Intelligent Design

A Dilemma for Haldane

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Another day; another bad day for Darwinism. This is so true that I rarely post here anymore. Why bother? Darwinism is beat up everyday by its adherents doing experiments.

Here’s another one.

The team investigated the validity of Haldane’s predictions for the probability of fixation of a beneficial allele. They used C. elegans because it reproduces asexually, thus ensuring “genetic identity” from one generation to the next.

While validating Haldane’s predictions for the initial introduction of both deleterious and beneficial alleles to a population, they found this:

If its [i.e., the allele’s] frequency was higher than 5% (when more than five different individuals in a population of 100 individuals), the allele was perceived as deleterious and it started to be eliminated by natural selection. But when the frequency was less than 5%, the allele was beneficial. The result of these complex dynamics is that genetic diversity could be maintained indefinitely, without one allele or the other ever being fixed in the population.

IIRC, several years ago, in a study involving bacteria, it was found that when a bacterial population utilizing one type of sugar was place in the environment of a different type sugar, then the population switched over to the new sugar type; however, the ‘allele’ for the original sugar was never COMPLETELY eliminated from the population. Only WGA could determine this.

What these two examples suggest is that the ‘genome’ has the ability to monitor the level of use of any particular ‘allele’, and that depending on its current ‘use’, the ‘allele’ that would be ‘deleterious’ for the current environment is held at some minimal level so that should the environment change in the future, the needed ‘allele’ [then ‘beneficial’] would be ready at hand. [Which makes sense given how improbable it is to generate an allele from scratch]

To my mind, this calls the very idea of Natural Selection into question. We already know—Dawkin’s tells us this—that Natural Selection is no more than the “Grim Reaper.” Thus, NS is no more than the elimination of “unfit” alleles through “death.” But, in this scenario—backed up by the two experiments I’m speaking of—it is the population itself which determines what is ‘deleterious’, and hence eliminated via “death,” and which is ‘beneficial.’ In this case, it is the genome—very likely communicating with itself via individual genomes—that is making the “SELECTION;” NOT ‘nature.’

This is potentially devastating to Darwinian thought. But, don’t worry, you can be sure that our Darwinian ‘true-believers’ will invent some new ‘epicycle’ to explain—in their minds only—this deathblow to population genetics.

47 Replies to “A Dilemma for Haldane

  1. 1
    jstanley01 says:

    The wheels of history may grind slow, but they grind fine. With Darwinism just like Ptolemaic astronomy (emphasis added)…

    Eventually, perfectly concentric spheres were abandoned as it wasn’t possible to develop a sufficiently accurate model under that ideal. However, while providing for similar explanations, the later deferent and epicycle model proved to be flexible enough to accommodate observations for many centuries.

    Except that, with the acceleration of discovery in the modern world, I’d give NDE’s ever-more-unlikely just-so stories a decade at most this side of the dustbin.

  2. 2
    OldArmy94 says:

    As much as I see Darwinian evolution as a completely fabricated mishmash of tales and fables, I do not see it being eliminated..EVER. Unlike other discarded theorems and paradigms, and I think “global warming/climate change” is headed toward oblivion, there is too much at stake from a philosophical and religious viewpoint for Darwinism to just disappear. It may be possibly displaced by another yet-unknown theory of life, but it will not surrender to a design-based ideal.

  3. 3
    nullasalus says:

    Unlike other discarded theorems and paradigms, and I think “global warming/climate change” is headed toward oblivion, there is too much at stake from a philosophical and religious viewpoint for Darwinism to just disappear.

    And there is the essential truth of the matter. Actual science, arguments, reason and evidence don’t matter all that much when it comes to many aspects of modern evolutionary theory, precisely because of what’s at stake philosophically, politically, and religiously.

    There is a silver lining: while the theory may not change, respect for ‘scientific consensus’ probably will go further and further into the toilet. I personally won’t worry too much if Darwinism remains the sacred cow of certain academics – if the cost of their vigilance is the loss of their reputation among the general public.

  4. 4

    PaV, absolutely nothing in that paper poses any problem for evolutionary theory at all! It’s a very elegant paper, and it demonstrates empirically a very important evolutionary principle.

