptics, SNP = single nucleotide polymorphism = point mutation.

    unfounded presupposition of ‘randomness’ again Nick???

    Already referenced Shapiro earlier, but to add that line of criticism,, Though SNP’s (random mutations) do get through to make some point mutations to DNA, the level of DNA repair that prevents them from happening is simply unfathomably complex:

    Quantum Dots Spotlight DNA-Repair Proteins in Motion – March 2010
    Excerpt: “How this system works is an important unanswered question in this field,” he said. “It has to be able to identify very small mistakes in a 3-dimensional morass of gene strands. It’s akin to spotting potholes on every street all over the country and getting them fixed before the next rush hour.” Dr. Bennett Van Houten – of note: A bacterium has about 40 team members on its pothole crew. That allows its entire genome to be scanned for errors in 20 minutes, the typical doubling time.,, These smart machines can apparently also interact with other damage control teams if they cannot fix the problem on the spot.
    http://www.sciencedaily.com/re.....123522.htm

    A Look at the Quality Control System in the Protein Factory – JonathanM – March 2012
    Excerpt: The DNA damage response (DDR) system is like a cellular special ops force. The moment such damage is detected, an intricate network of communication and recruitment launches into action. If the cellular process for making proteins were a factory, this would be the most advanced quality-control system ever designed.
    http://www.evolutionnews.org/2.....57791.html

    Repair mechanisms in DNA include:

    A proofreading system that catches almost all errors
    A mismatch repair system to back up the proofreading system
    Photoreactivation (light repair)
    Removal of methyl or ethyl groups by O6 – methylguanine methyltransferase
    Base excision repair
    Nucleotide excision repair
    Double-strand DNA break repair
    Recombination repair
    Error-prone bypass
    http://www.newgeology.us/presentation32.html

    Although evolution depends on ‘mutations/errors’ to DNA to make evolution plausible, there are multiple layers of error correction in the cell to protect against any “random changes” to DNA from happening in the first place:

    The Evolutionary Dynamics of Digital and Nucleotide Codes: A Mutation Protection Perspective – February 2011
    Excerpt: “Unbounded random change of nucleotide codes through the accumulation of irreparable, advantageous, code-expanding, inheritable mutations at the level of individual nucleotides, as proposed by evolutionary theory, requires the mutation protection at the level of the individual nucleotides and at the higher levels of the code to be switched off or at least to dysfunction. Dysfunctioning mutation protection, however, is the origin of cancer and hereditary diseases, which reduce the capacity to live and to reproduce. Our mutation protection perspective of the evolutionary dynamics of digital and nucleotide codes thus reveals the presence of a paradox in evolutionary theory between the necessity and the disadvantage of dysfunctioning mutation protection. This mutation protection paradox, which is closely related with the paradox between evolvability and mutational robustness, needs further investigation.”
    http://www.arn.org/blogs/index....._contradic

    Contradiction in evolutionary theory – video – (The contradiction between extensive DNA repair mechanisms and the necessity of ‘random mutations/errors’ for Darwinian evolution)
    http://www.youtube.com/watch?v=dzh6Ct5cg1o

    The Darwinism contradiction of repair systems
    Excerpt: The bottom line is that repair mechanisms are incompatible with Darwinism in principle. Since sophisticated repair mechanisms do exist in the cell after all, then the thing to discard in the dilemma to avoid the contradiction necessarily is the Darwinist dogma.
    http://www.uncommondescent.com.....r-systems/

    Nick perhaps you want random unguided mutations to be true, but the fact is that mutations that happen to DNA are, as Shapiro has pointed out so eloquently, for the vast majority of times regulated, directed, changes to DNA that are governed. i.e. non-random with respect to true randomness! It is simply unwarranted for you to claim that this example is truly random, much less do you seem realize how trivial this example of cyclical variation is to the burden of proof for explain where moth wings and highly integrated DNA repair mechanisms came in the first place!

    etc.. etc.. etc…

  84. 84
    A Gene says:

    There is no “carbonaria gene.” So state the authors. The gene pathway that leads to melanism is the same in the typicals and in the ‘carbonaria.’ What changes, apparently, is some kind of molecular ‘factor’.

    It sounds like it’s the regulation of the gene that’s changed (which makes a lot of sense). It could be that it’s still the same gene, if the mutation is in the regions that control expression. Or it could be at another locus, which interacts with the region that control expression. I think this could reasonably be called a gene too.

  85. 85
    PaV says:

    Nick Matzke:

    Furthermore, recent studies in the last few years have narrowed down the region of the genome that controls melanism. As was mentioned, they also found classic genomic signatures of a selective sweep there (reduced diversity in that region). And this is exactly what you would expect if Majerus’s suggestion — that a point mutation swept through the population — is correct.

    It was correct of you to point out that the genes for melanism didn’t change in the carbonaria morph. As the authors wrote: there is no ‘carbonaria gene.’ Was this what Darwinists expected? No. Why do I say that? Because they wrote that “surprisingly” none of the candidate genes turned out to be linked to the gene pathway associated with melanism.

    Yes, there appears to be a SNP. But, does this fit Majerus’ model? Not really—and for the same reason given above.

    Now, it could be argued that this confirms neo-Darwinian premises. But are we sure?

    Ted Sargeant’s reasons for invoking “induction” regarding B. betuleria is because the change occurred too rapidly. (He notes 47 years for the ‘carbonaria’ to develop, which, he writes, corresponds to a selection factor of .50, which is quite high as selection factors go.)

    At the time Sargeant questioned the “classical” theory regarding B. betularia, one of the denouncements of his theory was that it was Lamarkian. But we now know that this is a detectable phenomena in plants, and IIRC, even in animals, via RNA-mediated epigenetic mechanisms. And we also now know that not all mutations are random. IOW, are we dealing here with a case of a “directed mutation”?

    You can’t just sit around and make half-baked comments suggesting that some already-refuted explanation is more plausible and expect to be taken seriously.

    The questions raised above are scientific questions, not religious ones.

    Your question deserves to be turned around. The real question should be: why should science take Darwinism seriously.

    The mathematics make no sense at all.

    Behe’s work, first his computer simulation and then his “Edge of Evolution” make this quite clear. If you want to convince ID folks about evolution, either show us all the “intermediate forms” that Darwin expected to find in the fossil record, or show us some mathematical way of explaining how new genetic information comes about. Or, better yet, both.

    The genetic evidence so far for the ‘carbonaria’ is of a controlling region SNP. And the authors suggest that it is but one, single mutation. How did all of the other information in the mutated sequence come about? How is this type of change in any way impressive? Why should we go from the occurence of SNPs in bringing about very simple adaptive change, to wholesale changes in body-types? On what basis is such an extrapolation to be carried out? Because otherwise we have to invoke intelligent agency? Is it materialism then that requires this extrapolation? Is that science? Why should logical people be required to ‘believe’ this stuff?

    Let’s point out that Darwinists insisted that “junk-DNA” had no function and was a confirmation of their theory. ID said that didn’t make much sense. Who turned out to be right?

    ID said that if an intelligent agent is involved in the operation of the genome, then “front-loading” is a distinct possibility, as well as being more likely—i.e., a non-gene-centric position. And now we know that sea squirts have genes that are used for limb formation, a fact that buttresses the notion of “front-loading” and which points to regulatory pathways as determinative, rather than simply genes. (

    Darwinism is running out of time. Nothing about it makes much sense. When will all the ad hoc explanations finally stop? Hopefully soon.

  86. 86
    wd400 says:

    PaV,

    You really do talk a load of rubbish sometimes.

    No one has ever claimed that that the peppered moths explained “wholesale changes in body-types” – just that they form a nice example of adaptation in a changing environment.

    Creationist’s apoplexy about the peppered moths, and the bizzare things you’ll say to avoid the simple interpretation of the results, on the hand, seems to suggest they form some sort of problem for you guys?

  87. 87
    Starbuck says:

    When evolutionary biologists use the null hypothesis to try to explain ancestor-descendant variations in genes, they look to examples such as the peppered moth for answers as to why neutral evolution fails. What would normally take neutral evolution 30 million years selection can do in two. Does this work for all cases? No, but it’s a good starting point and when it works we learn a lot.

  88. 88
    PaV says:

    wd400:

    Who’s talking a load of rubbish here?

    The peppered moth is THE ICON of evolution. And evolution is supposed to tell us how bacteria became humans.

    And now you’re saying this: the peppered moth is “just …. a nice example of adaptation in a changing environment.”

    I’ve been saying for years that if Darwin entitled his book The Origin of Adaptations, that I’d probably not find too much wrong with it.

    Who are you kidding with this line of defense? You can’t have your cake,and eat it too.

    The reason I question the “classic” tale told of B. betularia is, first, because I suspect that neo-Darwinism can do even less than what it appears to be able to do. That’s just a personal suspicion based on a whole host of considerations. Hence, it borders on intuition.

    And, second, related to the first, I think that the amount of true “randomness” in mutations is far less than we think.

    And, third, because it seems that the gene frequencies of the alleles—whatever that means, if anything (whole genome analysis will eventually tell us just what it means; but, in the case at point, there WASN’T a “carbonaria gene”, an allele, but, rather, a modification factor, so how can we even talk about “changing gene/allele frequencies”?)—are changing so quickly, back and forth, traditional pop. gen. formulas don’t favor such an explanation. This is why Ted Sargeant had reservations. And, this is exactly why Haldane published his paper that later came to be known as Haldane’s Dilemma. (But, of course, there’s never a dilemma that a good “ad hoc”, Darwinian “just-so” story can’t remedy.)

    But, wd400, you’re right: all this is is a simple case of “adaptation.” New body-types aren’t going to emerge via these mechanism even if we had billion, trillion years available.

  89. 89
    PaV says:

    Starbuck:

    What would normally take neutral evolution 30 million years selection can do in two. Does this work for all cases? No, but it’s a good starting point and when it works we learn a lot.

    I see you’re ready to throw neutral drift under the bus. But, of course, neutral theory developed because of the concept of “genetic load” owing to the fact that directional selection, such as you assume to be taking place here with B. betularia, requires lots of individuals to die. The “surprising” (Why do we hear biologists use that word over and over again? Is it because they have everything wrong?) level of protein polymorphisms led Kimura to propose the NT.

    So, as usual, you’re a Darwinist who will concede the inadequacies of one theory, only because he’s convinced of the power of another one. But, unfortunately, neither one is powerful enough—in a mathematical way—of explaining viable genetic pathways leading from sea squirts to humans, (let alone from cats to dogs) nor a combination of both.

    We’re incredibly huge orders of magnitude away from any sensible mathematical solution.

  90. 90
    wd400 says:

    See, this is the rubbish I’m talking about.

    Apart from all the noise, do you mind explaining why you think a “modification factor” that segregates in a simple Mendelian fashion isn’t an allele?

    Or what the near-fixation of one allele has to do with Haldane’s paper, which is about the cost fixation of multiple alleles (and based on shakey assumptions, which Haldane makes explicit if you actually read the paper).

    Seems a lot like the classic Gish Gallop to me…

  91. 91
    Starbuck says:

    I am not throwing nt under the bus, just that it is the the null hypothesis , and sometimes the null hypothesis is correct , but when it isn’t we look to other explanations, like selection. We test , we poke, we prod. There’s no atheistic conspiracy we just want to understand.

  92. 92
    PaV says:

    Well, wd400, two years later we now know that you were wrong and I was right.

    Look at this link.

  93. 93
    wd400 says:

    Ummmm…. no.

  94. 94
    PaV says:

    Ummmm…..yes.

    The link you provide is the very same link you’ll find in the link I provided to Dr. Hunter’s “Darwin’s God” blog.

    This from an article about this finding:

    By examining the DNA of hundreds more typica moths and ruling out mutations one by one, the team ended up with one candidate: the large transposable element that had landed in the cortex gene. But the jumping gene didn’t land in the DNA that encodes the protein. Instead it landed in an intron — a stretch of DNA that gets chopped out after the gene is copied into RNA and before a protein is made.

    Should I bring up the ignoble history of Haldane driving Barbra McClintock out of population genetics because “she didn’t know what she was talking about”? And what made Haldane make this claim? McClintock said that ‘transposable elements’ are “non-random.” How dare her?

    Well, as we know, she went on to receive the Nobel Prize for her work on transposons.

    Therefore, we can definitively say that if they were “non-random” in 1953, they’re still “non-random”; you know, “directed.” And you can take that to the Nobel Prize award ceremony.

    If you can’t admit here, in this instance, that you were wrong, then you never will.

  95. 95
    wd400 says:

    The link you provide is the very same link you’ll find in the link I provided to Dr. Hunter’s “Darwin’s God” blog.

    Yes. I know. In this thread I said that the black colouration was a simple mendelian trait that arose from a single mutation which rapidly spread to near-fixation. The paper says the same thing.

    You said a lot of confused things about epigenetics and directed mutation. The paper doesn’t say anything about that.

    It’s that simple

    (Do you have a citation for the Haldane thing — I think you’ve probably mis-remembered this)

  96. 96
    PaV says:

    “A simple Mendelian trait.” Is a ‘transposon’ a “simple Mendelian trait”?

    That the transposon is handed down from one generation to the next is almost entirely immaterial. What matters is how it arose.

    Now your pet theory, really hypothesis, is RM+NS. I argued that, to the contrary, it was likely some directed effect caused by some kind of environmental cue.

    As I mentioned, Barbara McClintock’s work with “jumping genes” (transposons) led her to the conclusion that these transposons were NOT random mutations. IOW, RM+NS is off the table. So, you were wrong. (Point mutations were ruled out as being causitive in this paper)

    There is likely some kind of set of internal mechanisms that react to the environment, with the transposons being part of these mechanicsms. That means we’re dealing with an ‘epigenetic’ origin of the mutation.
    You are simply wrong here–other than your assertion that changes brought about in one generation are then transmitted to the next. What a surprise assertion that is! Does the transposons have any choice in being handed down? And, if this insertion occurs in an intron, I think terming this a Mendelian trait misses the mark.

    As to Haldane, I invite you to look it up yourself if you’re interested. It’s up to you to prove that what I stated is wrong. Otherwise, what I said stands.

  97. 97
    wd400 says:

    You’re wrong about almost everything here, I’m afraid. I don’t know if it’s just your ignorance or motivated reasoning, but neither seems curable…

  98. 98
    bornagain77 says:

    “I don’t know if it’s just your ignorance or motivated reasoning, but neither seems curable…”

    Says the man who adamantly believes, without one shred of evidence, that unguided material processes can out program and engineer our best programmers and engineers.

    A few notes to that effect:

    “a one-celled bacterium, e. coli, is estimated to contain the equivalent of 100 million pages of Encyclopedia Britannica. Expressed in information in science jargon, this would be the same as 10^12 bits of information. In comparison, the total writings from classical Greek Civilization is only 10^9 bits, and the largest libraries in the world – The British Museum, Oxford Bodleian Library, New York Public Library, Harvard Widenier Library, and the Moscow Lenin Library – have about 10 million volumes or 10^12 bits.”
    – R. C. Wysong

    ‘The information content of a simple cell has been estimated as around 10^12 bits, comparable to about a hundred million pages of the Encyclopedia Britannica.”
    Carl Sagan, “Life” in Encyclopedia Britannica: Macropaedia (1974 ed.), pp. 893-894

    HISTORY OF EVOLUTIONARY THEORY – WISTAR DESTROYS EVOLUTION
    Excerpt: A number of mathematicians, familiar with the biological problems, spoke at that 1966 Wistar Institute,, For example, Murray Eden showed that it would be impossible for even a single ordered pair of genes to be produced by DNA mutations in the bacteria, E. coli,—with 5 billion years in which to produce it! His estimate was based on 5 trillion tons of the bacteria covering the planet to a depth of nearly an inch during that 5 billion years. He then explained that,, E. coli contain(s) over a trillion (10^12) bits of data. That is the number 10 followed by 12 zeros. *Eden then showed the mathematical impossibility of protein forming by chance.
    http://www.pathlights.com/ce_e.....hist12.htm

    Moreover, the regulatory network of a e-coli is found to be much more elegant than the operating system of Linux:

    The Multi-dimensional Genome–impossible for Darwinism to account for– by Dr Robert Carter – video
    (15:52 minute mark: Comparing the Computer Operating Systems of Linux to the much more sophisticated operating systems of Regulatory Networks in e-coli)
    https://youtu.be/K3faN5fU6_Y?t=952

    Comparing genomes to computer operating systems – Van – May 2010
    Excerpt: we present a comparison between the transcriptional regulatory network of a well-studied bacterium (Escherichia coli) and the call graph of a canonical OS (Linux) in terms of topology,,,
    http://www.ncbi.nlm.nih.gov/pubmed/20439753
    regulatory network of a well-studied bacterium (Escherichia coli) and the call graph of a canonical OS (Linux) – Picture of comparison
    http://www.ncbi.nlm.nih.gov/pm.....figure/F1/

    Along that line, it is also found that bacteria ‘solve optimization problems for collective decision making that are beyond what we, human beings, can solve with our most powerful computers’

    Learning from Bacteria about Social Networking (Information Processing) – video
    Excerpt: I will show illuminating movies of swarming intelligence of live bacteria in which they solve optimization problems for collective decision making that are beyond what we, human beings, can solve with our most powerful computers.
    http://www.youtube.com/watch?v=yJpi8SnFXHs

    And here is, according to a Darwinist, a ‘horrendously complex’ metabolic pathway chart of a ‘simple’ cell:

    ExPASy – Biochemical Pathways – interactive schematic
    http://biochemical-pathways.com/#/map/1

    Even the most stripped down bacteria imaginable, gives us every indication that life was Intelligently Designed

    Microbe with stripped-down DNA may hint at secrets of life – Mar 24, 2016
    Excerpt: The newly created bacterium has a smaller genetic code than does any natural free-living counterpart, with 531,000 DNA building blocks containing 473 genes. (Humans have more than 3 billion building blocks and more than 20,000 genes).
    But even this stripped-down organism is full of mystery. Scientists say they have little to no idea what a third of its genes actually do.
    “We’re showing how complex life is, even in the simplest of organisms,” researcher J. Craig Venter told reporters. “These findings are very humbling.”,,,
    The genome is not some one-and-only minimal set of genes needed for life itself. For one thing, if the researchers had pared DNA from a different bacterium they would probably have ended up with a different set of genes.,,,
    The genome is “as small as we can get it and still have an organism that is … useful,” Hutchison said.,,,
    http://hosted.ap.org/dynamic/s.....INNY_GENES

    Three Subsets of Sequence Complexity and Their Relevance to Biopolymeric Information – David L. Abel and Jack T. Trevors – Theoretical Biology & Medical Modelling, Vol. 2, 11 August 2005, page 8
    “No man-made program comes close to the technical brilliance of even Mycoplasmal genetic algorithms. Mycoplasmas are the simplest known organism with the smallest known genome, to date. How was its genome and other living organisms’ genomes programmed?”
    http://www.biomedcentral.com/c.....2-2-29.pdf

    To Model the Simplest Microbe in the World, You Need 128 Computers – July 2012
    Excerpt: Mycoplasma genitalium has one of the smallest genomes of any free-living organism in the world, clocking in at a mere 525 genes. That’s a fraction of the size of even another bacterium like E. coli, which has 4,288 genes.,,,
    The bioengineers, led by Stanford’s Markus Covert, succeeded in modeling the bacterium, and published their work last week in the journal Cell. What’s fascinating is how much horsepower they needed to partially simulate this simple organism. It took a cluster of 128 computers running for 9 to 10 hours to actually generate the data on the 25 categories of molecules that are involved in the cell’s lifecycle processes.,,,
    ,,the depth and breadth of cellular complexity has turned out to be nearly unbelievable, and difficult to manage, even given Moore’s Law. The M. genitalium model required 28 subsystems to be individually modeled and integrated, and many critics of the work have been complaining on Twitter that’s only a fraction of what will eventually be required to consider the simulation realistic.,,,
    http://www.theatlantic.com/tec.....rs/260198/

    And yet wd400, although he has not one shred of evidence that unguided material processes can produce such unfathomable complexity, has the audacity to label those who disagree with him as ignorant.