    Evolutionary theory is about reproductive success in the current environment. That environment includes other populations in the habitat, as well as your own.

    What is beneficial or deleterious in one environment may or may not be in a different environment. If the environment changes (is “dynamic”) as the article says, then alleles will fluctuate as to whether they are deleterious, advantageous or neutral.

    This is exactly why crude models of population genetics don’t work – the allele frequency itself alters the environment that determines the selection coefficient of the allele.

    It’s not “Darwinian evolution” that is “a completely fabricated mishmash of tales and fables” – the “completely fabricated mishmash of tales and fables” are the tales told by ID proponents about Darwinian evolution!

  5. 5
    wd400 says:

    Dear me, frequency dependant selection is not a new discovery.

  6. 6
    Phinehas says:

    Some have openly admitted on this blog that all natural causes must be eliminated as possibilities before they would accept design as an option. That’s quite the gap-filler and, no doubt, adequate protection for their position from any and all evidence.

  7. 7

    That sounds more like a version of ID: if we can eliminate all natural causes we can conclude Design. That’s essentially Dembski’s position.

    It’s not a sound methodology.

    We could conclude Design if a someone proposed a testable Design model and it fitted the data better than a non-Design model.

    But nobody ever proposes a testable i.e. a predictive Design model.

  8. 8
    Chesterton says:

    Well Elizabeth that paper couldn´t show fixation of new alleles. As drift is at least a key factor for darwinian evolution, not to be easily demostrable open some questions.

  9. 9

    Lots of alleles never fix, especially in a large population. That’s how diversity is maintained. And sometimes, their is selection for a proportion in the population, as with sickle cell. If the sickle cell allele gets too prevalent, too many people get sickle cell anaemia, die, early, and alleles are lost. But when the prevalence drops, too few people get the protective sickle cell trait, and the number climbs again.

    So it reaches homeostasis, below fixation.

    Exactly the same is happening here. It’s a beautiful example of optimising evolution in action, not problem for it.

  10. 10
    wd400 says:

    As drift is at least a key factor for darwinian evolution, not to be easily demostrable open some questions.

    Drift is not Darwinian, and the fixation of alleles by drift is easily demonstrable (in fact, it’s an inevitable consequence of non-infinite populations). What’s interesting about this experiment is that (Darwinian) selection is acting to maintain diversity that would usually be lost by drift (or by directional selection). As Elizabeth says, it’s a nice example of the way in which natural selection can maintain genetic diversity.

  11. 11
    Axel says:

    ‘But nobody ever proposes a testable i.e. a predictive Design model.’

    Well, Elizabeth, at the link to a site listing the opinions of many very eminent theist scientists, which I posted on UD, yesterday, one of the contributors, whose name I forget now, has stated that atheism is virtually history, since modern science has rendered theism an experimental science. I’ll dig it up tomorrow, if this thread is still visible.

    I’ll also be posting some devastating comments by Nobel prize winners concerning atheism. Maxwell said you have to be an imbecile to be one, so you’d better sharpen up.

    Proof of theism is of course, proof of design. You materialists have no way of explaining the non-locality of photons, do you? And so little to say about it.

    I suggested the other day that asking for proof of Design is like asking a fish to prove it lives in water. I see that Von Braun compared asking for proof of Design with wanting to hold up a candle to look at the sun.

  12. 12
    Axel says:

    What was a hilarious, if highly predictable, response of the disaffected, teenage-atheist types, who normally delight in ‘group’ sneering at religious believers, was palpable shock, immediately falling back on theodicy, a la Nick Madzke. Never mind the science!

  13. 13
    Barb says:

    I found this amusing, as it relates to Haldane: Bible translator Ronald Knox was once engaged in a theological discussion with scientist John Scott Haldane. “In a universe containing millions of planets,” reasoned Haldane, “is it not inevitable that life should appear on at least one of them?”

    “Sir,” replied Knox, “if Scotland Yard found a body in your cabin trunk, would you tell them: ‘There are millions of trunks in the world—surely one of them must contain a body?’ I think they would still want to know who put it there.”—The Little, Brown Book of Anecdotes.

  14. 14
    Chesterton says:

    So it reaches homeostasis, below fixation.

    Exactly the same is happening here. It’s a beautiful example of optimising evolution in action, not problem for it.

    But evolution it is not homestasis is changing.

    What’s interesting about this experiment is that (Darwinian) selection is acting to maintain diversity that would usually be lost by drift (or by directional selection)

    But selection is not about chosing the best fit not keeping all?

  15. 15
    bornagain77 says:

    Of related note to asexual populations (of bacteria) maintaining a genome over long periods of time:

    The Paradox of the “Ancient” (250 Million Year Old) Bacterium Which Contains “Modern” Protein-Coding Genes:
    “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland ;
    http://mbe.oxfordjournals.org/...../19/9/1637

    These following studies, by Dr. Cano on ancient bacteria, preceded Dr. Vreeland’s work:

    “Raul J. Cano and Monica K. Borucki discovered the bacteria preserved within the abdomens of insects encased in pieces of amber. In the last 4 years, they have revived more than 1,000 types of bacteria and microorganisms — some dating back as far as 135 million years ago, during the age of the dinosaurs.,,, In October 2000, another research group used many of the techniques developed by Cano’s lab to revive 250-million-year-old bacteria from spores trapped in salt crystals. With this additional evidence, it now seems that the “impossible” is true.”
    http://www.physicsforums.com/s.....p?t=281961

    Dr. Cano had found ‘slight but significant’ differences between ancient and modern bacteria:

    Revival and identification of bacterial spores in 25- to 40-million-year-old Dominican amber
    Dr. Cano and his former graduate student Dr. Monica K. Borucki said that they had found slight but significant differences between the DNA of the ancient, 25-40 million year old amber-sealed Bacillus sphaericus and that of its modern counterpart, (thus ruling out that the change is a modern contaminant, yet at the same time confounding materialists, since the change to the genome is not nearly as great as evolution’s ‘genetic drift’ theory requires.)
    http://www.sciencemag.org/cgi/...../5213/1060

    Out of curiosity, I e-mailed both Dr. Vreeland and Dr. Cano to ask them if either of them had performed a ‘fitness test’ between the ancient and modern bacteria, since I knew that the ‘fitness test’ performed between antibiotic resistant bacteria and normal bacteria had never been violated,,,

    Is Antibiotic Resistance evidence for evolution? – ‘The Fitness Test’ – video
    http://www.metacafe.com/watch/3995248

    Thank Goodness the NCSE Is Wrong: Fitness Costs Are Important to Evolutionary Microbiology
    Excerpt: it (an antibiotic resistant bacterium) reproduces slower than it did before it was changed. This effect is widely recognized, and is called the fitness cost of antibiotic resistance. It is the existence of these costs and other examples of the limits of evolution that call into question the neo-Darwinian story of macroevolution.
    http://www.evolutionnews.org/2.....s_wro.html

    Dr. Vreeland wrote me back and said that ‘only a creationist would ask such a question’! He then lectured me for a couple of paragraphs on how well established evolution was as a scientific theory whilst never telling me whether he had performed the fitness test or not. Dr. Cano, on the other hand, was far more forthright with me and stated in response to my question as to if he had performed a ‘fitness test’ between the ancient bacteria and the modern bacteria:

    “We performed such a test, a long time ago, using a panel of substrates (the old gram positive biolog panel) on B. sphaericus. From the results we surmised that the putative “ancient” B. sphaericus isolate was capable of utilizing a broader scope of substrates. Additionally, we looked at the fatty acid profile and here, again, the profiles were similar but more diverse in the amber isolate.”
    – Dr. RJ Cano commenting on ‘fitness test’ which compared ancient bacteria almost identical modern bacteria

    Thus, the most solid evidence available for the most ancient DNA scientists are able to ‘revive’ does not support evolution happening on the molecular level of bacteria. In fact, according to the fitness test of Dr. Cano, the change witnessed in bacteria conforms to the exact opposite, Genetic Entropy, a slight loss of functional information/complexity for the bacteria over extremely long periods of time, since fewer substrates and fatty acids are utilized by the modern strains.