    The truth is, the willful ignorance manifested in wd400s false bravado towards PaV makes rocks appear as genius in comparison!

  99. 99
    Dionisio says:

    PaV @92:

    Why did you write “…two years later…”?

    From Aug 6 2012 to Nov 20 2016?

    BTW, is this the paper Dr Hunter referred to?

    http://rnajc.ucsf.edu/sites/rn.....e17951.pdf

  100. 100
    PaV says:

    Dionisio:

    I looked quickly at the date and thought I saw 2014. Simple as that. And, yes, that is the paper.

  101. 101
    PaV says:

    wd400:

    I said that if you didn’t admit you were wrong here, you never would. You’re stuck in an old paradigm.

  102. 102
    wd400 says:

    Feel free to point out anything in this paper (and not your own imagination or misunderstanding of it) that requires a new paradigm.

  103. 103
    bornagain77 says:

    “Feel free to point out anything in this paper (and not your own imagination or misunderstanding of it) that requires a new paradigm.”

    Says the man who himself, given naturalism, is a merely a figment of imagination with no free will.

    The Confidence of Jerry Coyne – Ross Douthat – January 6, 2014
    Excerpt: then halfway through this peroration, we have as an aside the confession that yes, okay, it’s quite possible given materialist premises that “our sense of self is a neuronal illusion.” At which point the entire edifice suddenly looks terribly wobbly — because who, exactly, is doing all of this forging and shaping and purpose-creating if Jerry Coyne, as I understand him (and I assume he understands himself) quite possibly does not actually exist at all? The theme of his argument is the crucial importance of human agency under eliminative materialism, but if under materialist premises the actual agent is quite possibly a fiction, then who exactly is this I who “reads” and “learns” and “teaches,” and why in the universe’s name should my illusory self believe Coyne’s bold proclamation that his illusory self’s purposes are somehow “real” and worthy of devotion and pursuit? (Let alone that they’re morally significant:,,) Read more here:
    http://douthat.blogs.nytimes.c.....oyne/?_r=0

  104. 104
    Dionisio says:

    PaV @100:

    I looked quickly at the date and thought I saw 2014. Simple as that. And, yes, that is the paper.

    Thank you for clarifying this to me. I appreciate it.
    BTW, that may happen to anyone, not a big deal. It happens to me often. Just wanted to make sure there wasn’t another more recent discussion between you and your politely dissenting interlocutor that I was not aware of. Didn’t want to comment on your discussion with your politely dissenting interlocutor before seeing all the related comments.

    Please, note that the following two questions are mainly for my own research study, hence they’re not directly related to this discussion with your interlocutor:

    1. When you saw Dr. Hunter’s reference to that paper, did you see the entire paper or just the abstract?
    2. Had you seen the text of the entire paper before the link to the PDF copy of that paper was posted @99?

    Now, back to your discussion with your politely dissenting interlocutor.
    The referenced paper has this paragraph in their conclusion:

    The carb-TE is a spectacular example of an adaptively advantageous transposon; its discovery fills a fundamental gap in the peppered moth story and furthers our appreciation of the mechanism underpinning rapid adaptation. A consensus on the general importance of transposable elements for adaptive evolution has yet to emerge.

    Note they’re referring to “mechanism underpinning rapid adaptation.”
    They’re talking about “adaptive evolution”, i.e. micro-evolution, which is possible because the biological systems are designed with a built-in framework that is conducive to such adaptation mechanisms, which explain the observed phenotype variety within each kind of biological systems.
    What else is new? That’s all. Same old, same old. Don’t we all agree on that?
    You’re on target. Your politely dissenting interlocutor isn’t.
    Just let’s be gracious to them. They don’t know what they’re talking about.
    You may tell them to read better the entire paper next time they want to discuss with you.
    I try not to discuss directly with them. My time is very limited. Can’t afford to squander it on trolling nonsense.

    PS. Please correct any inaccuracies in my comments.
    Thank you.

  105. 105
    Dionisio says:

    #104 addendum

    http://www.genetics.org/content/204/1/3.full.pdf

    BTW, I think on several occasions gpuccio has expressed his interesting opinion on the transposons in relation to ID.

  106. 106
    bornagain77 says:

    PaV and Dionisio, this is of related interest to epigenetic mechanisms:

    Yale’s Steven Novella Argues with Michael Behe — Here’s Why Novella Is Wrong – Cornelius Hunter – November 23, 2016
    Excerpt: the press release informed the public that the (MEGA) experiment provided “A powerful, unvarnished visualization of bacterial movement, death, and survival; evolution at work, visible to the naked eye.” Likewise, Novella called it “a nice demonstration of evolution at work in a limited context.” There’s only one problem: The experiment did not demonstrate evolution, it falsified evolution.
    http://www.evolutionnews.org/2.....03309.html

  107. 107
  108. 108
    Dionisio says:

    bornagain77 @106:

    Thank you for sharing that interesting report.

    Every new scientific research report is bad news for Neo-Darwinian ideas.

  109. 109
    Dionisio says:

    bornagain77:

    After opening the link you posted @106, with an interesting article by Dr. Hunter, I looked at another recent article he posted in his own blog:

    http://darwins-god.blogspot.co.....-code.html

    In that article Dr. Hunter refers to this paper by two scientists from Kazakhstan, who apparently don’t care much about being as “politically correct” as their western colleagues or simply didn’t realize their title choice for their paper may be prone to different interpretations. Well, that could happen to any title anyway. 🙂

    Here’s the paper (>3yo) by the two scientists from Kazakhstan:
    https://arxiv.org/pdf/1303.6739v1.pdf

  110. 110
    PaV says:

    Dionisio:

    No, I had only read the abstract, and I didn’t see the paper until you linked to it.

    You stated this: “Note they’re referring to “mechanism underpinning rapid adaptation.”
    They’re talking about “adaptive evolution”, i.e. micro-evolution, which is possible because the biological systems are designed with a built-in framework that is conducive to such adaptation mechanisms, which explain the observed phenotype variety within each kind of biological systems.
    What else is new? That’s all. Same old, same old. Don’t we all agree on that?”

    The “classic” story surrounding the peppered moth is that because of industrial pollution and the concomitant darkening of tree barks, the moth, subject to ‘selection pressure,’ changed its allele frequencies.

    That’s the classic story. And, within the traditional pop. gen. way of thinking, this would mean some point mutation occurred, or that some kind of recombination occurred. So, either a protein was itself changed (SNP), or, expression of a protein was changed. And, of course, all of this would be “random.”

    This is the critical remark. We are NOT dealing with a “random” event, just as your statement above implies. And, I invoked Barbara McClintock because she was run out of the academy (let’s just say that she no longer felt comfortable in the pop. gen. community, much like what happened to Sternberg at the Smithsonian, and to Duesberg at Berkeley) precisely because she was claiming that TE’s were responsible for rapid adaptive events AND that they were “non-random.”

    No one in their right mind would quibble with adaptation occurring. What is at stake, always, is the mechanism that’s involved.

    From this paper we know that a TE is involved, and, that it is nicely fitted into an intron region, which, of course, should not affect the protein involved in any way. Taken together, this simply means that RM+NS means almost nothing here. But, this is an ICON of evolution. If neo-Darwinism fails to explain its origin, then neo-Darwinism is dead! But, of course, many in the evolution camp are already saying this. Against all of this, wd400 is holding out to the end.

    I personally don’t think that there is much to traditional evolutionary thinking. I believe that what has historically been called “microevolution” is not really that at all, but simply built in mechanisms at work using environmental cues. If you’ve paid attention over the years, you’ll see that I’ve asked wd400 on many occasions to explain the very rapid change in phenotype that occurred in Pod podicarus, an Adriatic lizard transplanted to another island. He says he can’t explain it.

    I said that the only way it can be explained is that the changed diet of the lizards brought the dramatic phenotypic changes, viz, cecal valves, about. I suggested 4 or 5 years ago that an experiment be run in which the diet was changed/controlled. Such an experiment was conducted, and, in fact, when the diet of the lizards were changed in the lab, the ‘exact’ changes took place in the lab specimens.

    I have every right to feel vindicated in my thinking. And it is, of course, ‘intelligent design’ that informs my thinking.

    So, not only do I think it is impossible to explain “macro-evolution” using Dawinian thought, I don’t even think that “microevolution” will hold up to scrutiny once the genome’s regulatory mechanisms are more fully explored.

    But, we’ll just have to ‘wait and see’ on that one.

  111. 111
    wd400 says:

    Taken together, this simply means that RM+NS means almost nothing here

    You still haven’t read the paper, have you?

  112. 112
    Dionisio says:

    PaV,

    Does anything happen to the RBC count of people living in low lands traveling to very high altitudes?

    That kind of adaptation is possible because the biological systems have a built-in framework that is conducive to such adaptation.

    That kind of adaptation is called phenotypical plasticity.

    There are many examples like that. Biological systems were designed with those built-in features.

  113. 113
    wd400 says:

    Phenotypic plasticity exists, of course. But it’s not relevant to the peppered moth example, where the phenotype is encoded by a single dominant allele (as has been known since the 1920s).

  114. 114
    PaV says:

    wd400:

    I’m sure the authors will invoke “selection” somewhere along the line, and then bow down to Darwinism; but, that proves nothing other than they only have one paradigm out of which to look at and analyze things.

    Up until this paper, let’s say from the “1920’s” on, was this thought to be anything other than some “random” mutation, and likely a SNP?

    Here, for example, is what Nick Matzke wrote early on:

    As for the mutational change from light to dark in the peppered moth, we don’t quite know the exact mutational change yet, but it could well be just a point mutation. It’s not exactly hard for a mutation to push up the amount of melanin in an organism.

    TE’s are not ‘random.’ That’s the whole upshot.

    Here’s a snippet from a report on the paper:

    Saccheri and colleagues compared that region in one black moth and three typical moths. The researchers found 87 places where the black moth differed from the light-colored moths. Most of the differences were changes in single DNA bases — the information-carrying chemicals in DNA. Such genetic variants are known as SNPs for single nucleotide polymorphisms. One difference was the insertion of a 21,925-base-long stretch of DNA into the region. This big chunk of DNA contained multiple copies of a transposable element, or jumping gene. Transposable elements are viruslike pieces of DNA that copy and insert themselves into a host’s DNA.

    By examining the DNA of hundreds more typica moths and ruling out mutations one by one, the team ended up with one candidate: the large transposable element that had landed in the cortex gene. But the jumping gene didn’t land in the DNA that encodes the protein. Instead it landed in an intron — a stretch of DNA that gets chopped out after the gene is copied into RNA and before a protein is made.

    So, the insert is in “junk DNA,” and it’s not a SNP

    If you can’t accept that as a new starting point, I can’t do anything about it. But just throwing the same old bromides at me, and insisting that I’m wrong; well, this gets us nowhere.

    That this “mutation”—all 22 kbases of it—started at some point in time, and was handed down meiotically. And, yes, they’ve located this as occurring around 1820. None of that amounts to a hill of beans. What matters is HOW did this mutation arise. The rest is mumbo-jumbo.

    Time will prove one of us right. I’m confident. What about you?

    As to the paper, if you would like to direct my attention to something there, please do. I may, or may not, respond, depending on whether I deem it a worthwhile use of my time. I’m not going to beat a dead horse here.

  115. 115
    wd400 says:

    I’m sure the authors will invoke “selection” somewhere along the line, and then bow down to Darwinism; but, that proves nothing other than they only have one paradigm out of which to look at and analyze things.

    They show strong evidence of selection.

    Up until this paper, let’s say from the “1920’s” on, was this thought to be anything other than some “random” mutation, and likely a SNP?

    No one knew what a SNP was in the 1920s. You are the only person how said anyting about a SNP in this thread.

    TE’s are not ‘random.’

    You keep saying this, but it’s not true. In this case we are talking about a single mutation. Is you claim really that this is a directed response, programmed to occur in a single moth then take over the population?

    As to the paper, if you would like to direct my attention to something there, please do.

    You are the one making the claims. Please demonstrate something in this paper requires a whole new paradigm to understand. Or perhaps just admit that you wrote this post before you even read the paper, you didn’t understand the results and you made a mistake in necroing this thread?

  116. 116
    Origenes says:

    WD400: In this case we are talking about a single mutation.

    For clarity, we are not talking about a single point mutation, therefore it would be helpful to say: “we are talking about a single insert“.

    From the paper:

    We conclude that the large insert is the carbonaria mutation. The carbonaria insert is 21,925 nucleotides long and is composed of a roughly 9-kb essentially non-repetitive sequence (except for approximately 370 nucleotides at the repeat unit junctions) that is tandemly repeated approximately two and one-third times, with only minor differences among the repeats (Fig. 1c). The insert bears the hallmark of a class II (DNA cut-and-paste) transposable element …

    Hunter:

    This observed mutation (the insertion of a long sequence of DNA into an intron), is much more complicated than a single point mutation. … and the fact it was inserted into an intron suggests that additional molecular and cellular mechanisms are required for the coloration change to occur.

    None of this fits evolutionary theory.

    For example, evolutionary theory requires that the needed random DNA mutational change is reasonably likely to occur. Given the moth’s effective population size, the moth’s generation time period, and the complexity of the mutation, the needed mutation is not likely to occur. Evolution would have to be inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome. This is an enormous space of mutational possibilities to search through.

    It doesn’t add up. Evolution does not have the resources in terms of time and effective population size to come anywhere close to searching this astronomical mutational space. It’s not going to happen.

    A much more likely explanation, and one that has been found to be true in so many other cases of adaptation (in spite of evolutionary pushback), is that the peppered moth coloration change was directed. The environmental change and challenge somehow caused the peppered moth to modify its color. This suggests there are preprogrammed, directed adaptation mechanisms, already in place that are ready to respond to future, potential, environmental changes, which might never occur.

  117. 117
    wd400 says:

    Insertions are a type of mutation, I’m not sure what you think this adds?

    It remains the fact we are talking about a single insertion. Do you really think a this is response is “directed” to occur in a single moth?

  118. 118
    Origenes says:

    WD400: Do you really think a this is response is “directed” to occur in a single moth?

    Do you really (really) think that that is what dr. Hunter proposes when he writes:

    A much more likely explanation, and one that has been found to be true in so many other cases of adaptation (in spite of evolutionary pushback), is that the peppered moth coloration change was directed. The environmental change and challenge somehow caused the peppered moth to modify its color. This suggests there are preprogrammed, directed adaptation mechanisms, already in place that are ready to respond to future, potential, environmental changes, which might never occur.

    ?

  119. 119
    wd400 says:

    I think Hunter probably didn’t read (or at least didn’t understand) the paper so didn’t realise how improbable his scenario was.

  120. 120
    rvb8 says:

    Amazing! I have now read through most of these posts. Nick and wd400 both explain that a single mutation(or perhaps an ‘insertion’, not sure) caused a gene which governs the production melanin (I think)to produce more pigment in a single, perhaps several moths. The mutation was random and unguided, the process of selection that followed, was anything but random.

    This happened before, or in and around the fifties. Britain at this time was highly polluted and many buildings were covered in soot. The mutation allowed the dark moths to be camouflaged against predators, escape predation, and successfully pass on this advantageous mutation.

    Now as Britain is a much less polluted place, the few moths that have another mutation reducing melanin, means the process is being reversed.

    Easy, logical, evidence based, supported by years of patient research. Not being a scientist but genuinely interested in letting scientists explain their work, this explanation is clearly the correct one.

    I have no idea what all the other sciencey babble is about. I do know it is incredibly difficult to read, illogical, God based, and supported by exactly zero research.

    Which idea will win through I wonder?

  121. 121
    Origenes says:

    wd400 @119,

    wd400: I think Hunter probably didn’t read (or at least didn’t understand) the paper so didn’t realise how improbable his scenario was.

    Do not simply state your opinions, but provide arguments for your views. For instance, when you wish to talk probabilities, you should take example from dr. Hunter, who does provide arguments:

    … evolutionary theory requires that the needed random DNA mutational change is reasonably likely to occur. Given the moth’s effective population size, the moth’s generation time period, and the complexity of the mutation, the needed mutation is not likely to occur. Evolution would have to be inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome. This is an enormous space of mutational possibilities to search through.
    It doesn’t add up. Evolution does not have the resources in terms of time and effective population size to come anywhere close to searching this astronomical mutational space. It’s not going to happen.

    [Darwin’s God]

  122. 122
    bornagain77 says:

    a few ‘non-random’ notes:

    Genome-wide characterization of non-reference transposons in crops suggests non-random insertion – 2 August 2016
    Results
    We identified 13,066, 23,866 and 35,679 non-ref TEs in rice, maize and sorghum, respectively. Genome-wide characterization analysis shows that most of non-ref TEs were unique and non-ref TE classes shows different among rice, maize and sorghum. We found that non-ref TEs have a strong positive correlation with gene number and have a bias toward insertion near genes, but with a preference for avoiding coding regions in maize and sorghum. The genes affected by non-ref TE insertion were functionally enriched for stress response mechanisms in all three crops.
    Conclusions
    These observations suggest that transposon insertion is not a random event and it makes genomic diversity, which may affect the intraspecific adaption and evolution of crops.
    https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-016-2847-3

    Non-random distribution of transposable elements in the nuclear genome of plants. – 1993
    Excerpt: We have studied the genomic distribution of five different families of plant transposable elements by analyzing their location in DNA fractions from maize and tobacco genomes fractionated according to base composition. The results show that each family of elements is preferentially integrated in one specific fraction of its respective host genome. This demonstrates that the distribution of transposable elements in the nuclear genome of plants is not random but compartmentalized,,,
    https://www.ncbi.nlm.nih.gov/pubmed/8389439

    Integration specificity of the hobo element of Drosophila melanogaster is dependent on sequences flanking the integration site – 1999
    http://link.springer.com/artic.....3712619487
    We analyzed the integration specificity of the hobo transposable element of Drosophila melanogaster. Our results indicate that hobo is similar to other transposable elements in that it can integrate into a large number of sites, but that some sites are preferred over others, with a few sites acting as integration hot spots.

    Large-scale discovery of insertion hotspots and preferential integration sites of human transposed elements – 2009
    http://nar.oxfordjournals.org/...../1515.full
    We first discovered that most TEs insert within specific ‘hotspots’ along the targeted TE… Finally, we performed a global assessment to determine the extent to which young TEs tend to nest within older transposed elements and identified a 4-fold higher tendency of TEs to insert into existing TEs than to insert within non-TE intergenic regions. Our analysis demonstrates that TEs are highly biased to insert within certain TEs, in specific orientations and within specific targeted TE positions. TE nesting events also reveal new characteristics of the molecular mechanisms underlying transposition.

    A Key Evidence for Evolution Involving Mobile Genetic Elements Continues to Crumble – Cornelius Hunter – July 13, 2014
    Excerpt: The biological roles of these place-jumping, repetitive elements are mysterious.
    They are largely viewed (by Darwinists) as “genomic parasites,” but in this study, researchers found the mobile DNA can provide genetic novelties recruited as certain population-unique, functional enrichments that are nonrandom and purposeful.
    “The first shocker was the sheer volume of genetic variation due to the dynamics of mobile elements, including coding and regulatory genomic regions, and the second was amount of population-specific insertions of transposable DNA elements,” Michalak said. “Roughly 50 percent of the insertions were population unique.”
    http://darwins-god.blogspot.co.....lving.html

    Non-Random and Targeted Mutations (Environmentally induced changes to the level of DNA, 6:34 minute mark of video) – video
    http://www.youtube.com/watch?v=qTChu5vX1VI

    Evolution Is Not Random,,, – Tanya Lewis, – 02 October 2014
    Excerpt: “So in the end, most mutation is not random, at least for the DNA sequences we analyzed here,”
    http://m.livescience.com/48103.....2_32724136

    WHAT SCIENTIFIC IDEA IS READY FOR RETIREMENT? Fully Random Mutations – Kevin Kelly – 2014
    Excerpt: What is commonly called “random mutation” does not in fact occur in a mathematically random pattern. The process of genetic mutation is extremely complex, with multiple pathways, involving more than one system. Current research suggests most spontaneous mutations occur as errors in the repair process for damaged DNA. Neither the damage nor the errors in repair have been shown to be random in where they occur, how they occur, or when they occur. Rather, the idea that mutations are random is simply a widely held assumption by non-specialists and even many teachers of biology. There is no direct evidence for it.
    On the contrary, there’s much evidence that genetic mutation vary in patterns. For instance it is pretty much accepted that mutation rates increase or decrease as stress on the cells increases or decreases. These variable rates of mutation include mutations induced by stress from an organism’s predators and competition, and as well as increased mutations brought on by environmental and epigenetic factors. Mutations have also been shown to have a higher chance of occurring near a place in DNA where mutations have already occurred, creating mutation hotspot clusters—a non-random pattern.
    http://edge.org/response-detail/25264

    “It is difficult (if not impossible) to find a genome change operator that is truly random in its action within the DNA of the cell where it works. All careful studies of mutagenesis find statistically significant non-random patterns”
    James Shapiro – Evolution: A View From The 21st Century – (Page 82)

    Duality in the human genome – Nov. 28, 2014
    Excerpt: 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.
    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.,,,
    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.
    http://medicalxpress.com/news/.....enome.html

    etc.. etc…

  123. 123
    Dionisio says:

    PaV @110:

    Agree with you. I did not want to imply ‘randomness’ at all. That’s left out to Interpretation.

    Someone could say that I met my wife in college by accident. I don’t believe that. But I won’t argue about it. Though could give -upon request- a strong reason for what I believe.
    Again, here’s part of the referenced paper:

    The carb-TE is a spectacular example of an adaptively advantageous transposon; its discovery fills a fundamental gap in the peppered moth story and furthers our appreciation of the mechanism underpinning rapid adaptation.

    A consensus on the general importance of transposable elements for adaptive evolution has yet to emerge.

    As you know, many folks like to stick to the pseudoscientific ‘evo’ jargon. One must ignore those terms when they obstruct the real meaning of the text.

  124. 124
    Origenes says:

    wd400, rvb8.

    WD400:

    Origenes: For clarity, we are not talking about a single point mutation, therefore it would be helpful to say: “we are talking about a single insert“.

    Insertions are a type of mutation, I’m not sure what you think this adds?

    Clarity!
    Notice the confused state that rvb8 is in:

    rvb8: Nick and wd400 both explain that a single mutation (or perhaps an ‘insertion’, not sure) caused a gene …

    Rvb8 labours under the idea that an “insertion”is not a “single mutation” — perhaps because he equates “single mutation” with “point mutation”. See the confusion? Also, what did Nick “explain” — back in 2012?

    Nick Matzke: … we don’t quite know the exact mutational change yet, but it could well be just a point mutation.

    We now know that Nick’s intuition failed him. What actually happened was an insert of 21,925 nucleotides. This is a very complicated event and therefore it’s tricky to refer to it as a mere “single mutation”. It gives rise to the wrong associations: “single mutation”, “point mutation”, “easy”, “logical” and so forth.
    See what this does to poor rvb8:

    rvb8: Easy, logical, evidence based, supported by years of patient research. Not being a scientist but genuinely interested in letting scientists explain their work, this explanation is clearly the correct one.

    No rvb8, from a Darwinian perspective, it’s neither “easy” nor “logical”…

    Dr. Hunter: … evolutionary theory requires that the needed random DNA mutational change is reasonably likely to occur. Given the moth’s effective population size, the moth’s generation time period, and the complexity of the mutation, the needed mutation is not likely to occur. Evolution would have to be inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome. This is an enormous space of mutational possibilities to search through.
    It doesn’t add up. Evolution does not have the resources in terms of time and effective population size to come anywhere close to searching this astronomical mutational space. It’s not going to happen.

    [dr. Hunter]

  125. 125
    Silver Asiatic says:

    Every once in a while we get a thread here that is so entertaining that I’m almost embarrassed to enjoy it so much — and here we have one! Watching wd400 trying to squirm out of this is simply delightful. He is totally exposed. It’s amazing how much is revealed in his little cryptic comments. “Nothing to see here, it’s just a mutation that spread through the population!” Ha ha. I love it.
    Great job by Origenes to expose rbv’s ignorance also. He doesn’t know if it was a point mutation or an insertion of 21,925 nucleotides – but for him it doesn’t matter. LOL.
    PaV has also done an admirable job in trying to tease out some answers from wd400 and as we know, that’s always a slow and painful process.
    The only place I think there is a slip-up is by including the speculation that the insertion was ‘directed’. It may well be the case, but that’s still speculative. And of course, instead of trying to defend his own position, wd400 jumped on that part of the claim.
    It doesn’t matter that much, it’s obvious that he’s trying to dig himself out of a hole, so he thinks a turn-around will work in this case. Very amusing!

  126. 126
    bornagain77 says:

    Silver Asiatic, if it were possible to ever get a straight answer out of wd400, I would like to ask him, since he holds practically everything in the cell to be the result of randomness instead of the result of purposeful intent, why is it impossible for Darwinists, in the peer reviewed literature, to describe the complexities of biological life without illegitimately using words that invoke agent causality and/or teleology, instead of just attributing the actions in the cell to randomness as wd400 is bent on doing?:

    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

    This working biologist agrees with Talbott’s assessment:

    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

  127. 127
    Silver Asiatic says:

    BA77

    Silver Asiatic, if it were possible to ever get a straight answer out of wd400 …

    I think we both know, that’s never going to happen. 🙂
    But I admire your persistent efforts to try.

    Actually, I admire many things about wd400 – not the least of which that he continues to participate here after so many years. But also that he is so totally committed to his worldview that he cannot permit the slightest concession to design or admit the smallest doubt about the power of Darwinian processes. I find that kind of charming in some ways – it’s like religious loyalty or patriotism to a cause.

    He’s also truly amazing in that he takes no interest at all in the philosophical (moral, spiritual, rational) implications of his belief system. It’s always just … zero. No response, or some cryptic one-liner at best. He’s a true atheist/materialist — a wonderful example to observe and study!

    I’ll also say he has corrected me (and us) several times, at least forcing a doctrinaire reading of Darwinian papers, and of course, strictly speaking, they’re not going to say something is evidence of ID. That’s what we read into it, but he is technically correct many times.

    Finally, and sincerely, he doesn’t get nasty about it. Unless we’d say being completely obdurate and closed to refutations of his point of view as being rude, it will usually just be the mind-bogglingly (fake?) naive phrase, like this one:

    Insertions are a type of mutation, I’m not sure what you think this adds?

    I love it! He equates the two radically different events as both “a type of mutation”, says nothing about the probability of that DNA segment insertion into the genome, and adds the question “I’m not sure what you think this adds?”

    He’s a master of understating the problem, deflecting attention and then claiming “he’s not sure” what we think the difference between point mutation and the insertion of 22K nucleotides really adds to the conversation.

    LOL. After 10 (?) years on this blog, wd400 is not sure of what we’re seeing here?

  128. 128
    wd400 says:

    Do not simply state your opinions, but provide arguments for your views. For instance, when you wish to talk probabilities, you should take example from dr. Hunter, who does provide arguments:

    Well you asked me what I thought, and that’s the only reason I can imagine Hunter would propose a scenario that is so ad odds with the paper. The paper establishes that the phenotype is the result of a single mutation, so if it was a “directed” mutation it was directed to occur in one moth.

    We now know that Nick’s intuition failed him. What actually happened was an insert of 21,925 nucleotides. This is a very complicated event and therefore it’s tricky to refer to it as a mere “single mutation”. It gives rise to the wrong associations: “single mutation”, “point mutation”, “easy”, “logical” and so forth.

    There is nothing very complex about a TE insertion. In humans, where TEs are relatively quiet, we probably each have a new insertion. In Drosopophila some elements like P and I end up copying themselves almost every generation. Aslmot as if “Evolution would have to be inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome”…

  129. 129
    wd400 says:

    SA,

    I’m really not sure you’ve read the same thread as I have.

    Literlly the only thing that (now) separates PaV’s assertions from the mainstream evolutionary explanation of this phenomenom is the idea that the mutation is directed. But it’s a pretty weird sort of “direction” when it only occurs in one moth.

    I love it! He equates the two radically different events as both “a type of mutation”, says nothing about the probability of that DNA segment insertion into the genome, and adds the question “I’m not sure what you think this adds?

    As I said above, you might want to read up a bit about the rate and effects of transposable element integrations.

    Moreover, remember that PaV necro’d this thread because he (without reading the paper…) thought its results supported his ravings above about epigenetics and directed mutation. It should be clear to anyone who read this that’s not the case. Just as I said at the time, it’s mutation to generate a simple Mendelian trait followed by strong selection to nearly fix the mutant allele.

  130. 130
    PaV says:

    wd400:

    This is how you view things:

    Well you asked me what I thought, and that’s the only reason I can imagine Hunter would propose a scenario that is so a[t] odds with the paper. The paper establishes that the phenotype is the result of a single mutation, so if it was a “directed” mutation it was directed to occur in one moth. . . .

    It remains the fact we are talking about a single insertion. Do you really think a this is response is “directed” to occur in a single moth?

    Since you completely lack imagination, let’s supply some:

    There are ‘directed’ mechanisms within the genome that, due to some environmental effect, begin to mutate certain innate operations of adaptation, or change within an organism. These mechanisms—always present—when affected by some ‘cue’, respond by heightening the mutational capabilities of the organism; however, not in a ‘general,’ but in a more ‘specific’ way, a way that isolates certain protein domains or regulatory targets.

    Thus, while ‘randomness’ is an element being used by the organism, the ONLY way that this ‘randomness’ has any effect is due to the ability of the organism to isolate, or specify, where the mutational mechanisms are to be activated. Hence, there is a ‘randomness’ to it—meaning that ‘one’ will end up with the needed ‘mutation’ (here, a rather colossal insert [Diogenes]), and will then spread via normal inheritance and ‘selection.’

    There, now do you see?

    PaV:TE’s are not ‘random.’

    wd400:
    You keep saying this, but it’s not true. In this case we are talking about a single mutation. Is you claim really that this is a directed response, programmed to occur in a single moth then take over the population?

    The TE’s are not random

    From this 2009 paper:

    Recent comprehensive sequence analysis of the maize genome now permits detailed discovery and description of all transposable elements (TEs) in this complex nuclear environment. . . .

    The majority, perhaps all, of the investigated retroelement families exhibited non-random dispersal across the maize genome, with LINEs, SINEs, and many low-copy-number LTR retrotransposons exhibiting a bias for accumulation in gene-rich regions.

    McClintock did her original work on maize.

  131. 131
    PaV says:

    wd400:

    Moreover, remember that PaV necro’d this thread because he (without reading the paper…) thought its results supported his ravings above about epigenetics and directed mutation. It should be clear to anyone who read this that’s not the case. Just as I said at the time, it’s mutation to generate a simple Mendelian trait followed by strong selection to nearly fix the mutant allele.

    Ravings? Really?

    Now, here’s what Wikipedia has to say about our beloved peppered moths:

    In peppered moths, the allele for dark-bodied moths is dominant, while the allele for light-bodied moths is recessive, meaning that the typica moths have a phenotype (visible or detectable characteristic) that is only seen in a homozygous genotype (an organism that has two copies of the same allele), and never in a heterozygous one. This helps explain how dramatically quickly the population changed when being selected for dark colouration.

    Now, the idea is this: the alleles are present for both the dark and light-bodied moths. Because more and more ‘light-bodied’ ones are visible and selectively eaten, the dark-bodied alleles accumulate and change the allele frequency.

    Is that what we see here?

    Answer, honestly, wd400.

  132. 132
    wd400 says:

    Since you completely lack imagination, let’s supply some:

    There are ‘directed’ mechanisms within the genome that, due to some environmental effect, begin to mutate certain innate operations of adaptation, or change within an organism. These mechanisms—always present—when affected by some ‘cue’, respond by heightening the mutational capabilities of the organism; however, not in a ‘general,’ but in a more ‘specific’ way, a way that isolates certain protein domains or regulatory targets.

    Thus, while ‘randomness’ is an element being used by the organism, the ONLY way that this ‘randomness’ has any effect is due to the ability of the organism to isolate, or specify, where the mutational mechanisms are to be activated. Hence, there is a ‘randomness’ to it—meaning that ‘one’ will end up with the needed ‘mutation’ (here, a rather colossal insert [Diogenes]), and will then spread via normal inheritance and ‘selection.’

    There, now do you see?

    Honestly, I do not. What has this to do with the paper? How does it fit with the fact this is a single mutation? What evidence is there for these directed mutations at all, let alone in this case?

    The majority, perhaps all, of the investigated retroelement families exhibited non-random dispersal across the maize genome, with LINEs, SINEs, and many low-copy-number LTR retrotransposons exhibiting a bias for accumulation in gene-rich regions.

    Do you really need to be taught that the “random” in RM+NS means random with respect to fitness? This paper is saying that some classes of TEs preferentially integrate in gene-rich or gene poor regions (which is likely a result of the fact some retroelements tend to insert themselves into other copies of their own sequence, creating large gene-poor regions in the process).

    Now, the idea is this: the alleles are present for both the dark and light-bodied moths. Because more and more ‘light-bodied’ ones are visible and selectively eaten, the dark-bodied alleles accumulate and change the allele frequency.

    Is that what we see here?

    Yes.

  133. 133
    Origenes says:

    wd400,

    wd400: … that’s the only reason I can imagine Hunter would propose a scenario that is so ad odds with the paper.

    The scenario that Dr. Hunter proposes is this:
    “A much more likely explanation, and one that has been found to be true in so many other cases of adaptation (in spite of evolutionary pushback), is that the peppered moth coloration change was directed. The environmental change and challenge somehow caused the peppered moth to modify its color. This suggests there are preprogrammed, directed adaptation mechanisms, already in place that are ready to respond to future, potential, environmental changes, which might never occur.” [Dr.Hunter],
    and you have provided zero arguments as to why this scenario is at odds with the findings in the paper.

    wd400: The paper establishes that the phenotype is the result of a single mutation, so if it was a “directed” mutation it was directed to occur in one moth.

    You don’t seem to understand what is meant by “directed”. And what’s up with your “in one moth”? Why do you hold that “preprogrammed, directed adaptation mechanisms”, present in all British peppered moths, is only activated in just one moth? On what basis do you think that this is Dr. Hunter’s position?

    If there is indeed a “one moth problem”, then this is only a problem for your position. Only if the insert was a random mutation, then a “one moth problem” emerges. So perhaps, you must answer your own question:

    wd400: Is you claim really that this is a directed response, programmed to occur RANDOM MUTATION in a single moth then take over the population?

  134. 134
    wd400 says:

    Origenes, I’m honestly not sure what you’re on about.

    Let’s break it down.

    This paper (and others before it) demonstrate this phenotype is the result of a single mutation. So it happened in one moth, other black moths inherited this trait from this ancestor rather than as the result of environmentally enduced change. That doesn’t seem compatible with a programmed response present in all British peppered moths (your own emphasis).

    Why did Hunter propose a program response, when it seems so unlikely given the paper? I presume because he didn’t read the paper. If he did he didn’t understand it, I guess.

    What “one moth problem” exists for random mutation?

  135. 135
    Origenes says:

    wd400,

    This paper (and others before it) demonstrate this phenotype is the result of a single mutation.

    For clarity: an insert of 21,925 nucleotides.

    wd400: So it happened in one moth …

    It is only your assumption that this happened in one moth. Show me where this is demonstrated in the paper.

    wd400: … rather than as the result of environmentally enduced change.

    I guess you mean “induced”. Whatever… it’s another unsubstantiated assumption on your part.

    wd400: That doesn’t seem compatible with a programmed response present in all British peppered moths (your own emphasis).

    Indeed. Your baseless assumptions are not compatible with Dr. Hunter’s scenario. Bravo!

    wd400: What “one moth problem” exists for random mutation?

    The exact same “one moth problem” that you envisioned for the (non-existent) scenario of “directed response, programmed to occur in a single moth then take over the population” [wd400 in post #115].

  136. 136
    wd400 says:

    How can a single mutation happen in more than one moth? I really don’t know what you are failing to grasp about this.

    The exact same “one moth problem” that you envisioned for the (non-existent) scenario of “directed response, programmed to occur in a single moth then take over the population” [wd400 in post #115].

    Again, I don’t see the problem.If the response is random with respect to fitness and rare we’d expect to occur only once. If it was directed (and therefore a common response to the same stimulus that many thousands of moths received) we’d expect to occur multiple times. Right?

  137. 137
    Origenes says:

    wd400: How can a single mutation happen in more than one moth?

    This can be the case if the “single mutation” is the result of, as Dr. Hunter terms it, “preprogrammed directed adaptation mechanisms” present in British peppered moths.

    wd400: I really don’t know what you are failing to grasp about this.

    Really? And I’m wondering why it is that I have to explain it to you again and again.

    wd400: Again, I don’t see the problem.

    After I pointed out that it can only be a problem for your position, you no longer see the “one moth problem”. How convenient.

    wd400: If the response is random with respect to fitness and rare we’d expect to occur only once.

    As a random event it is astronomically unlikely. So much so that we expect it to never happen.

    wd400: If it was directed (and therefore a common response to the same stimulus that many thousands of moths received) we’d expect to occur multiple times. Right?

    Right. We would expect multiple dark coloured moths — which is actually confirmed by observation.

  138. 138
    wd400 says:

    I don’t think you understand what is meant by “single mutation”. It means a single event. All of the black moths inherited a gene variant that was created by a single mutation.

  139. 139
    Origenes says:

    wd400,

    Are you serious? Do you derive ‘single random mutation in one individual moth’ from the term “single mutation”? Is that how you argue for your Darwinian position?

    It also doesn’t follow:
    A non-random directed mutation can be described as a “single mutation” wrt an individual moth, however by doing so it is certainly not implied that this happens in one individual moth only. Quite the contrary.
    Given the presence of relevant preprogrammed directed adaptation mechanisms in British peppered moths, we would obviously expect exposure to a specific “single mutation” by multiple moths.

  140. 140
    wd400 says:

    Are you serious? Do you derive ‘single random mutation in one individual moth’ from the term “single mutation”? Is that how you argue for your Darwinian position?