    A few assorted supplemental notes:

    Learning from Bacteria about Social Networks – video
    Description: Bacteria do not store genetically all the information required to respond efficiently to all possible environmental conditions. Instead, to solve new encountered problems (challenges) posed by the environment, they first assess the problem via collective sensing, then recall stored information of past experience and finally execute distributed information processing of the 109-12 bacteria in the colony,,, 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

    Biophoton Communication: Can Cells Talk Using Light? – May 2012
    Excerpt: The question he aims to answer is whether the stream of photons has any discernible structure that would qualify it as a form of communication.,, Biophoton streams consist of short quasiperiodic bursts, which he says are remarkably similar to those used to send binary data over a noisy channel. That might help explain how cells can detect such low levels of radiation in a noisy environment.
    http://www.technologyreview.co.....alk-using/

    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

    Verse and Music:

    Romans 1:20
    For since the creation of the world God’s invisible qualities—his eternal power and divine nature—have been clearly seen, being understood from what has been made, so that people are without excuse.

    LECRAE-IT’S YOUR WORLD – song
    Excerpt of Lyrics – He uses intelligent design
    Like eloquence confined
    Life elements assigned by
    Elohim my God
    He left his fingerprints
    You thinking that our origins are coincidence
    Our symmetry alone makes
    Evolution look ridiculous
    And since our complexity is more than irreducible
    The fact our design had a designer is irrefutable
    I use science too to make a statement like this
    The existence of an atheist proves God exists
    http://www.youtube.com/watch?v=TS5fYvyy5Y8

  16. 16
    Daniel King says:

    PaV:

    Darwinism is beat up everyday by its adherents doing experiments.

    What’s wrong with those people?

    I applaud the ID advocates here for avoiding such self-destructive behavior.

    Convenient, isnt’t it?

  17. 17
    goodusername says:

    If its [i.e., the allele’s] frequency was higher than 5% (when more than five different individuals in a population of 100 individuals), the allele was perceived as deleterious and it started to be eliminated by natural selection. But when the frequency was less than 5%, the allele was beneficial. The result of these complex dynamics is that genetic diversity could be maintained indefinitely, without one allele or the other ever being fixed in the population.

    Unless I’m missing something, this sounds like a usual case of an evolutionary stable state, whereby a trait is beneficial only when it is present below a certain percentage of the population, and therefore tends to be fixed at that percentage.
    It’s a major theme of Dawkins’ book The Selfish Gene from 1976.

  18. 18
    bornagain77 says:

    OT: podcast: “Censorship Loses: New Scientific Volume Challenges Neo-Darwinism”
    http://intelligentdesign.podom.....9_03-07_00

  19. 19
    bornagain77 says:

    as to “It’s a major theme of Dawkins’ book The Selfish Gene from 1976.”

    Unfortunately for those who would wish to cite ‘The Selfish Gene’ in support of neo-Darwinian evolution, all the major foundational presuppositions under-girding what Dawkins held to be true in his book ‘The Selfish Gene’ are now shown to be false:

    Modern Synthesis Of Neo-Darwinism Is False – Denis Nobel – video
    http://www.metacafe.com/w/10395212

    ,, In the preceding video, Dr Nobel states that around 1900 there was the integration of Mendelian (discrete) inheritance with evolutionary theory, and about the same time Weismann established what was called the Weismann barrier, which is the idea that germ cells and their genetic materials are not in anyway influenced by the organism itself or by the environment. And then about 40 years later, circa 1940, a variety of people, Julian Huxley, R.A. Fisher, J.B.S. Haldane, and Sewell Wright, put things together to call it ‘The Modern Synthesis’. So what exactly is the ‘The Modern Synthesis’? It is sometimes called neo-Darwinism, and it was popularized in the book by Richard Dawkins, ‘The Selfish Gene’ in 1976. It’s main assumptions are, first of all, is that it is a gene centered view of natural selection. The process of evolution can therefore be characterized entirely by what is happening to the genome. It would be a process in which there would be accumulation of random mutations, followed by selection. (Now an important point to make here is that if that process is genuinely random, then there is nothing that physiology, or physiologists, can say about that process. That is a very important point.) The second aspect of neo-Darwinism was the impossibility of acquired characteristics (mis-called “Larmarckism”). And there is a very important distinction in Dawkins’ book ‘The Selfish Gene’ between the replicator, that is the genes, and the vehicle that carries the replicator, that is the organism or phenotype. And of course that idea was not only buttressed and supported by the Weissman barrier idea, but later on by the ‘Central Dogma’ of molecular biology. Then Dr. Nobel pauses to emphasize his point and states “All these rules have been broken!”.
    Professor Denis Noble is President of the International Union of Physiological Sciences.