    That’s the plain meaning of the phrase, yes. It’s not about “arguing” for a position, it’s just what those words mean.

    A non-random directed mutation can be described as a “single mutation” wrt an individual moth, however by doing so it is certainly not implied that this happens in one individual moth only. Quite the contrary.
    Given the presence of relevant preprogrammed directed adaptation mechanisms in British peppered moths, we would obviously expect exposure to a specific “single mutation” by multiple moths.

    Well, again, “single mutation” means a gene variant that arose just once. This paper, and others before it, demonstrated that this phenotype is the result of a single mutation in that sense. So the scenario Hunter imagined is ruled out. Clear?

  141. 141
    Origenes says:

    wd400: This paper, and others before it, demonstrated that this phenotype is the result of a single mutation in that sense. So the scenario Hunter imagined is ruled out. Clear?

    Nope. The paper does not demonstrate “a single mutation in that sense”. It does not demonstrate randomness. Clear?

  142. 142
    wd400 says:

    Well, I’m afraid you are just wrong about this. The pattern of linage disequilibrium and decreased genetic diversity associated with the allele only makes sense if the gene arose once the was quickly driven to high frequency ( a so called “selective sweep”).

  143. 143
    Origenes says:

    wd400: The pattern of lin[k]age disequilibrium and decreased genetic diversity associated with the allele only makes sense if the gene arose once …

    For clarity: you are claiming that the data only make sense if the insert happened in one single moth. If the insert happened in 10 moths, 100 moths or a thousand moths the data no longer make sense. Do I understand you correctly?

  144. 144
    wd400 says:

    Yes.

  145. 145
    Silver Asiatic says:

    wd

    Thanks for your reply.

    Literlly the only thing that (now) separates PaV’s assertions from the mainstream evolutionary explanation of this phenomenom is the idea that the mutation is directed. But it’s a pretty weird sort of “direction” when it only occurs in one moth.

    If so, then I’d agree with your view, as I said earlier, I don’t think a case can be made for a “directed mutation” having occured based on this data alone. I think this could contribute to an argument for that kind of thing, but thus far it is speculative, and there’s nothing in the paper to support it.

    However, as I read it, PaV and Origenes and Cornelius Hunter are pointing first to the improbability of that mutation/insertion. That’s what is driving the speculation about directed, or pre-programmed mutation.

    As I said above, you might want to read up a bit about the rate and effects of transposable element integrations.

    I think many of us are interested in this. As I see it, the probability of that kind of mutation occuring is very small, and Origenes quoted Hunter a couple of times pointing out how difficult it would be to model this kind of complex insertion event.
    So, with that, if you have anything we could read that would support the idea that this was not an astronomically improbable event, then that would help quite a lot.

    Moreover, remember that PaV necro’d this thread because he (without reading the paper…) thought its results supported his ravings above about epigenetics and directed mutation. It should be clear to anyone who read this that’s not the case. Just as I said at the time, it’s mutation to generate a simple Mendelian trait followed by strong selection to nearly fix the mutant allele.

    Ok, again I agree that this does not necessarily show a directed mutation, but it certainly does not if this mutation is of the ordinary sort we would expect – in other words, it’s not significantly different than the odds of a point mutation occurring in the same way.

    My concern on your response is that you did not address the difference between a point mutation and an insertion of a segment 22 thousand nucleotides.

    As you state, it’s a mutation to generate a simple Mendelian trait – yes, the trait is simple, but the mutation is not.

    For me, that’s where the focus of the argument is. If you do not accept that the insertion was a highly improbable event, then you’re obviously not going to see any need to propose it as a directed mutation.

  146. 146
    bornagain77 says:

    of note:

    Peppered Moth Still Not Evolving by Brian Thomas, M.S.
    ,,, what began as a population of light and dark moth varieties existed through the industrial revolution as a population of light and dark moth varieties. No net evolution occurred. And that’s essentially what geneticists confirmed in their new study.,,,
    5. A hiccup in healthy cell processes that randomly pasted the 21,925-long TE into this particular gene would justify the Nature study authors calling it a “mutation.” However, processes could have pasted the TE into this gene as part of an internal variation-generating protocol. But this implies ingeniously designed automated genetic-script editing. The team did not test these options, but whether the TE placement happened by accident or design, the cut-and-paste process itself followed a focused strategy using cellular machinery and protocols.
    http://www.icr.org/article/pep.....-evolving/

    and again, other TE studies show the placement of TEs to be ‘non-random’
    http://www.uncommondescent.com.....ent-621062

    “The majority, perhaps all, of the investigated retroelement families exhibited non-random dispersal across the maize genome,”
    http://journals.plos.org/plosg.....en.1000732

    Thus the placement of TEs in moths, from the best evidence now available from other research, does not suggest that the placement of TEs in moths was a random event. In fact, taking into consideration the complexity, and many molecular machines, involved in ‘cutting and pasting’ several thousand bases into the genome as a ‘new’ regulatory element, and the odds against it happening purely by chance, it is ludicrous to suggest it was a ‘random/accidental’ event.

    But ludicrous is apparently fine and dandy with wd400.

  147. 147
    bornagain77 says:

    of related note:

    butterfly mimicry – images
    https://www.google.com/search?q=butterfly+mimicry&biw=1351&bih=650&source=lnms&tbm=isch&sa=X&sqi=2&ved=0ahUKEwiYyPa8pMTQAhVhjVQKHbEDA2YQ_AUIBigB

    Problems with evolution of (Butterfly) mimicry “huge” – with picture of leaf mimic butterfly – April 2014
    http://www.uncommondescent.com.....icry-huge/

    Bernard d’Abrera on Butterfly Mimicry and the Faith of the Evolutionist – October 5, 2011
    Excerpt:  renowned butterfly scholar and photographer Bernard d’Abrera considers the mystery of mimicry.,,,
    For it to happen in a single species once through chance, is mathematically highly improbable. But when it occurs so often, in so many species, and we are expected to apply mathematical probability yet again, then either mathematics is a useless tool, or we are being criminally blind.,,, Evolutionism (with its two eldest daughters, phylogenetics and cladistics) is the only systematic synthesis in the history of the universe that proposes an Effect without a Final Cause. It is a great fraud, and cannot be taken seriously because it outrageously attempts to defend the philosophically indefensible.
    http://www.evolutionnews.org/2.....51571.html

    A mural on moth wings
    Excerpt: It’s the only mimic insect I know that paints an entire scene. It looks like a watercolor. Two red-eyed muscomorph flies feed from fresh bird droppings, complete with light glinting off their wings. I’ve never seen anything like it!
    http://www.myrmecos.net/2011/0.....oth-wings/

    Fruit fly with the wings of beauty – July 2012
    Excerpt: But a closer examination of the transparent wings of Goniurellia tridens reveals a piece of evolutionary(?) art. Each wing carries a precisely detailed image of an ant-like insect, complete with six legs, two antennae, a head, thorax and tapered abdomen.
    http://www.thenational.ae/news.....-of-beauty

    SEM (scanning electron microscope) of butterfly wings – images
    https://www.google.com/search?q=SEM+of+butterfly+wings&client=firefox-a&hs=Rov&rls=org.mozilla:en-US:official&channel=np&source=lnms&tbm=isch&sa=X&ei=-oegUtWrJMepyAGyo4D4Aw&ved=0CAkQ_AUoAQ&biw=1280&bih=621

    Butterfly wings inspire new high-tech surfaces – November 7, 2012
    Excerpt: The researchers wanted to test how butterfly wings and rice leaves might display some of the characteristics of other surfaces they’ve studied, such as shark skin, which is covered with slippery, microscopic grooves that cause water to flow smoothly around the shark. They also tested fish scales, and included non-textured flat surfaces for comparison. After studying all the textures close up, the researchers made molds of them in silicone and cast plastic replicas. To emulate the waxy coating on the rice leaves and the slippery coating on shark skin (which in nature is actually mucous), they covered all the surfaces with a special coating consisting of nanoparticles. In one test, they lined plastic pipes with the different coated textures and pushed water through them. The resulting water pressure drop in the pipe was an indication of fluid flow. For a pipe about the size of a cocktail straw, a thin lining of shark skin texture coated with nanoparticles reduced water pressure drop by 29 percent compared to the non-coated surface. The coated rice leaf came in second, with 26 percent, and the butterfly wing came in third with around 15 percent. Then they dusted the textures with silicon carbide powder – a common industrial powder that resembles natural dirt – and tested how easy the surfaces were to clean. They held the samples at a 45-degree angle and dripped water over them from a syringe for two minutes, so that about two tablespoons of water washed over them in total. Using software, they counted the number of silicon carbide particles on each texture before and after washing. The shark skin came out the cleanest, with 98 percent of the particles washing off during the test. Next came the rice leaf, with 95 percent, and the butterfly wing with about 85 percent washing off. By comparison, only 70 percent washed off of the flat surface. Bushan thinks that the rice leaf texture might be especially suited to helping fluid move more efficiently through pipes, such as channels in micro-devices or oil pipelines. As to the Blue Morpho’s beautiful wings, their ability to keep the butterfly clean and dry suggests to him that the clapboard roof texture might suit medical equipment, where it could prevent the growth of bacteria.
    http://phys.org/news/2012-11-b.....faces.html

    “Insect Wings Shred Bacteria to Pieces” – March 2013 – with video
    http://www.uncommondescent.com.....to-pieces/

  148. 148
    bornagain77 says:

    Metamorphosis: The Beauty & Design of Butterflies
    https://www.youtube.com/watch?v=AZk6nZGH9Xo
    https://www.youtube.com/watch?v=Vx4i9Rn4moA&list=PLO673u2zYHhmtTNnZ-nIEV2sO3aMpWO3s&index=1

    Brilliant Butterfly Feature Challenges Darwinian Selection by Brian Thomas, M.S. – September 2013
    Excerpt: The PNAS study authors wrote, “Morpho butterflies are a brilliant spectacle of nature’s capacity for photonic engineering.” However, there is no reason—other than sheer bias—to credit nature with engineering butterfly optic structures that even human engineers have not yet been able to replicate.
    http://www.icr.org/article/7710/

    Deciphering butterflies’ designer colors: – July 17, 2013
    Excerpt: The three tropical butterflies the researchers studied all display iridescence, a property of materials that change color depending on the viewing angle, but they do so with different colors. Papilio ulysses, the Ulysses butterfly or blue mountain swallowtail, appears bluish green when seen from above. Its cousin Papilio peranthus, by contrast, looks yellowish green from above, and a third relative, Papilio blumei, the green swallowtail, is more of a deep green. All three shift toward deep blue when viewed from a sharp angle.
    To probe the physics behind the wings’ structural colorations, the scientists examined a cross-section of each species’ wing under a scanning electron microscope. The team found that the wings contain specialized architectures in which solid flat layers known as cuticles alternate with thin “air” layers known as laminae. The laminae aren’t entirely empty space, however; they also contain pillars of the cuticle material, which gives the wing a repeating crystal-like structure. This structure is similar to what is known as a Bragg reflector—essentially a multi-layered mirror that reflects only certain wavelengths, or colors, of light.
    The researchers then measured the light spectrum reflected from the wing at different angles, using a technique called angle-resolved reflection spectroscopy. They found that the varying colors of the three species’ wings arise from slight differences in crystal parameters. P. ulysses has seven cuticle layers, for example, while P. peranthus has eight. The thicknesses of the cuticles and air layers also vary between species. Cheah notes that even though these differences are slight, they have a major effect on the butterflies’ appearance. “It all comes from the fact the wing structure has subtle differences between these three types of butterfly,” he says.
    http://phys.org/news/2013-07-d.....rials.html

    Look at This Incredible Insect Wing Design – Cornelius Hunter – May 17, 2013
    Excerpt: And so using this rational, mathematical, approach to biology the researchers were able to do something that consistently eludes evolutionists—produce a successful prediction:
    “An optimal cell size of a grid-like structure such as the wing can be predicted using the “critical crack length” of the membrane, which is determined by the material’s fracture toughness and the stress applied. … An “optimal” wing cell should have a diameter of around 1132 µm. Is this the case in locust wings? Our results show that the distribution of the wing cell size in locust wings corresponds very well to this prediction, with the most common wing-cell “class” being between 1000 and 1100 µm.”
    http://darwins-god.blogspot.co.....-wing.html

    The vein patterns in fruit fly wings never vary by “more than the width of a single cell” – Sept. 18, 2014
    Excerpt: Gregor and his colleagues used computer analysis and superimposition to measure and compare wing vein patterns in fruit flies. Even when grown at different temperatures, genetically similar flies had as little variation between two flies’ wings as between the left and right wings of a single fly. And genetically less-similar flies’ wings differed by no more than one cell’s width, suggesting exquisitely precise developmental control over vein patterns. “At every single step, we are at the precision of one half to one cell, so no [additional] error-reducing mechanisms [are] necessary,” says Gregor.
    If the data hold, it would point to “a remarkable amount of communication between the two sides of the body,” he says. It would mean development is really incredibly precise.”
    http://www.uncommondescent.com.....ngle-cell/

  149. 149
    Origenes says:

    wd400:

    Origenes:
    For clarity: you are claiming that the data only make sense if the insert happened in one single moth. If the insert happened in 10 moths, 100 moths or a thousand moths the data no longer make sense. Do I understand you correctly?

    Yes.

    How does this data distinguish between the offspring of one single carbonaria moth — the female lays about 2,000 eggs — and multiple carbonaria moths who were exposed to preprogrammed directed adaptation mechanisms (Dr. Hunter’s scenario)?
    Obviously, it cannot be done. Only your Darwinian assumptions can rule out Dr. Hunter’s scenario.

  150. 150
    wd400 says:

    Obviously, it cannot be done. Only your Darwinian assumptions can rule out Dr. Hunter’s scenario

    How would you know? Why are you so confident about a subject you know so little about?

    The key difference is that offspring from a single mutant would all receive the new allele on a single genetic background. If lots of different moths produced the mutation in would occur on different genetic backgrounds.

    The mutation is still associated with a particular set of genetic variants (that don’t cause the phenotype), something that happens when a single mutation is spread through a population more quickly than recombination can connect if to different genetic backgrounds.

    So it’s a single mutation. Hunter’s scenario is wrong.

  151. 151
    wd400 says:

    SA,

    You can read up yourself, but as I said insertion is what TEs do. We don’t know enough about these moths to know the rate of insertion per generation, but in other species there can be multiple insertions per generation. In humans it’s a little less than one, not much more than the rate of protein coding point mutations.

    Transposons are so good and getting into and modifying sequences that scientists use them to generate mutations to study gene function: https://en.m.wikipedia.org/wiki/Transposon_mutagenesis

  152. 152
    Origenes says:

    WD400: The key difference is that offspring from a single mutant would all receive the new allele on a single genetic background. If lots of different moths produced the mutation in would occur on different genetic backgrounds.

    Doesn’t follow. If lots of moths, who share the same relevant haplotype, produce the same precision insertion due to preprogrammed directed adaptation mechanisms — consistent with Dr. Hunter’s proposal — I don’t see any problems whatsoever.

  153. 153
    wd400 says:

    You can keep constructing epicycles to support Hunter’s idea (like, why would any moths share such a long haplotype in the original population, let alone why only those moths with this long haplotype of mostly neutral variants would produce this mutation…) or try to engage with the data in an attempt to understand it rather than prop an idea that you prefer. It’s really up to you.

  154. 154
    bornagain77 says:

    “You can keep constructing epicycles”

    spits coffee out laughing!,,,

    A Philosophical Question…Does Evolution have a Hard Core ?
    Some Concluding Food for Thought
    Excerpt: So basically, the demarcation problem is a fun game philosophers enjoy playing, but when they realize the implications regarding the theory of evolution, they quickly back off…
    http://www.samizdat.qc.ca/cosm.....ore_pg.htm

    Imre Lakatos, although he tipped toed around the failure of Darwinism to have a rigid demarcation criteria in science, he was brave enough to state that a good scientific theory will make successful predictions in science and a pseudo-scientific theory will generate ‘epicycle theories’ to cover up embarrassing failed predictions.

    “In degenerating programmes, however, theories are fabricated only in order to accommodate known facts”
    – Imre Lakatos (November 9, 1922 – February 2, 1974) a philosopher of mathematics and science, , quote as stated in 1973 LSE Scientific Method Lecture

    And on that score, Darwinism squarely qualifies as a pseudo-science:

    “When their expectations turn out to be false, evolutionists respond by adding more epicycles to their theory that the species arose spontaneously from chance events. But that doesn’t mean the science has confirmed evolution as Velasco suggests. True, evolutionists have remained steadfast in their certainty, but that says more about evolutionists than about the empirical science.”
    ~ Cornelius Hunter

    Here’s That Algae Study That Decouples Phylogeny and Competition – June 17, 2014
    Excerpt: “With each new absurdity another new complicated just-so story is woven into evolutionary theory. As Lakatos explained, some theories simply are not falsifiable. But as a result they sacrifice realism and parsimony.”
    – Cornelius Hunter
    http://darwins-god.blogspot.co.....uples.html

    “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

    Following in Lakatos’s footsteps, Dr. Hunter has compiled a list of some of the major false predictions generated by evolutionary theory that Darwinists have to make excuses for. False predictions that are fundamental to evolutionary theory, i.e. go to the ‘core’ of the theory, as it were, and falsify it from the inside out using Lakatos’s demarcation criteria.

    Darwin’s (failed) Predictions – Cornelius G. Hunter – 2015
    This paper evaluates 23 fundamental (false) predictions of evolutionary theory from a wide range of different categories. The paper begins with a brief introduction to the nature of scientific predictions, and typical concerns evolutionists raise against investigating predictions of evolution. The paper next presents the individual predictions in seven categories: early evolution, evolutionary causes, molecular evolution, common descent, evolutionary phylogenies, evolutionary pathways, and behavior. Finally the conclusion summarizes these various predictions, their implications for evolution’s (in)capacity to explain phenomena, and how they bear on evolutionist’s claims about their theory.
    https://sites.google.com/site/darwinspredictions/home

    And here is a broader overview of the many failed predictions of naturalism/materialism, in comparison to the many successful predictions of Theism, in regards to the major scientific discoveries that have now been revealed by modern science:

    Theism compared to Materialism/Naturalism – a comparative overview of the major predictions of each philosophy – video
    https://youtu.be/QQ9iyCmPmz8

    Verse:

    1 Thessalonians 5:21
    but test everything; hold fast what is good.

  155. 155
    Origenes says:

    wd400: You can keep constructing epicycles to support Hunter’s idea (like, why would any moths share such a long haplotype in the original population …

    Didn’t I mention (#149) that a female moth lays about 2,000 eggs? So, why is this in any way unlikely?

    wd400: … let alone why only those moths with this long haplotype of mostly neutral variants would produce this mutation…)

    It is your assumption that these variants are neutral. They may very well not be neutral wrt the insertion.
    Anyway, this is your selective skepticism speaking.

    wd400: … or try to engage with the data in an attempt to understand it rather than prop an idea that you prefer. It’s really up to you.

    Indeed. Let’s do just that. Which brings us back to Dr.Hunter:

    Dr. Hunter: … evolutionary theory requires that the needed random DNA mutational change is reasonably likely to occur. Given the moth’s effective population size, the moth’s generation time period, and the complexity of the mutation, the needed mutation is not likely to occur. Evolution would have to be inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome. This is an enormous space of mutational possibilities to search through.
    It doesn’t add up. Evolution does not have the resources in terms of time and effective population size to come anywhere close to searching this astronomical mutational space. It’s not going to happen.