  20. 20
    wd400 says:

    But selection is not about chosing the best fit not keeping all?

    Yes. The most fit in the environment in any given generation. The environment includes the other genes present in the population, so, sometimes the fitness of an allele depends on its frequency in the population.

    One way to think of this is to say it’s as if selection is trying to maintain a maximally fit population – if there were less of these new alleles they would be favoured so become more frequent. But if there were more of them they would be further selected against and become less frequent. In time they arrive the equilibrium frequency (+/- a bit of drift from generation to generation).

    These are acrually a really nice example of the sorts of models we often run with undergrad geneticists, but with actual animals. Which is pretty cool.

  21. 21
    Brent says:

    Daniel K @16,

    I applaud the ID advocates here for avoiding such self-destructive behavior.

    Convenient, isnt’t it?

    Why yes, quite. And all the more, in fact, since it is a natural byproduct of being right.

  22. 22
    Mung says:

    Elizabeth Liddle:

    Lots of alleles never fix, especially in a large population. That’s how diversity is maintained.

    Diversity is maintained by alleles which are never fixed, especially in large populations. The HOW is a bit vague.

    Care to say more?

  23. 23

    I could, but you could just do a literature search, or even construct a model.

    Hint: feedback.

  24. 24
    Mung says:

    Or I could try to discover what is meant by diversity and how it is measured. And I could try to discover what is meant by disparity and how it is measured. And I might discover that disparity is not a measure of diversity. And I might discover that you’re equivocating over the term diversity.

    Probably better that you just clarify whatever point it is that you thing you’re making.

  25. 25

    You could do those things, Mung.

    Here’s a place you could start:

    Diversity, disparity, and evolutionary rate estimation for unresolved Yule trees

    Disparity is one of the terms that goes into a diversity estimate.

  26. 26
    TheisticEvolutionist says:

    Not many people know this but John Scott Haldane (the father of neo-Darwinist J. B. S. Haldane) was a leading critic of genetic determinism/reductionism and he certainly would of rejected Dawkins concept of selfish genes and neo-Darwinism.

    See for example his book “Mechanism, Life and Personality. An Examination of the Mechanistic Theory of Life and Mind” (1913) which was a criticism of materialism and reductionism and supported a form of holistic organicism in biology. He believed the organism as fundamental to biology: “we perceive the organism as a self-regulating entity”, “every effort to analyse it into components that can be reduced to a mechanical explanation violates this central experience”.

    His views would be similar to Denis Noble, viewing the organism as a connected system or whole and not just reducing them to gene alone.

  27. 27
    Timaeus says:

    Hey, guys! I want to raise an apparently minor concern about our presentation here on UD.

    Lately, in many of our columns, I’ve noticed atrocious spelling errors, sometimes even in the headlines.

    Here, for example, we have “dilemna” instead of “dilemma.”

    This isn’t just a fussy point about English. ID people are often classed as “creationists,” and “creationists” are often stereotyped (by reference to polls attempting to connect religious belief with fewer years of formal education, etc.) as less educated than the general population, as anti-education, anti-culture, etc. When an ID website features frequent spelling errors, this just confirms the stereotype. You don’t see many spelling errors in columns written by Dawkins, Coyne, Collins, Miller, etc.

    If columns are originally typed up in a word processor, they can be spell-checked before copying and pasting to the UD author site. Of course, spell-checkers don’t catch everything, so I recommend that writers also have good, large, thorough English dictionary of the traditional kind at hand. Also, if the writer has a wife, parent, brother or friend who is better at English (including not only spelling but grammar, usage, and punctuation), it wouldn’t hurt to fly columns by that person before posting them.

    I realize, of course, that some apparent spelling errors can be just typos, and don’t indicate ignorance of spelling. But even typos shouldn’t find their way into titles or columns here; proofreading is in order.

    If the secular humanists and materialists all write polished stuff and we write sloppy stuff, it just confirms prejudices. Noncommitted readers may say: “If these ID guys don’t know their English very well, maybe they aren’t very educated, and maybe they don’t know their science any better.”