    [dr. Hunter]

  156. 156
    wd400 says:

    Epicycles it is then!

    You might want to reflect on how desperately you are keeping Hunter’s scenario alive in some form. Like, how greatly does this programmed response present in all moths (your words…) happening in one clutch of eggs improve the odds compared to it happening in one moth? And remember these moths are diploid and reproduce sexually, so there are at least 4 haplotypes surrounding the insertion site in any clutch and two in each offspring. So, do even make this tiny improvement to the odds of Hunter’s scenario you need to explain why the mutation happened in only one of these backgrounds.

    As I say, i encourage you to take a step back, stop trying to defend someone simply because they propose an idea you’d like to be true and engage with the data. Per the piece you keep quoting, “inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome” is exactly what TEs do.

  157. 157
    bornagain77 says:

    correction:

    You might want to reflect on how desperately you are keeping Darwin’s’s scenario alive in some form.

    There all better.

    False Darwinian prediction: Mutations are not adaptive – Cornelius Hunter
    Excerpt: The second problem is that organisms use strategies to direct the mutations according to the threat. Adaptive mutations have been extensively studied in bacteria. Experiments typically alter the bacteria food supply or apply some other environmental stress causing mutations that target the specific environmental stress. (Burkala, et. al.; Moxon, et. al; Wright) Adaptive mutations have also been observed in yeast (Fidalgo, et. al.; David, et. al.) and flax plants. (Johnson, Moss and Cullis) One experiment found repeatable mutations in flax in response to fertilizer levels. (Chen, Schneeberger and Cullis) Another exposed the flax to four different growth conditions and found that environmental stress can induce mutations that result in “sizeable, rapid, adaptive evolutionary responses.” (Chen, Lowenfeld and Cullis) In response to this failed prediction some evolutionists now are saying that evolution somehow created the mechanisms that cause mutations to be adaptive.
    https://sites.google.com/site/darwinspredictions/mutations-are-not-adaptive

  158. 158
    Origenes says:

    wd400: Per the piece you keep quoting, “inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome” is exactly what TEs do.

    This is similar to the following “discussion”:

    X: IPhones arise by sheer dumb luck.

    Y: You must be mistaken, because an IPhone arising by sheer dumb luck would be a very unlikely event.

    X: Not at all. We see IPhones everywhere.

  159. 159
    bornagain77 says:

    On the unfalsifiable pseudo-scientific nature of Darwinian evolution:

    As far as having a rigid mathematical basis to test against as other overarching theories of science have, Darwinian evolution is a untestable, and therefore unfalsifiable, pseudo-science, whereas, on the other hand, Intelligent Design is very much a testable, and therefore falsifiable, science since it is based on the rigid math within ‘conservation of information’ theorems (Dembski; Marks).
    http://www.uncommondescent.com.....ent-620985

    Of related note: In so far as Darwinian evolution is dependent on the premises of reductive materialism, (which I would argue Darwinism is absolutely dependent on the premises of reductive materialism), and regardless of whether Darwinists ever personally accept the falsification or not, Darwinian evolution is now empirically falsified by advances in quantum biology. Specifically, reductive materialism cannot explain the ‘non-local’, beyond space and time, effect of quantum entanglement/information in molecular biology:

    “What happens is this classical information (of DNA) is embedded, sandwiched, into the quantum information (of DNA). And most likely this classical information is never accessed because it is inside all the quantum information. You can only access the quantum information or the electron clouds and the protons. So mathematically you can describe that as a quantum/classical state.”
    Elisabeth Rieper – Classical and Quantum Information in DNA – video (Longitudinal Quantum Information resides along the entire length of DNA discussed at the 19:30 minute mark; at 24:00 minute mark Dr Rieper remarks that practically the whole DNA molecule can be viewed as quantum information with classical information embedded within it)
    https://youtu.be/2nqHOnVTxJE?t=1176

    Molecular Biology – 19th Century Materialism meets 21st Century Quantum Mechanics – video
    https://www.youtube.com/watch?v=rCs3WXHqOv8

    Looking beyond space and time to cope with quantum theory – 29 October 2012
    Excerpt: “Our result gives weight to the idea that quantum correlations somehow arise from outside spacetime, in the sense that no story in space and time can describe them,”
    http://www.quantumlah.org/high.....uences.php

    Quantum correlations do not imply instant causation – August 12, 2016
    Excerpt: A research team led by a Heriot-Watt scientist has shown that the universe is even weirder than had previously been thought.
    In 2015 the universe was officially proven to be weird. After many decades of research, a series of experiments showed that distant, entangled objects can seemingly interact with each other through what Albert Einstein famously dismissed as “Spooky action at a distance”.
    A new experiment by an international team led by Heriot-Watt’s Dr Alessandro Fedrizzi has now found that the universe is even weirder than that: entangled objects do not cause each other to behave the way they do.
    http://phys.org/news/2016-08-q.....ation.html

    i.e. Quantum information is experimentally shown to be a non-local’, beyond space and time, effect that is irreducible to reductive materialistic explanations. And as such, since Darwinian evolution is based on reductive materialistic premises, then Darwinian evolution is experimentally falsified as the scientific explanation for molecular biology.

    Moreover, I would also argue, along with Penrose and Hameroff, that this non-local quantum information provides physical evidence that is very suggestive for the existence of the ‘soul’:

    “Let’s say the heart stops beating. The blood stops flowing. The microtubules lose their quantum state. But the quantum information, which is in the microtubules, isn’t destroyed. It can’t be destroyed. It just distributes and dissipates to the universe at large. If a patient is resuscitated, revived, this quantum information can go back into the microtubules and the patient says, “I had a near death experience. I saw a white light. I saw a tunnel. I saw my dead relatives.,,” Now if they’re not revived and the patient dies, then it’s possible that this quantum information can exist outside the body. Perhaps indefinitely as a soul.”
    – Stuart Hameroff – Quantum Entangled Consciousness – Life After Death – video (5:00 minute mark)
    https://youtu.be/jjpEc98o_Oo?t=300

    LIFE AFTER DEATH: Shock claim of evidence showing consciousness may continue as a SOUL
    THE human conscious lives on after death, scientists have sensationally claimed. By Sean Martin – Sun, Nov 6, 2016
    Excerpt: Sir Roger states if a person temporarily dies, this quantum information is released from the microtubules and into the universe.
    However, if they are resuscitated the quantum information is channeled back into the microtubules and that is what sparks a near death experience.
    Sir Roger added: “If they’re not revived, and the patient dies, it’s possible that this quantum information can exist outside the body, perhaps indefinitely, as a soul.”
    http://www.express.co.uk/news/.....tinue-SOUL

    What Penrose and Hameroff are referring to is the fact that in quantum mechanics it is quantum information that is primarily conserved, and not necessarily energy and matter that are primarily conserved, as energy and matter are primarily conserved in classical mechanics: (November 2016)
    http://www.uncommondescent.com.....ent-620372

  160. 160
    wd400 says:

    “inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome” is exactly what TEs do.

    This is similar to the following “discussion”:

    X: IPhones arise by sheer dumb luck.

    Y: You must be mistaken, because an IPhone arising by sheer dumb luck would be a very unlikely event.

    X: Not at all. We see IPhones everywhere.

    I think if you reflect on this you’ll see there is really no relation between the two.

    To make it simpler — Hunter said to generate this mutation would require “inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome”. Well, we know that is happening all the time. TEs copy (or cut and paste) themselves into new positions in the genome all the time. Most of the time these new insertions have no effect, sometimes they create diseases and very rarely the mutation is advantageous.

  161. 161
    Origenes says:

    wd400: Hunter said to generate this mutation would require “inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome”.
    Well, we know that is happening all the time. TEs copy (or cut and paste) themselves into new positions in the genome all the time.
    Most of the time these new insertions have no effect, sometimes they create diseases and very rarely the mutation is advantageous.

    You are implying that these insertions are random, which would be consistent with your non-teleological Darwinian expectations.
    Dr. Hunter wrote in 2009:

    … new findings are now revealing more about how rice can rapidly adapt. In this case the smart adaptations were caused by transposable elements which are small segments of DNA that evolutionists thought inconveniently plopped themselves down in the genome whereever they happened to land. The transposable elements would help only rarely when a lucky insertion occurred.

    In post #122 Bornagain77 provides several references to studies which show that transposon insertion is not a random event.
    Dr. Hunter’s point is straightforward and simple: transposable elements increases the search space, and all you have done so far is ignore this irrefutable fact. Here it is again:

    … evolutionary theory requires that the needed random DNA mutational change is reasonably likely to occur. Given the moth’s effective population size, the moth’s generation time period, and the complexity of the mutation, the needed mutation is not likely to occur. Evolution would have to be inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome. This is an enormous space of mutational possibilities to search through.
    It doesn’t add up. Evolution does not have the resources in terms of time and effective population size to come anywhere close to searching this astronomical mutational space. It’s not going to happen.
    [Dr. Hunter]

    ——
    p.s. Dr.Hunter’s website darwinspredictions.com has been hacked.

  162. 162
    bornagain77 says:

    Origenes, darwinspredictions.com can now be accessed here:

    https://sites.google.com/site/darwinspredictions/home

  163. 163
    bornagain77 says:

    As to unexpected ‘non-random’ patterns, Sternberg has this article

    Discovering Signs in the Genome by Thinking Outside the BioLogos Box – Richard Sternberg – March 17, 2010
    Excerpt: The scale on the x-axis is the same as that of the previous graph–it is the same 110,000,000 genetic letters of rat chromosome 10. The scale on the y-axis is different, with the red line in this figure corresponding to the distribution of rat-specific SINEs in the rat genome (i.e., ID sequences). The green line in this figure, however, corresponds to the pattern of B1s, B2s, and B4s in the mouse genome….

    *The strongest correlation between mouse and rat genomes is SINE linear patterning.
    *Though these SINE families have no sequence similarities, their placements are conserved.
    *And they are concentrated in protein-coding genes.,,,

    ,,, instead of finding nothing but disorder along our chromosomes, we are finding instead a high degree of order.

    Is this an anomaly? No. As I’ll discuss later, we see a similar pattern when we compare the linear positioning of human Alus with mouse SINEs. Is there an explanation? Yes. But to discover it, you have to think outside the BioLogos box.
    http://www.evolutionnews.org/2.....32961.html

    Beginning to Decipher the SINE Signal – Richard Sternberg – March 18, 2010
    Excerpt: So for a pure neutralist model to account for the graphs we have seen, ~300,000 random mutation events in the mouse have to match, somehow, the ~300,000 random mutation events in the rat.
    What are the odds of that?
    http://www.evolutionnews.org/2.....32981.html

  164. 164
    Silver Asiatic says:

    wd400

    You can read up yourself, but as I said insertion is what TEs do. We don’t know enough about these moths to know the rate of insertion per generation, but in other species there can be multiple insertions per generation.

    The dispute here is whether this particular TE was a single, random insertion or whether it was triggered by some cue or is part of some other non-random process.

    From a paper BA77 quoted on TEs in plants:

    The results show that each family of elements is preferentially integrated in one specific fraction of its respective host genome. This demonstrates that the distribution of transposable elements in the nuclear genome of plants is not random but compartmentalized …

    So, there’s evidence of non-randomness here. Why not the same in the moth genome? Are you too quick to declare it a single random event without further analysis?

  165. 165
    wd400 says:

    SA,

    Well, as I’ve said many times, the fact this is a mutation that happened in one moth seems to rule out the idea it’s a programmed response. You can always invoke untestable =divine intervention or similar for this one mutation, but there’s not reason to think this one TE insertion was different than the millions of others.

    These other quotes turn on different meanings of “random”. We know from studies like these that some TEs preferentially insert into genomic regions with a hight proportion of “A”s and “T”s, or near a particular motif, or even into other copies of themselves. Combine that with selection removing from elements that insert into genes and get non-random patterns of TEs in the genome. But that doesn’t mean TE insertion is random with respect to fitness, which is the important point.

  166. 166
    PaV says:

    wd400:

    Well, as I’ve said many times, the fact this is a mutation that happened in one moth seems to rule out the idea it’s a programmed response. You can always invoke untestable =divine intervention or similar for this one mutation, but there’s not reason to think this one TE insertion was different than the millions of others.

    You don’t know that the ‘mutation’ happened in “one moth”: you’re presuming that based on your confidence in population genetics. And here, your confidence in pop gen is ‘linked’ to evidence from “linkage disequilibrium.” That is, the haplotypes they make reference to in the Naturearticle we are now discussing from June of this year, are what are identified and used when using linkage disequilibrium techniques.

    Yet, there is the example of the entire “Man Out of Africa” Theory—(modern man moved up from Africa about 200,000 ya, and then diversified. [We know this, BTW, because of the presence of a “bottleneck”. Remember our discussion about that years ago?]). This theory is based on linkage disequilibrium and, yet, just recently, a European human skull was found in a cave that dates to 700,000 ya.

    The ‘Petralona man’, or Archanthropus of Petralona, as it has since been called, was found to be 700,000 years old, making it the oldest human europeoid (presenting European traits) of that age ever discovered in Europe. Dr Poulianos’ research showed that the Petralona man evolved separately in Europe and was not an ancestor of a species that came out of Africa.

    Oops!!

    How many times have I said that you are way too confident of the techniques of pop gen.

    But, even granting that the date is right; and even granting that it was “one moth” that inserted the TE, you still have no way in the world to rule out whether this was brought about epigenetically or not. This reality is completely blind to the techniques you rely on. [Further, I proposed a mechanism above that involved random mutations, but a mechanism, nevertheless, that is part of the organism’s cellular “protocol.” Hence, the probabilities fall well outside that, let’s say, of random drift.]

    If you want to insist that linkage disequilibrium somehow assures you of this, then I would respond that our discussion on “bottlenecks” (where you never sufficiently responded to my critique that “bottlenecks” are blind because of the way they are defined, and that they could be hundreds of thousands of years off) and now the results of ‘linkage disequilibrium,’ or shall I say the known failure of the technique in terms of human ancestry, should give pause to anyone who takes it seriously.

    I was just looking at this article by Richard Sternberg at ENV about SINE’s, and their positioning between rats and mice. Guess what, the SINES on a particular chromosome line up. I think you would do well to read it.

  167. 167
    wd400 says:

    PaV,

    You don’t need much pop gen to understand the evidence for a single origin: why would the allele be so closely associated with a particular genetic background if it had been generated by multiple separate mutations?

    For the rest of this little survey of tangentially related factoids:

    Out of Africa refers to Homo sapiens even your alternative archeology site doesn’t claim this skull is from our species.

    I can’t find anything resembling meaning in this passage

    [Further, I proposed a mechanism above that involved random mutations, but a mechanism, nevertheless, that is part of the organism’s cellular “protocol.” Hence, the probabilities fall well outside that, let’s say, of random drift.]

    What “protocols”, who said anything about drift?

    I’ll read the ENV link, but it wouldn’t surprise me that there was coarse similarity in SINE insertion sites among mice and rats. SINEs tend to insert in GC rich sequences, and not into LINEs. If composition of the chromosomes are conserved you may well get SINEs inserting into the same windows in each genome.

  168. 168
    PaV says:

    wd400:

    You don’t need much pop gen to understand the evidence for a single origin: why would the allele be so closely associated with a particular genetic background if it had been generated by multiple separate mutations?

    Are you trying to tell me that if there were 10, or 20, or even thirty, with this new mutation, and they began to interbreed, that you could tell the difference in 2010?

    Hard to believe.

    But, again, you are blind to what the actual mechanism causing the insert was. That’s the whole point here. That’s why you’re wrong and I’m right; because all indications are that some internal “engineering” brought this about.

    Out of Africa refers to Homo sapiens even your alternative archeology site doesn’t claim this skull is from our species.

    Well, if the skull is from 700,000 years ago, then why would it be H.sapien? Here’s the problem you need to address: if homo sapiens came “out of africa” and then diversified, where did the “europeoid” features come from? I guess you could say that there was some kind of “human” (
    homo’) population in Europe that the Africa H. sapiens mixed with; but, if we know that H. erectus developed into H. sapiens in Africa, and you have a skull that is like H. erectus in Europe and is 700,000 years old, isn’t it entirely possible that it, too, developed into something similar to H. sapiens?

    I’ll add that I’ve looked around a little, and it seems that the aborigines in Australia have two haplotype clusters (not the 17 in Africa), and that there is good evidence that there is NO African haplotypes found among the Aborigines. So, here’s the question: are Aborigines H.sapiens, or not?

    Or, maybe, as I saw in one paper criticizing the OOA Theory: it’s a premise “based on a mixture of statistics and best guesses.”

    What “protocols”, who said anything about drift?

    Use a different word, if you prefer. James Shapiro talks about NGE; so, just think of the “protocol” as an internally guided, and regulated system that responds to environmental stimuli in a generic way, but that through some kind of a feedback system is able to use the cellular mechanisms at its disposal in a genetically targeted way. Just use your imagination. Darwin said that biologists of his day didn’t have enough imagination. Maybe it’s still true.

    As to “drift,” this was just shorthand for organismal mutation rates acting over the entire genome. I thought for sure you would understand the shorthand. You know: the standard ID argument for the implausibility of specific mutations. (The answer comes back: “Oh, but because of “random drift,” somewhere in the population the ‘mutation’ already exists.” You see, Darwinism is never wrong. It just can’t be.)

    SINEs tend to insert in GC rich sequences, and not into LINEs. If composition of the chromosomes are conserved you may well get SINEs inserting into the same windows in each genome.

    Sternberg points out that the positions have been “preserved.” So, you’re problem is explaining why the positions are “preserved” from rats to mice.

  169. 169
    wd400 says:

    God, what a load of rubbish.

    But, again, you are blind to what the actual mechanism causing the insert was. That’s the whole point here. That’s why you’re wrong and I’m right; because all indications are that some internal “engineering” brought this about.

    Can we have just one skerrick of evidence for this claim?

    but, if we know that H. erectus developed into H. sapiens in Africa, and you have a skull that is like H. erectus in Europe and is 700,000 years old, isn’t it entirely possible that it, too, developed into something similar to H. sapiens?

    This was literally the multiregional hypothesis that the evidence proved wrong (there have been Homo species out of Africa much longer than 7ka). So, no, it’s not very likely.

    I’ll add that I’ve looked around a little, and it seems that the aborigines in Australia have two haplotype clusters (not the 17 in Africa),

    This is a prediction of OOA, decreased diversity as you extend from the source population.

    and that there is good evidence that there is NO African haplotypes found among the Aborigines. So, here’s the question: are Aborigines H.sapiens, or not?

    They are. Why do you think the words before this would leave any doubt as to this?

    Use a different word, if you prefer. James Shapiro talks about NGE; so, just think of the “protocol” as an internally guided, and regulated system that responds to environmental stimuli in a generic way, but that through some kind of a feedback system is able to use the cellular mechanisms at its disposal in a genetically targeted way

    And do any of these protocols exist, outside of your (and prehaps James Shaprio’s) imagination?

    As to “drift,” this was just shorthand for organismal mutation rates acting over the entire genome.

    You used a term with a precise meaning to describe entirely different than that meaning? And you’re surprised I didn’t get what you were saying?

    Sternberg points out that the positions have been “preserved.” So, you’re problem is explaining why the positions are “preserved” from rats to mice.

    I’m not sure what you mean by preserved, but the paper only demonstrates that SINEs in mice and rats share broad (each point in those graphs represents 2 million base pairs) similarity in preferences for insertion sites, related to the fact they like GC rich sequences and LINEs occupy other regions.

  170. 170
    bornagain77 says:

    wd400 at 165 and elsewhere states:

    “random with respect to fitness”

    Just don’t ask for a precise, mathematically useful, quantification of ‘fitness’

    Fitness: A Battle is Raging
    The rigor of this approach, however, is lessened because there is as yet no universally agreed upon measure of fitness; fitness is either defined metaphorically, or defined only relative to the particular model or system used. It is fair to say that due to this lack, there is still no real agreement on what exactly the process of natural selection is. This is clearly a problem.
    http://telicthoughts.com/fitne.....#more-7550

    Although wd400 has used the weasel term ‘random with respect to fitness’ a few times in this thread, and elsewhere, to try to dodge the evidence that mutations are being directed in the genome, (such as this following evidence),,

    Rapid Evolution of Citrate Utilization by Escherichia coli by Direct Selection Requires citT and dctA. – Minnich – Feb. 2016
    The isolation of aerobic citrate-utilizing Escherichia coli (Cit(+)) in long-term evolution experiments (LTEE) has been termed a rare, innovative, presumptive speciation event. We hypothesized that direct selection would rapidly yield the same class of E. coli Cit(+) mutants and follow the same genetic trajectory: potentiation, actualization, and refinement. This hypothesis was tested,,,
    Potentiation/actualization mutations occurred within as few as 12 generations, and refinement mutations occurred within 100 generations.,,,
    E. coli cannot use citrate aerobically. Long-term evolution experiments (LTEE) performed by Blount et al. (Z. D. Blount, J. E. Barrick, C. J. Davidson, and R. E. Lenski, Nature 489:513-518, 2012, http://dx.doi.org/10.1038/nature11514 ) found a single aerobic, citrate-utilizing E. coli strain after 33,000 generations (15 years). This was interpreted as a speciation event. Here we show why it probably was not a speciation event. Using similar media, 46 independent citrate-utilizing mutants were isolated in as few as 12 to 100 generations. Genomic DNA sequencing revealed an amplification of the citT and dctA loci and DNA rearrangements to capture a promoter to express CitT, aerobically. These are members of the same class of mutations identified by the LTEE. We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved.
    http://www.ncbi.nlm.nih.gov/pubmed/26833416

    Michael Behe’s Quarterly Review of Biology Paper Critiques Richard Lenski’s E. Coli Evolution Experiments – December 2010
    Excerpt: After reviewing the results of Lenski’s research, Behe concludes that the observed adaptive mutations all entail either loss or modification–but not gain–of Functional Coding ElemenTs (FCTs)
    http://www.evolutionnews.org/2.....41221.html

    Evolution of an Irreducibly Complex System – Lenski’s E. Coli – Feb. 2015
    Conclusion:
    When viewed objectively, without the blinders of materialistic philosophy, Lenski’s experiments are strong evidence for, and a powerful vindication of, Behe’s arguments in particular, and the skeptics of Darwinism in general.
    At the end of the day, Lenski’s E. coli are just another in a long line of Darwinian claims that, upon closer inspection, fail to live up to their hype: from moth coloration to finch beaks to antibiotic resistance in bacteria. In each case, when these examples are carefully studied, instead of supporting the grander claims of the evolutionary creation story, they inadvertently demonstrate the pathetic impotence of Darwinian mechanisms and underscore the need for an alternative source of innovation in the history of life.
    http://www.uncommondescent.com.....ent-551158

    ,,, Although wd400 has used the weasel term ‘random with respect to fitness’ a few times in this thread to try to dodge the evidence presented to him that mutations are being directed in the genome, the fact of the matter is that random mutations are central to Darwinian thinking. Moreover, this randomness postulate of materialists, at least the way materialists use it, is indistinguishable from the Theist’s own appeal to a miracle.

    Evolution and the Illusion of Randomness – Talbott – Fall 2011
    Excerpt: The situation calls to mind a widely circulated cartoon by Sidney Harris, which shows two scientists in front of a blackboard on which a body of theory has been traced out with the usual tangle of symbols, arrows, equations, and so on. But there’s a gap in the reasoning at one point, filled by the words, “Then a miracle occurs.” And the one scientist is saying to the other, “I think you should be more explicit here in step two.”
    In the case of evolution, I picture Dennett and Dawkins filling the blackboard with their vivid descriptions of living, highly regulated, coordinated, integrated, and intensely meaningful biological processes, and then inserting a small, mysterious gap in the middle, along with the words, “Here something random occurs.”
    This “something random” looks every bit as wishful as the appeal to a miracle. It is the central miracle in a gospel of meaninglessness, a “Randomness of the gaps,” demanding an extraordinarily blind faith. At the very least, we have a right to ask, “Can you be a little more explicit here?”
    http://www.thenewatlantis.com/.....randomness

    Wolfgang Pauli comments on the shell game that Darwinists play with the word ‘chance’ here

    Pauli’s ideas on mind and matter in the context of contemporary science – Harald Atmanspacher
    Excerpt: “In discussions with biologists I met large difficulties when they apply the concept of ‘natural selection’ in a rather wide field, without being able to estimate the probability of the occurrence in a empirically given time of just those events, which have been important for the biological evolution. Treating the empirical time scale of the evolution theoretically as infinity they have then an easy game, apparently to avoid the concept of purposesiveness. While they pretend to stay in this way completely ‘scientific’ and ‘rational,’ they become actually very irrational, particularly because they use the word ‘chance’, not any longer combined with estimations of a mathematically defined probability, in its application to very rare single events more or less synonymous with the old word ‘miracle.’”
    Wolfgang Pauli (pp. 27-28)
    http://www.igpp.de/english/tda/pdf/paulijcs8.pdf

    Robert C. Sproul points out: “By calling the unknown cause ‘chance’ for so long, people begin to forget that a substitution was made. . . . The assumption that ‘chance equals an unknown cause’ has come to mean for many that ‘chance equals cause.’”

    The Universal Determinism Dichotomy (UDD) – David L. Abel – 2015
    Excerpt: We sometimes appeal to yet-to-be-discovered laws when trying to explain what appears to be chance phenomena. Most theorists, however, attempt to reduce Chance Contingency to unknown and/or very complex physical causation, as summarized by Peale.12 Thus Chance Contingency as a true cause may be only “apparent.”
    Sproul argues effectively that chance is not a cause of anything. Chance is nothing more than a statistical description of unknown or complex physical causation. Chance, therefore, cannot have any physical effects, since it is not a physical cause. 13,,,
    13. Sproul RC. – Not a Chance: the Myth of Chance in Modern Science and Cosmology. Grand Rapids, MI: Baker Books; 1994
    https://www.academia.edu/12267097/The_Universal_Determinism_Dichotomy_UDD_

    Thus to say a mutation “happened randomly by chance’, as it is usually used by Darwinists, is in reality a ‘placeholder for ignorance’ instead of being an appeal to a known cause.
    Thus, when an atheist states that something happened by chance, we have every right to ask, as Talbott pointed out, “Can you be a little more explicit here?”

    Nobel laureate Jacques L. Monod, for one, used this chance-equals-cause line of reasoning.

    “Pure chance, absolutely free but blind, [is] at the very root of the stupendous edifice of evolution,” Monod wrote. “Man knows at last that he is alone in the universe’s unfeeling immensity, out of which he emerged only by chance.”

    ‘By chance’ Monod does what many other materialists do—he elevates chance to a creative principle that is indistinguishable from the Theist’s own appeal to a miracle. Chance, as it is used by materialists, is, in fact, offered as a ‘God substitute’ by materialists as the ‘uncaused cause’ by which the universe and by which all life on earth came to be.

    Moreover, if we try be ‘a little more explicit here’ as Talbott stated, then we find that the ‘randomness postulate’ of materialists falls apart upon closer examination.

  171. 171
    bornagain77 says:

    It is interesting to note that if one wants to build a better random number generator for a computer program then a better source of entropy is required to be found to drive the increased randomness:

    Cryptographically secure pseudorandom number generator
    Excerpt: From an information theoretic point of view, the amount of randomness, the entropy that can be generated is equal to the entropy provided by the system. But sometimes, in practical situations, more random numbers are needed than there is entropy available.
    http://en.wikipedia.org/wiki/C....._generator

    Yet there are two major problems, for the materialist, with entropy being found to be the primary source of randomness in the universe.

    The first problem is that Entropy is the most finely tuned initial condition of the universe, and Entropy is also governed by a constant.

    The Physics of the Small and Large: What is the Bridge Between Them? Roger Penrose
    Excerpt: “The time-asymmetry is fundamentally connected to with the Second Law of Thermodynamics: indeed, the extraordinarily special nature (to a greater precision than about 1 in 10^10^123, in terms of phase-space volume) can be identified as the “source” of the Second Law (Entropy).”
    http://irafs.org/irafs_1/cd_ir.....enrose.pdf

    Bruce Gordon, PhD math, discusses the initial entropy of the universe in this following video
    The Multiverse confirms the Ontological Argument for God
    https://www.youtube.com/watch?v=MgDn_k11ups&t=12s

    The Austrian physicist Ludwig Boltzmann first linked entropy and probability in 1877. However, the equation as shown, involving a specific constant, was first written down by Max Planck, the father of quantum mechanics in 1900. In his 1918 Nobel Prize lecture, Planck said: This constant is often referred to as Boltzmann’s constant, although, to my knowledge, Boltzmann himself never introduced it – a peculiar state of affairs, which can be explained by the fact that Boltzmann, as appears from his occasional utterances, never gave thought to the possibility of carrying out an exact measurement of the constant. Nothing can better illustrate the positive and hectic pace of progress which the art of experimenters has made over the past twenty years, than the fact that since that time, not only one, but a great number of methods have been discovered for measuring the mass of a molecule with practically the same accuracy as that attained for a planet.
    http://www.daviddarling.info/e.....ation.html

    Thus the randomness inherent in the Entropy of the universe is actually proof for Theism and is not proof for Atheism, as the materialist apparently falsely believes in his appeal to randomness.

    The second major problem, for the materialist, is that Entropy, i.e. the universal tendency of things to decay towards disorder, almost directly contradicts the claims of Darwinists that increases in functional complexity/information/order can easily be had. IOW, not only does Evolution not have any known universal law to appeal to, as other overarching theories of science have, the second law of thermodynamics, i.e. Entropy, a law with great mathematical explanatory power in science, almost directly contradicts Darwinian claims that increases in functional complexity/information can be easily had:

    Why Tornados Running Backward do not Violate the Second Law – Granville Sewell – May 2012 – article with video
    Excerpt: So, how does the spontaneous rearrangement of matter on a rocky, barren, planet into human brains and spaceships and jet airplanes and nuclear power plants and libraries full of science texts and novels, and supercomputers running partial differential equation solving software , represent a less obvious or less spectacular violation of the second law—or at least of the fundamental natural principle behind this law—than tornados turning rubble into houses and cars? Can anyone even imagine a more spectacular violation?
    http://www.uncommondescent.com.....econd-law/

    “Gain in entropy always means loss of information, and nothing more.”
    Gilbert Newton Lewis – preeminent Chemist of the first half of last century

    Thus, the materialist’s appeal to ‘uncaused randomness’ to try to get around Theism backfires on the materialist since, number 1, Entropy, i.e. the source for randomness in the universe, is proof for Theism not atheism, and 2, the type of ‘decaying randomness’ inherent in Entropy is completely antithetical to the claims of Darwinists that increasing complexity and order are supposedly easy to achieve:

    Verse and quote:

    Psalm 102:25-27
    Of old You laid the foundation of the earth, And the heavens are the work of Your hands. They will perish, but You will endure; Yes, they will all grow old like a garment; Like a cloak You will change them, And they will be changed. But You are the same, And Your years will have no end.

    “We have the sober scientific certainty that the heavens and earth shall ‘wax old as doth a garment’….
    Dark indeed would be the prospects of the human race if unilluminated by that light which reveals ‘new heavens and a new earth.’”
    Sir William Thomson, Lord Kelvin (1824 – 1907) – pioneer in many different fields, particularly electromagnetism and thermodynamics.

  172. 172
    Silver Asiatic says:

    wd

    Well, as I’ve said many times, the fact this is a mutation that happened in one moth seems to rule out the idea it’s a programmed response. You can always invoke untestable =divine intervention or similar for this one mutation, but there’s not reason to think this one TE insertion was different than the millions of others.

    Well, patterns within the moth genome could have been shaped, simultaneously by insertion events like this. We don’t know what the mutation rate is or how to model the range of variation we could expect with the number of different sized segments that could be copy/inserted, and the effects they could have. We don’t know how improbable this particular advantageous mutation was. But it remains true that we don’t know what influenced the mutation (if anything), even if it was a single event.

    We know from studies like these that some TEs preferentially insert into genomic regions with a hight proportion of “A”s and “T”s, or near a particular motif, or even into other copies of themselves. Combine that with selection removing from elements that insert into genes and get non-random patterns of TEs in the genome.

    That’s another area for study and it could be that mutational-biases like this are caused more directly by environmental factors which trigger a clustering of TEs or affect the mutation rate itself. Ok, I don’t think we can tie any of that back to this particular study (for one reason, the authors didn’t explore it), but I find this to be a much more open question. An ‘edited’, complex segment of code spliced into a non-coding region, which ultimately drove the morphological variation is a lot more difficult to explain, in probabilistic terms, than a simple point mutation in the coding region.
    Also, how do we know these events are random with regards to fitness and not, rather, a response of the organism to fitness pressures (and as some claim, the organism adjusts its own DNA in response)?

  173. 173
    bornagain77 says:

    In another thread wd400 wrote:

    “Since fitness is that thing that matters in evolution, that’s something to measure.”
    – wd400
    http://www.uncommondescent.com.....ent-518518

    And yet, as we saw in post 170, there is no universally agreed upon measure of fitness:

    Fitness: A Battle is Raging
    The rigor of this approach, however, is lessened because there is as yet no universally agreed upon measure of fitness; fitness is either defined metaphorically, or defined only relative to the particular model or system used. It is fair to say that due to this lack, there is still no real agreement on what exactly the process of natural selection is. This is clearly a problem.
    http://www.uncommondescent.com.....r-fitness/

    The fact that fitness cannot be accurately measured in any meaningful sense, and therefore rigorously quantified as mathematical a law of nature, is made self-evident by the following:

    Op-Ed: Time to Ditch Natural Selection? – Oct. 3, 2015
    Excerpt: If NS were a law of nature, we would see every organism trending along the same trajectory: for instance, bearing more offspring. But NS explains opposite outcomes with equal ease (see Oct 1 entry for examples). It explains why the sloth is slow and the cheetah is fast. It explains why the roundworm is round and the flatworm is flat. It explains why some animals bear lots of young and why some bear few. We are led to believe that NS explains up, down, in, out and sideways by some mysterious, aimless force, and whatever results was caused by NS.,,,
    In journal papers, you can find neo-Darwinians measuring coefficients of selection and using them in differential equations. They speak of positive selection, negative selection, balancing selection, purifying selection, and epigenetic selection. In my experience, this is all hand-waving. It is jargon masquerading as science.,,
    read more here:
    http://crev.info/2015/10/op-ed.....selection/

    Moreover, even though ‘fitness’ figures centrally in the equations of population genetics, ‘fitness’ actually falsifies Darwinian evolution as a scientific theory. Specifically, in the following video and article, Donald Hoffman has, through numerous computer simulations of population genetics, in which ‘fitness’ figured centrally in the equations, proved that if Darwinian evolution were actually true then ALL of our perceptions of reality would be illusory.

    Donald Hoffman: Do we see reality as it is? – Video – 9:59 minute mark
    Quote: “,,,evolution is a mathematically precise theory. We can use the equations of evolution to check this out. We can have various organisms in artificial worlds compete and see which survive and which thrive, which sensory systems or more fit. A key notion in those equations is fitness.,,, fitness does depend on reality as it is, yes.,,, Fitness is not the same thing as reality as it is, and it is fitness, and not reality as it is, that figures centrally in the equations of evolution. So, in my lab, we have run hundreds of thousands of evolutionary game simulations with lots of different randomly chosen worlds and organisms that compete for resources in those worlds. Some of the organisms see all of the reality. Others see just part of the reality. And some see none of the reality. Only fitness. Who wins? Well I hate to break it to you but perception of reality goes extinct. In almost every simulation, organisms that see none of reality, but are just tuned to fitness, drive to extinction that perceive reality as it is. So the bottom line is, evolution does not favor veridical, or accurate perceptions. Those (accurate) perceptions of reality go extinct. Now this is a bit stunning. How can it be that not seeing the world accurately gives us a survival advantage?”
    https://youtu.be/oYp5XuGYqqY?t=601

    The Evolutionary Argument Against Reality – April 2016
    The cognitive scientist Donald Hoffman uses evolutionary game theory to show that our perceptions of an independent reality must be illusions.
    Excerpt: “The classic argument is that those of our ancestors who saw more accurately had a competitive advantage over those who saw less accurately and thus were more likely to pass on their genes that coded for those more accurate perceptions, so after thousands of generations we can be quite confident that we’re the offspring of those who saw accurately, and so we see accurately. That sounds very plausible. But I think it is utterly false. It misunderstands the fundamental fact about evolution, which is that it’s about fitness functions — mathematical functions that describe how well a given strategy achieves the goals of survival and reproduction. The mathematical physicist Chetan Prakash proved a theorem that I devised that says: According to evolution by natural selection, an organism that sees reality as it is will never be more fit than an organism of equal complexity that sees none of reality but is just tuned to fitness. Never.”
    https://www.quantamagazine.org/20160421-the-evolutionary-argument-against-reality/

    Although Hoffman tried to limit his results to just our visual perceptions, as Plantinga had pointed out years before Hoffman came along, there is no reason why the results do not also extend to undermining our cognitive faculties as well:

    The Case Against Reality – May 13, 2016
    Excerpt: Hoffman seems to come to a conclusion similar to the one Alvin Plantinga argues in ch. 10 of Where the Conflict Really Lies: we should not expect — in the absence of further argument — that creatures formed by a naturalistic evolutionary process would have veridical perceptions.,,,
    First, even if Hoffman’s argument were restricted to visual perception, and not to our cognitive faculties more generally (e.g., memory, introspection, a priori rational insight, testimonial belief, inferential reasoning, etc.), the conclusion that our visual perceptions would be wholly unreliable given natural selection would be sufficient for Plantinga’s conclusion of self-defeat. After all, reliance upon the veridicality of our visual perceptions was and always will be crucial for any scientific argument for the truth of evolution. So if these perceptions cannot be trusted, we have little reason to think evolutionary theory is true.
    Second, it’s not clear that Hoffman’s application of evolutionary game theory is only specially applicable to visual perception, rather than being relevant for our cognitive faculties generally. If “we find that veridical perceptions can be driven to extinction by non-veridical strategies that are tuned to utility rather than objective reality” (2010, p. 504, my emphasis), then why wouldn’t veridical cognitive faculties (more generally) be driven to extinction by non-veridical strategies that are tuned to utility rather than objective reality? After all, evolutionary theory purports to be the true account of the formation of all of our cognitive faculties, not just our faculty of visual perception. If evolutionary game theory proves that “true perception generally goes extinct” when “animals that perceive the truth compete with others that sacrifice truth for speed and energy-efficiency” (2008), why wouldn’t there be a similar sacrifice with respect to other cognitive faculties? In fact, Hoffman regards the following theorem as now proven: “According to evolution by natural selection, an organism that sees reality as it is will never be more fit than an organism of equal complexity that sees none of reality but is just tuned to fitness” (Atlantic interview). But then wouldn’t it also be the case that an organism that cognizes reality as it is will never be more fit than an organism of equal complexity that cognizes none of reality but is just tuned to fitness? On the evolutionary story, every cognitive faculty we have was produced by a process that was tuned to fitness (rather than tuned to some other value, such as truth).
    http://www.gregwelty.com/2016/.....t-reality/

    Thus, in what should be needless to say, a worldview that undermines the scientific method itself by holding all our observations of reality, and cognitive faculties, are illusory is NOT a worldview that can be firmly grounded within the scientific method!

    Steps of the Scientific Method
    Observation/Research
    Hypothesis
    Prediction
    Experimentation
    Conclusion
    http://www.sciencemadesimple.c.....ethod.html

    Moreover, completely contrary to what Hoffman found for Darwinian theory, it turns out that accurate perception, i.e. conscious observation, of reality, far from being unreliable and illusory, is experimentally found to be far more integral to reality, i.e. far more reliable of reality, than the math of population genetics predicted. In fact, in the following experiment it was found that reality doesn’t exist without an observer.

    New Mind-blowing Experiment Confirms That Reality Doesn’t Exist If You Are Not Looking at It – June 3, 2015
    Excerpt: The results of the Australian scientists’ experiment, which were published in the journal Nature Physics, show that this choice is determined by the way the object is measured, which is in accordance with what quantum theory predicts.
    “It proves that measurement is everything. At the quantum level, reality does not exist if you are not looking at it,” said lead researcher Dr. Andrew Truscott in a press release.,,,
    “The atoms did not travel from A to B. It was only when they were measured at the end of the journey that their wave-like or particle-like behavior was brought into existence,” he said.
    Thus, this experiment adds to the validity of the quantum theory and provides new evidence to the idea that reality doesn’t exist without an observer.
    http://themindunleashed.org/20.....at-it.html

    Apparently science itself could care less if atheists are forced to believe, because of the mathematics of population genetics, that their observations of reality, and cognitive faculties, are illusory!

    Verse:

    2 Peter 1:16
    For we have not followed cunningly devised fables, when we made known unto you the power and coming of our Lord Jesus Christ, but were eyewitnesses of his majesty.

  174. 174
    PaV says:

    As I begin my response to your screed, let me remind you that the reason this thread has been raised from the dead is because newly analyzed sequences of Biston betularia, both typica and carboneria, show that it is not a “point mutation” but an TE insert into an ‘intron’ that differentiates the two forms.

    I stated that this proves me right, and you wrong. Further, I said that if you didn’t admit you were wrong here, you would never admit you were wrong—and, along with you, your fellow evolutionary biologists.
    All of this only shows that Darwinism is “unfalsifiable” since nothing—no evidence whatsoever—will get you to reconsider the assertions the theory makes.

    God, what a load of rubbish.

    Just to make sure: you’re not describing evolutionary biology, are you? What you try to convince me and others of is just that: rubbish.

    But, again, you are blind to what the actual mechanism causing the insert was. That’s the whole point here. That’s why you’re wrong and I’m right; because all indications are that some internal “engineering” brought this about.

    Can we have just one skerrick of evidence for this claim?

    This is rich. Is it your claim that, just by chance, a 22,000 nucleotide sequence decided to insert itself, not in an exon—which would mean a protein is modified, but into an “intron,” which will be excised and to evolutionary biologists is no more than “junk DNA.” [That is, termed “junk” until such time that experiments demonstrate that ‘introns’ actually have functions, and play a role in regulation of proteins. Then, you say, well we knew all along that it had some role in regulation. Well, why did you call it junk, then?]

    All of this happened by chance, you say? Well, give me “one skerrick” of evidence for this claim?

    Actually, your claim is rubbish. The probablilities are plain against such a thing happening by accident. My claim at least makes some sense. But isn’t that how science is supposed to work? Theory says one thing; something is discovered that makes one question what the theory says, and then a new view of things is conjectured, and then tested. Just like Barbara McClintock did.

    From the 2014 paper in Chromosoma, “Transposons, environmental changes, and heritable induced phenotypic variability”:

    [From the introduction]That data demonstrated that Hsp90 is involved in repression of transposon activity by playing a significant role in piwi-interacting RNA (piRNAs)-dependent RNA interference (RNAi) silencing. The important implication is that the fixed phenotypic abnormalities observed in Hsp90 mutants are probably related to de novo induced mutations by transposon activation. In this case, Hsp90 could be considered as a mutator. . . .
    [Further down]
    In other words, evolution is gradual but does not progress at a constant speed. This inconstant speed could be due, at least in part, to the activity of transposons that would act as evolutionary accelerators in the presence of environmental changes. . . .
    [From the conclusion]
    Environmental changes, in their ability to induce transposon activation, could be formally considered as both hypermutators and selectors at the same time, leading to an acceleration of the evolutionary process. On the other hand, transposons can be viewed as a trigger of the speciation process through the production of variability and reproductive isolation of new species. This suggests an effective process for rapid evolutionary change and makes it clear why transposons and host genomes, although biological antinomies, have coevolved mechanisms that regulate transposition and mutational outcomes under environmental stress and optimize reciprocal survival in normal environmental conditions. The defense mechanisms and their alterations allow mutual survival of host and mobile elements.

    Rubbish, you say?

    but, if we know that H. erectus developed into H. sapiens in Africa, and you have a skull that is like H. erectus in Europe and is 700,000 years old, isn’t it entirely possible that it, too, developed into something similar to H. sapiens?

    This was literally the multiregional hypothesis that the evidence proved wrong (there have been Homo species out of Africa much longer than 7ka). So, no, it’s not very likely.

    And my contention is that your faith in pop. gen. methods is too firm.

    From the original article I linked to above, I cite the paragraph you were referring to in rebuttal:

    Today, most academics who have analyzed the Petralona remains say that the cranium of the Archanthropus of Petralona belongs to an archaic hominid distinguished from Homo erectus, and from both the classic Neanderthals and anatomically modern humans, but showing characterists of all those species and presenting strong European traits. A skull dating back 700,000 which is either Homo sapien or part Homo sapien is in direct conflict with the Out of Africa theory of human evolution.

    It’s either “Homo sapien or part Homo sapien”: that is, it has modern European characteristics. The ‘find’ was denounced, of course.
    And from a website on “Out of Africa” theories and such:

    Out of Asia Theory
    Some scientists have theorized that an early hominid such as homo habilis left Africa two million years ago and moved into Asia, where it evolved into Homo erectus then spread to Europe and back to Africa. This theory is based on the fact that the Homo erectus specimens found in Asia are older than those found in Africa.

    Evidence for this theory includes extraordinarily old dates for Homo species that appeared in Indonesia and China just as Homo erectus was emerging in Africa. Berkeley’s Carl Swisher told Time magazine that “elephants left Africa several times during their history” and “lots of animals expand their ranges. the main factor may have been an environmental change that made the expansion easier. No other animals needed stone tools to get out of Africa.” [Source: Michael Lemonick, Time, March 14, 1994]
    One primatologist told National Geographic: “The idea that all hominids originated in Africa is a myth created by people working in Africa. Sure, they’ve found a lot there, but if we’d invested that much time and money in Asia we would find fossil hominids just as old there too.”
    Homo erectus tools have been found in Africa and Europe but not in Asia. Scientists say that the reason for this is that they may have used equally effective bamboo tools— instead of stone ones—that decay and leave behind no evidence.

    A “myth.” Yes, but buttressed by linkage disequilibrium!

    And I love that final piece: “bamboo tools . . . that decay and leave behind no evidence.”
    That’s evolution for you: an explanation for what we see, based on what we don’t see. Wonderful! What better science could there be?

    I’ll add that I’ve looked around a little, and it seems that the aborigines in Australia have two haplotype clusters (not the 17 in Africa),

    This is a prediction of OOA, decreased diversity as you extend from the source population.

    Ahah! A prediction! But did it “predict” than no haplotypes whatsoever would be found? Diversity is one thing; absence another.

    and that there is good evidence that there is NO African haplotypes found among the Aborigines. So, here’s the question: are Aborigines H.sapiens, or not?

    They are. Why do you think the words before this would leave any doubt as to this?

    Homo sapiens, per the OOA theory, arose in Africa and then spread. How do you explain the absence of any genetic link to Africa? This seems to bother other scientists.

    Use a different word, if you prefer. James Shapiro talks about NGE; so, just think of the “protocol” as an internally guided, and regulated system that responds to environmental stimuli in a generic way, but that through some kind of a feedback system is able to use the cellular mechanisms at its disposal in a genetically targeted way

    And do any of these protocols exist, outside of your (and prehaps James Shaprio’s) imagination?

    Unfortunately, you have little of it.

    As to “drift,” this was just shorthand for organismal mutation rates acting over the entire genome.

    You used a term with a precise meaning to describe entirely different than that meaning? And you’re surprised I didn’t get what you were saying?

    Why would you think I was literally talking about “random drift.” Had I brought it up before?

    Now, your response to this would predictably be: “Well, that’s precisely it. You hadn’t brought it up. How was I to understand what you meant?”

    To which I reply: I was speaking of the probabilities of ”random drift.” Why? Because, in the absence of selection, the probabilities affecting sequences in general are those of random drift. And how can selection work on something that hasn’t arisen yet? Hence, we’re basically dealing with the same prohibitive improbabilities in both cases. Most of us, here at UD, pick up on these things quite easily.

    but the paper only demonstrates that SINEs in mice and rats share broad (each point in those graphs represents 2 million base pairs) similarity in preferences for insertion sites, related to the fact they like GC rich sequences and LINEs occupy other regions.

    Do you not see that you are making a circular argument. The fact that GC rich sequences have conserved positions is what needs explaining. It’s not the answer; it’s the question.

  175. 175
    wd400 says:

    PaV,

    I don’t have time to focus on all of your confused ramblings. So, very briefly…

    You did indeed claim that the fact this is a TE insertion “proved you right”. You have yet to demonstrate why that would be the case. All I said from the start that this was a simple Mendelian trait that arose by mutation then spread rapidly through the population. This is precisely what is seen in the paper.

    If you want to argue that TE insertion is non-random you’ll need some evidence. If you read about TEs you’ll see they are inserting themselves all the time, mostly with no effect sometimes creating diseases very rarely being adaptive. You can claim all those adaptive ones are programmed, but there is no reason to imagine this is the case. Even HSP example doesn’t generate adaptive mutations at a greater rate.

    And then you still have the problem that this mutation happened once. What kind of programmed response happens in one of the thousands upon thousands of moths that were subjected to the same stimulus.

    You are just wrong about to claim that Aboriginal Australians have no genetic link to African populations. I don’t know where you got this idea.

    I guess I thought you were literally talking about “random drift” because you said “random drift”. I don’t think that’s an unreasonable assumption.

    Finally, the GC rich regions don’t have conserved positions in rat and mouse. They graph is made by aligning chunks of the rat genome with the mouse chromosome.

    You are welcome to google up some more links, misunderstand them, and write a confused rant about them. But I don’t think I’ll be replying any more.

  176. 176
    bornagain77 says:

    Of related note to 173 in regards to ‘fitness’:

    Prehoda’s Goof: Mutational Fitness Effects Cannot Be Predicted – November 28, 2016
    Excerpt: The new PNAS paper by Bank et al., “On the (un)predictability of a large intragenic fitness landscape,” takes a serious look at the effects of mutational interactions.,,,
    The point of the study is that epistatic interactions are profoundly unpredictable. By performing one of the largest-ever surveys of epistasis on engineered mutations to Hsp90, a well-known protein, they concluded that it is extremely difficult to predict what will happen.,,,their conclusion has far-reaching implications for all evolutionary predictions,,,,
    “our results highlight the inherent difficulty imposed by the duality of epistasis for predicting evolution. In the absence of epistasis (i.e., in a purely additive landscape), evolution is globally highly predictable because the population will eventually reach the single-fitness optimum, but the path taken is locally entirely unpredictable. Conversely, in the presence of (sign and reciprocal sign) epistasis evolution is globally unpredictable,”
    http://www.evolutionnews.org/2.....03316.html

  177. 177
    bornagain77 says:

    Of Note: Dr Hunter has posted his article on ENV:

    Peppered Moth: How Evolution’s Poster Child Became the Rebuttal – Cornelius Hunter November 27, 2016
    Excerpt:,,, The mutating of the protein sequence was the whole idea behind evolution: DNA mutations which lead to changes in a protein can lead to a phenotype change with fitness improvement, and there would be subject to natural selection.
    That is not what we are seeing in the much celebrated peppered moth example. The DNA mutation is much more complicated (~20,000 nucleotides inserted), and the fact it was inserted into an intron suggests that additional molecular and cellular mechanisms are required for the coloration change to occur.
    None of this fits evolutionary theory.
    http://www.evolutionnews.org/2.....03315.html

  178. 178
    Silver Asiatic says:

    wd’s comment @ 86:

    No one has ever claimed that that the peppered moths explained “wholesale changes in body-types” – just that they form a nice example of adaptation in a changing environment.

    and PaV’s excellent response @88 – answered a big question for me in this debate.

    We don’t even have to talk about epigenetics or the non-randomness of transposable elements (as appropriate as it may be). In fact, it might actually help wd’s argument if the insertion was driven by epigenetic triggers, because without that we have, in wd’s words: “Most of the time these new insertions have no effect, sometimes they create diseases and very rarely the mutation is advantageous.”

    This particular insertion of a 22,000 nucleotide sequence has to qualify as the “very rarely” kind. What if it was only 19,000 nucleotides? Or what if 25,000? Or any other size more or less? What if it was inserted in a slighly different location? It just happens that one conferred an advantage. What kind of probability analysis is (or could be) done on this?

    But anyway, ok, conceding that it just happened that way, we’re still not at the real issue here. We’ve got a ‘very rarely’ complex insertion … and after an incredibly improbable event, what fitness benefit did it confer? Again, as wd explains: “just that they form a nice example of adaptation”.

    That’s it. A slight increase melanin – some darker pigmentation in the wing.

    If that was the end of this evolutionary story, probably most of us would walk away bored and uninterested.

    But that’s not it. That kind of rare insertion, for a change of color in the wings, and at the same time:

    PaV: The peppered moth is THE ICON of evolution. And evolution is supposed to tell us how bacteria became humans.

    Bacteria to humans.

    It’s easy to forget that’s actually what they’re claiming. And the peppered moth is evidence for it.

  179. 179
    wd400 says:

    This particular insertion of a 22,000 nucleotide sequence has to qualify as the “very rarely” kind. What if it was only 19,000 nucleotides? Or what if 25,000? Or any other size more or less? What if it was inserted in a slighly different location?

    Indeed. Do you know if any of these scenarios would produce the same phenotype, or are you just guessing?

  180. 180
    Silver Asiatic says:

    wd400

    Do you know if any of these scenarios would produce the same phenotype, or are you just guessing?

    Two of the scenarios I proposed are these:

    “… any other size more or less?”

    and

    “… slightly different location”

    I could have said actually:

    “… any different location”

    When we combine those two variables, we’d have all possible sizes (one to a million?) and all possible locations (unknown huge number). I forgot to add a third variable, not only length but specification of sequence, but anyway.

    No, I haven’t tested all of those yet. But I’d think that would be the task for the evolutionist. We saw nothing about it in the paper.

    And what if that particular insertion was the only possible scenario that produced the same phenotype?

    We’d have a one in a trillion, trillion chance or something like that. I’m underestimating. Maybe it’s 1 in 10^50 chance or much more?

    Would that cause you some concern? Would you lose confidence in evolutionary claims? Bacteria to humans. And it took a one in 10^50 mutation just to change pigment on a moths wing.

    I would hope you’d start questioning the theory at that point. I certainly would.

  181. 181
    bornagain77 says:

    SA, apparently ‘evolution is undeniably true’ is the axiom that Darwinists start out with in their theory. The truthfulness of Darwinian evolution is not a conclusion that they have reached by experiment. The truthfulness of evolution is simply never questioned by Darwinists:

    Response to John Wise – October 2010
    Excerpt: A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.
    http://www.evolutionnews.org/2.....38811.html

    “One century of studies on mutations has not provided a single verified example of a gene mutation that led to adaptive morphological change in metazoans.
    (Cabej 2012)

    Mutation + Selection = Stasis – October 8th, 2014
    Excerpt: As a trained physicist, Desai applied a statistical perspective using robots to precisely manipulate hundreds of lines of yeast to perform large scale evolutionary experiments. Scientists have long studied genetic evolution of microbes, but until now, only a few strains at a time.
    Robotically managing 640 lines of yeast from a single parent cell, Desai’s team was efficiently tooled to statistically analyze evolution at this level for the first time.
    In an interview with Singer, Joshua Plotkin, an evolutionary scientist at the University of Pennsylvania, commented, “This is the physicist’s approach to evolution, stripping down everything to the simplest possible conditions… They could partition how much of evolution is attributable to chance, how much to the starting point, and how much to measurement noise.”,,,
    While early mutations in the experiment initially variably influenced fitness, fitness in the final generations was the same. “Scientists,” Singer noted, “don’t know why all genetic roads in yeast seem to arrive at the same endpoint”.,,,,
    “I think many people think about one gene for one trait, a deterministic way of evolution solving problems,” David Reznick, a biologist at the University of California-Riverside, told Singer. “This says that’s not true.”
    Unexpectantly, Desai’s team discovered genetic mutations plus selection yields stasis in the microbe model– not evolution.
    http://www.darwinthenandnow.co.....on-stasis/

    Peer-Reviewed Research Paper on Plant Biology Favorably Cites Intelligent Design and Challenges Darwinian Evolution – Casey Luskin December 29, 2010
    Excerpt: Many of these researchers also raise the question (among others), why — even after inducing literally billions of induced mutations and (further) chromosome rearrangements — all the important mutation breeding programs have come to an end in the Western World instead of eliciting a revolution in plant breeding, either by successive rounds of selective “micromutations” (cumulative selection in the sense of the modern synthesis), or by “larger mutations” … and why the law of recurrent variation is endlessly corroborated by the almost infinite repetition of the spectra of mutant phenotypes in each and any new extensive mutagenesis experiment instead of regularly producing a range of new systematic species…
    (Wolf-Ekkehard Lönnig, “Mutagenesis in Physalis pubescens L. ssp. floridana: Some Further Research on Dollo’s Law and the Law of Recurrent Variation,” Floriculture and Ornamental Biotechnology Vol. 4 (Special Issue 1): 1-21 (December 2010).)
    http://www.evolutionnews.org/2.....42191.html
    Dr. Wolf-Ekkehard Lönnig, (retired) Senior Scientist (Biology), Max Planck Institute for Plant Breeding Research, Emeritus, Cologne, Germany.

  182. 182
    PaV says:

    wd400:

    When you say something like this:

    All I said from the start that this was a simple Mendelian trait that arose by mutation then spread rapidly through the population. This is precisely what is seen in the paper

    —you’re basically saying almost nothing. I guess you don’t see that.

    Either something is transmitted via epigenetics, or, as has been shown recently, absolutely transmitted outside of nuclear DNA, or, it is inherited via nuclear DNA in Mendelian fashion.

    We’re just finding out about these other ways of passing on cellular information.

    But, if something happens within an organism, and it affects nuclear DNA, or mt-DNA, for that matter, and is inherited in the traditional manner, then, according to your position, this is Darwinian—plain and simple. Well, this covers almost everything. It leaves out little. And so, it says almost nothing. How, is this informative?

    Mendelian genetics has been known for over a hundred years. No one disputes this. What evolutionary biologists need to demonstrate is that the mechanisms by which “mutations” (another ‘catch-all’ term among so many others) occur in organisms, occur in such a way as to bring about large scale changes; and, to demonstrate, as well, that these mutations are, indeed, ‘random.’

    You need a lot more than: “If something happens in an organism, and it’s inherited, this proves Darwin was right, and that neo-Darwinian analysis is cogent.”

    To equate a TE in the midst of an intron with a SNP–and you do this, since you don’t make a distinction[cf. the blocked out quote above]—is an incredible position to take. That’s why this thread has been revived. This is NOT the kind of mutation you, or any other evol. biol., had in mind. You just need to admit this.

    But, you won’t budge. Fine. The dust-heap of history awaits.

    Even HSP example doesn’t generate adaptive mutations at a greater rate.

    This comment flies in the face of the article I cited. I just don’t understand your statement.

    +++++++++++++++++++

    You know, one time, when I was working as an engineer, and we were logging an oil well in Beverly Hills, the logging runs kept stopping. This happened a few times. It was a brand new type of log, and it was very costly time wise and otherwise.

    Now, I found myself in the midst of the logging experts, who had used this logging machine many times before. It was their logging truck we were sitting in. I noticed that it was about the same amount of elapsed time each time before the equipment just shut down.

    So, after the second run, I began timing the runs. I timed the next two runs. They were exactly the same amount of time.

    So, I turned to the “experts,” and said: “It’s the same amount of time each time. It’s probably the electric breaker. Do you have a back-up breaker.” They said, “Yes, we do.”

    Well, we ran it the third time; this time using the back-up. No problems.

    Point of the story: We need to learn from our mistakes.
    We need to ‘smell out’ the right answer.

    But, then there’s orthodoxy that gets in the way. Right?

    The guys who worked for the company who invented the logging device could have said: “You don’t know anything about this logging device. Leave it to us “experts” to solve.”

    But they didn’t

  183. 183
    PaV says:

    This quote from one of BA77’s posts above is worth looking at in isolation:

    Pauli’s ideas on mind and matter in the context of contemporary science – Harald Atmanspacher
    Excerpt: “In discussions with biologists I met large difficulties when they apply the concept of ‘natural selection’ in a rather wide field, without being able to estimate the probability of the occurrence in a empirically given time of just those events, which have been important for the biological evolution. Treating the empirical time scale of the evolution theoretically as infinity they have then an easy game, apparently to avoid the concept of purposesiveness. While they pretend to stay in this way completely ‘scientific’ and ‘rational,’ they become actually very irrational, particularly because they use the word ‘chance’, not any longer combined with estimations of a mathematically defined probability, in its application to very rare single events more or less synonymous with the old word ‘miracle.’”

    Wolfgang Pauli (pp. 27-28)
    http://www.igpp.de/english/tda/pdf/paulijcs8.pdf

    It’s like reading one of my posts!

    Now, wd400, you know why I keep bringing up the use of the “infinite allele” model.

  184. 184
    wd400 says:

    The reason you keep bringing up the “infinite allele” model is that you don’t know what it means.

    Here’s the last thing I asked you in the “old” version of this thread.

    Apart from all the noise, do you mind explaining why you think a “modification factor” that segregates in a simple Mendelian fashion isn’t an allele?

    Still seems pretty relevant, to me. In this orginal thread (the one that you think is vindicated by the new paper) you claimed there was no allele for this trait (bizarrely while also accepting in segregates in Mendelian fashion…). this paper found the allele. Are you sure it’s a vindication for you?

  185. 185
    AhmedKiaan says:

    You guys seem to think if you play enough word games, something will happen. But the word games have been going on for decades, and nothing happens. Scientists keep doing science. Science keeps advancing. Cranks keep posting long screeds to blogs.

    I’m originally from the physics world, and I saw this all the time. Every week we got manifestoes in the mail about how Einstein was wrong, quantum theory is wrong, the round earth is wrong, etc. Cranks do a lot of typing, but they never accomplish anything.

  186. 186
    AhmedKiaan says:

    Smart cranks eventually realize their job is to understand how they got it so wrong.

    There aren’t many smart cranks. For the most part, they just keep typing, year after year.

  187. 187
    bornagain77 says:

    As the experiments in post 181 indicated, Darwinists have no clue how genotypes generate phenotypes

    With a Startling Candor, Oxford Scientist Admits a Gaping Hole in Evolutionary Theory – November 2011
    Excerpt: As of now, we have no good theory of how to read [genetic] networks, how to model them mathematically or how one network meshes with another; worse, we have no obvious experimental lines of investigation for studying these areas. There is a great deal for systems biology to do in order to produce a full explanation of how genotypes generate phenotypes,,,
    http://www.evolutionnews.org/2.....52821.html

    Not Junk After All—Conclusion – August 29, 2013
    Excerpt: Many scientists have pointed out that the relationship between the genome and the organism — the genotype-phenotype mapping — cannot be reduced to a genetic program encoded in DNA sequences. Atlan and Koppel wrote in 1990 that advances in artificial intelligence showed that cellular operations are not controlled by a linear sequence of instructions in DNA but by a “distributed multilayer network” [150]. According to Denton and his co-workers, protein folding appears to involve formal causes that transcend material mechanisms [151], and according to Sternberg this is even more evident at higher levels of the genotype-phenotype mapping [152]
    http://www.uncommondescent.com.....onclusion/

    To put it more clearly, the ‘form/shape’ any particular organism may take simply is not reducible to the ‘bottom up’ materialistic explanations of Darwinian evolution:

    What Do Organisms Mean? Stephen L. Talbott – Winter 2011
    Excerpt: Harvard biologist Richard Lewontin once described how you can excise the developing limb bud from an amphibian embryo, shake the cells loose from each other, allow them to reaggregate into a random lump, and then replace the lump in the embryo. A normal leg develops. Somehow the form of the limb as a whole is the ruling factor, redefining the parts according to the larger pattern. Lewontin went on to remark: “Unlike a machine whose totality is created by the juxtaposition of bits and pieces with different functions and properties, the bits and pieces of a developing organism seem to come into existence as a consequence of their spatial position at critical moments in the embryo’s development. Such an object is less like a machine than it is like a language whose elements… take unique meaning from their context.[3]”,,,
    http://www.thenewatlantis.com/.....nisms-mean

    “Last year I had a fair chunk of my nose removed in skin cancer surgery (Mohs). The surgeon took flesh from a nearby area to fill in the large hole he’d made. The pictures of it were scary. But in the healing process the replanted cells somehow ‘knew’ how to take a different shape appropriate for the new location so that the nose now looks remarkably natural. The doctor said he could take only half the credit because the cells somehow know how to change form for a different location (though they presumably still follow the same DNA code) . — I’m getting the feeling that we’ve been nearly as reductionist in the 20-21st century as Darwin and his peers were when they viewed cells as little blobs of jelly.”
    leodp – UD blogger
    http://www.uncommondescent.com.....ent-563451

    The Insurmountable Problem of “Form/Shape” for Darwinian Explanations – video (2016)
    https://youtu.be/WQxJRvpCOK0

    And since Darwinian explanations can not possibly explain the ‘form/shape’ of an organism, then any claim that ‘bottom up’ Darwinian processes can explain the transformation of all species on earth from pre-existing forms of life is pure hogwash.

  188. 188
    kairosfocus says:

    AK, in another thread, you have accused the President Elect of the USA of treason. You have been challenged to substantiate, to apologise, to withdraw or face consequences. Running off to another thread and pretending that something serious is not on the table that potentially decisively goes to character is NOT an option here at UD. KF

  189. 189
    PaV says:

    wd400:

    The reason you keep bringing up the “infinite allele” model is that you don’t know what it means.

    Well, I’ve just gotten out my worn, highlighted copy of Gillespie’s Population Genetics: A Concise Course. I even had a marker on p.29, where I have highlighted: “infinite allele model.”

    Let me quote Gillespie:
    When a mutation does occur, it is assumed to be to [sic] a unique allele, one that differs by state from all alleles that have ever existed in the population. A population that has been around for a long time will have seen a very large number of different alleles. Consequently, our model of mutation is often call the infinite allele model.

    So, you see, I do know what the ‘infinite allele model’ is. Will you retract your claim?

    Apart from all the noise, do you mind explaining why you think a “modification factor” that segregates in a simple Mendelian fashion isn’t an allele?

    I’ve already answered your question in my own way. You can’t seem to grasp it. Not my fault. Let me try another way. Here goes:

    Evolutionary theory is like the “Blob”!

    Do I have your attention? Yeah, exactly like in the movie, where this strange, alien life form invades earth, and absorbs into itself whatever it comes into contact.

    This is what evolutionary biologists do. There are too many protein polymorphisms found through gel electorphoresis, so Kimura, basing himself on the genetic load involved (and following here one of the patriarchs of pop. gen., Haldane) disjoins himself from “biological evolution,” and begins to talk about “molecular evolution”. This is otherwise known as the Neutral Theory. Well, the wars were waged. Now, Kimura’s Neutral Drift, a challenge to Darwinian theory, is considered to be just another part of evolutionary theory; not a challenge. You see, it got “swallowed up” by the great big “Blob”known as Darwinian evolutionary theory.

    Then there’s the familiar story of “junk DNA.” Why, of course, there’s no such thing as “intelligent design” because look at all of the “junk” in DNA. This is just all leftover stuff from gene duplications that went nowhere. You know: pseudogenes. Then pseudogenes are found to have function. All kinds of other “junk DNA” is found to have function, and the evolutionary biologists—like you—say: “We’ve known that all along. It only makes sense that all of this DNA should have some kind of function.” You see, it, too, got “swallowed up” by the great big “Blob”known as evolutionary biology.

    And, along these same lines, when evolutionary biologists were convinced of that only “coding” DNA was significant (while, in fairness, acknowledging that non-coding DNA was likely involved in regulation of some sort), “genes” meant “coding” DNA, and nothing else. Now that function is found for “junk DNA”, or “non-coding” DNA, this, too, is now termed “genes”—swallowed up by that great big “Blob” known as evolutionary biology. What confusion this causes. But to use different terminology would be to admit evolutionary biologists missed something big time—a “no-no” not permitted publicly by evo. biol.

    And, now, with a TE found inserted into an intron of the very “icon” of evolution, the peppered moth, you blithely say: In this orginal thread (the one that you think is vindicated by the new paper) you claimed there was no allele for this trait . . ..

    So, it, too is an “allele”—whatever that means. Like whatever a “species” means. Or whatever a “gene” is supposed to mean. A science that survives through equivocation is not going in the right direction.

    Evolutionary biology is an alien life form.

    Have I made my point clear?

  190. 190
    PaV says:

    Ahmed K:

    There aren’t many smart cranks. For the most part, they just keep typing, year after year.

    I think that Nobel Prize winning physicists who believe in the “multiverse” theory are cranks. How about you?

  191. 191
    bornagain77 says:

    PaV, I think your analogy between evolutionary biology and ‘The Blob’ is very good and deserves to be headlined, but I could be a crank who just likes old cornball science fiction movies. 🙂

    Life Form: Oddly Appropriate Segues – GEICO
    https://www.youtube.com/watch?v=X7n5wrFdmgI

  192. 192
  193. 193
    wd400 says:

    It would be much more becoming to simply say you were wrong.

    The spam that you’ve spewed forth to cover this is also wrong, but you’ve been told this many times and show no ability to learn anything than conflicts with the story you’ve created.

  194. 194
    bornagain77 says:

    “show no ability to learn anything than conflicts with the story you’ve created.”

    That’s especially rich coming from a Darwinist.

  195. 195
    AhmedKiaan says:

    Donald Trump got in trouble multiple times for refusing to do business with people who share your ethnicity, KF. And there’s no doubt he is corrupt, and has no moral character.

    UD really shouldn’t enforce a Republican political ideology. That would be a bad idea.

  196. 196
    kairosfocus says:

    AK, you now try to further complain that he is a racist. Again, that would need warrant but the primary issue still stands, you have put treason on the table, substantiate or withdraw. And this is not “republican ideology,” it is the premise that we should not accuse people of capital crimes without providing serious substance. I say this as a general principle, I have never nor will I endorse Mr Trump, as though that would be of relevance. It is evident from your evasive response that you do not have substance to back your accusation, but wish to dance wrong but strong. You are not welcome at any thread I own, good day. KF

  197. 197
    MatSpirit says:

    kairosfocus @188 “AK, in another thread, you have accused the President Elect of the USA of treason. You have been challenged to substantiate, to apologise, to withdraw or face consequences. Running off to another thread and pretending that something serious is not on the table that potentially decisively goes to character is NOT an option here at UD. KF”

    KF, apparently you are not familiar with American politics. As long as I can remember, which goes back to the early 50’s and the Republican/McCarthy era, members of the President Elect’s party have knowingly, deliberately and habitually called the members of the Democratic party traitors, corrupt, liars (at a Constitutionally mandated State of the Union address no less), Communists and any other scurrilous lies that enter their heads.

    Are you now threatening to ban a poster for reflecting that talk back to its source?

  198. 198
    PaV says:

    wd400:

    . . . [you] show no ability to learn anything tha[t] conflicts with the story you’ve created.

    Weren’t they just having a conference in England to move from the Modern Synthesis—your field—to the “Extended Synthesis.”

    It seems like it’s your “story” that needs correcting. Or am I missing something?

  199. 199
    PaV says:

    BTW, some of you might find this Phys.Org article interesting.

  200. 200
    kairosfocus says:

    MS, that matters not, cross complaining in blanket style as you just did does not erase the fact that AK accused someone of a capital crime, ducked the challenge to substantiate or withdraw and has now clearly implied utter want of substance through evasiveness and attempted compounding of unsubstantiated accusations. Tolerance for such false accusations — for cause — is zero. KF

  201. 201
    MatSpirit says:

    In American politics, “traitor” means anyone a Republican doesn’t like.

  202. 202
    Dionisio says:

    KF,

    This thread is about biology, but your not-so-politely-dissenting interlocutor AK seems to be upset for what happened earlier this month in the US and wants to vent his deep frustration in this thread. I feel sorry for him.

    This site does not seem to associate with any political party in any country, including the US, correct?
    I did not vote in the US election. Also, as far as I know, you’re not a US citizen, hence didn’t vote in the US election.

    Now, after reading AK comments filled with so much frustration, one can understand what he probably meant when he posted the following message in another thread the day before the US election:

    AhmedKiaan @30:
    November 7, 2016 at 2:42 pm
    I’m going to be celebrating a win tomorrow night.

    http://www.uncommondescent.com.....ent-620414

  203. 203
    PaV says:

    MatSpirit:

    In American politics, “criticizing” conservatives on the part of the Left means pulling them out of their cars and beating them to a pulp.

  204. 204
    AhmedKiaan says:

    Instead, my win will be leaving in 4 months. I guess in retrospect it makes sense that the first African-American president is followed by a white backlash so severe that the President Elect is literally endorsed by the KKK, David Duke, the Alt-Right Neo Nazis, etc. It’s just sad. But America had racist presidents in the past, and survived. I wonder how long Trump will be president before the damage is so severe that even the GOP pretends to have integrity and impeaches him.

  205. 205
    AhmedKiaan says:

    Hey PaV, can you get some courage and write up what you honestly believe about the medical community and HIV and whatnot? That would be funny to read.

  206. 206
    MatSpirit says:

    PaV, where did that happen?

  207. 207
    kairosfocus says:

    MS:

    US CONST, Art 3 Sec 3:

    Treason against the United States, shall consist only in levying War against them, or in adhering to their Enemies, giving them Aid and Comfort. No Person shall be convicted of Treason unless on the Testimony of two Witnesses to the same overt Act, or on Confession in open Court.

    The Congress shall have Power to declare the Punishment of Treason, but no Attainder of Treason shall work Corruption of Blood, or Forfeiture except during the Life of the Person attainted.

    You are further substantiating my point on the sort of hateful false accusations being tossed around without sound substantiation. In this case, on a matter that is normally a capital crime with very serious forfeiture provisions.

    The cumulative result of which is to utterly corrode community.

    It is time to stop the foolishness.

    KF

    PS: PAV is citing an actual recent very ugly incident.

  208. 208
    MatSpirit says:

    KF: “You are further substantiating my point on the sort of hateful false accusations being tossed around without sound substantiation. In this case, on a matter that is normally a capital crime with very serious forfeiture provisions.

    The cumulative result of which is to utftterly corrode community.

    It is time to stop the foolishness.”

    My point exactly. I’ve been listening to conservatives tossing hateful false accusations of treason around without any substantiation whatsoever since I was in high school and I know the history of such scurrilous accusations goes back decades further. I’ve watched it corrode my country. Pardon me if I don’t have a whole lot of sympathy for conservatives who don’t like it when maybe one tenth of one percent of what they so reclessly fling at others blows back in their faces.

    I think you’re getting a little over excited here. Why don’t you sit back, relax a little and take your mind things for a while? Maybe you could diagram some fishing reels or draw some world maps with important looking lines on them. Try to include at least one choke point.

    P.S. Could you even imagine violence during the Romney campaign? Of course not. He (and his father George) were the last of the decent Republicans. Not so for The Donald.

  209. 209
    kairosfocus says:

    MS, turnabout projective accusation and cross complaining; something marital counsellors advise against for cause — and which will utterly corrode public discussion; as in even assuming such as you project to be true it would be a call for across the board reform not tu quoque fallacies. I am not an American and at this point am inclined to have a very negative assessment of your overall political culture and future as a direct result. FYI, you would have been well advised to notice that I am responding to specifically abusive commentary and evasion of responsibility by AK, in part as establishing and defending standards of responsible behaviour at UD. Your attempted piling on simply demonstrates the need for what I am doing. Good day. KF

  210. 210
    MatSpirit says:

    That paragraph reads like you’re drunk. Answering a critic’s charge is not “turnabout projective accusation and cross complaining”. I don’t know why you brought up marriage counseling and refuse to speculate. What really corrodes public discussion are reflexive accusations of disloyalty, race baiting and blaming your opponents for the problems your party has caused.

    I realize you’re not an American and hope you remain safe on your tiny Carribean island that 99.99% of Americans couldn’t find on a map.

    If you think you’ve got a negative view of American political culture, try living here for a while. The last time we had a born again Christian who thought he’d been sent by God to save America get into the White house despite losing the popular vote, we got attacked in New York and Washington, the born again fool started a war with an innocent country that we’re still mired in, ISIS got started in the carnage of Iraq and the whole world economy collapsed. I can’t wait to see what this one does.

    If I hated America, I’d be cheering, but the only people I see who are happy with the last election are ISIS, Putin, conservatives and especially conservative Christians who have finally elected a thrice married philanderer who makes Bill Clinton look like a choir boy. God only knows why.

  211. 211
    DATCG says:

    KF,

    I request you delete please starting with AK thru yours and Mat’s comments.

    The take down by PaV of neo-Darwinism amid many other comments was great. I was so enjoying reading it. And I’d hope other readers would not see the distractions at the end. PaV deserves better.

    I’d suggest removing the last remaining comments by AK, politics, etc., and finally Mat’s revisionist history on politics.

    It just killed a great thread.

    Remove my comment as well.

    And I hope PaV would do another post on this latest information if it was not already done. Thanks.

    Great work PaV! And all others!

  212. 212
    kairosfocus says:

    DATCG, I am not thread owner. KF

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