    As I say, it may seem like a small point, but we are in the persuasion business, and when you are trying to persuade people, they notice everything about you — not just your arguments and your evidence, but your whole presentation. If you show up at a job interview with a gravy stain on your jacket and your tie on crooked, you may well lose the job even though you know more about the business than the person with the stain-free suit and the tie looking like James Bond’s.

    This is something that can be cleaned up easily, with minimal care and attention. Can we work on it?

  28. 28
    Gregory says:

    At least you’re not and don’t want to be part of an IDist Movement or IDist ‘Community,’ timaeus, right? 😛

    You’re “pulling back” from UD, right timaeus?

    Oh, hang on, should they (‘guys’-only!) use your Alabama-American English, timaeus, or be free to use British or Canadian English instead?

    C’mon IDists, git smurter kwickly, so that timaeus will finally be proud enough to join you! 🙂

  29. 29
    Chesterton says:

    One way to think of this is to say it’s as if selection is trying to maintain a maximally fit population – if there were less of these new alleles they would be favoured so become more frequent. But if there were more of them they would be further selected against and become less frequent. In time they arrive the equilibrium frequency (+/- a bit of drift from generation to generation).

    These are acrually a really nice example of the sorts of models we often run with undergrad geneticists, but with actual animals. Which is pretty cool.

    I understand is the frequency variation of alleles. I do not see how these mechanism that seems to tend to keep homehostasis can be extrapolated to a mechanism that led to the increasing diversity of life forms.

  30. 30
    Neil Rickert says:

    This is potentially devastating to Darwinian thought.

    I doubt it.

    The type of behavior described in the paper is what I would have expected. I agree it is not strictly Darwinian, and it is partly because I expect this kind of behavior that I say I am not a Darwinist. But people at UD and biologists keep telling me that I really am a Darwinist, so the distinction can’t be large.

    I expect this kind of behavior, because it is what would seem to be necessary for evolution to work well. And it seems to follow that Darwinian natural selection would itself adapt to the needs of evolution (or population survival) by adopting this not-strictly-Darwinian strategy.

    Your post asserts:

    They used C. elegans because it reproduces asexually, thus ensuring “genetic identity” from one generation to the next.

    That does not appear to be strictly correct. The authors write:

    These tiny organisms primarily reproduce by self-fertilization, which assures that genetic identity is maintained.

    Perhaps my terminology is off, but I see “asexual” as implying that only mitosis is used, while self-fertilization implies the use of meiosis. And it is meiosis that mixes things up enough to maintain some level of variation.

  31. 31
    scordova says:

    Hey, guys! I want to raise an apparently minor concern about our presentation here on UD.

    Lately, in many of our columns, I’ve noticed atrocious spelling errors, sometimes even in the headlines.

    Here, for example, we have “dilemna” instead of “dilemma.”

    This isn’t just a fussy point about English. ID people are often classed as “creationists,” and “creationists” are often stereotyped (by reference to polls attempting to connect religious belief with fewer years of formal education, etc.) as less educated than the general population, as anti-education, anti-culture, etc. When an ID website features frequent spelling errors, this just confirms the stereotype. You don’t see many spelling errors in columns written by Dawkins, Coyne, Collins, Miller, etc.

    We’ll try, but with a readership of about 100, I view this blog as draft and trial areas for ideas to get free editorial and peer review.

    The commenters like yourself and others have provided editorial corrections, for which I am extremely grateful.

    I review what I write several times, but things slip through the cracks because I often misread what I’ve written. I sometimes don’t find it until I come back 2 weeks later.

    Thank you for your corrections and all of your editorial improvements of what I’ve written. You’ve helped me present my ideas better. Thank you.

  32. 32
    sigaba says:

    We’ll try, but with a readership of about 100, I view this blog as draft and trial areas for ideas to get free editorial and peer review.

    You’ve gotta be kidding me. These are the foundations of a new science?

    Spelling errors are probably because everyone upgraded their Macs and the autocorrector is working overtime.

  33. 33
    PaV says:

    wd400 [@5]:

    Dear me, frequency dependant selection is not a new discovery.

    Case closed, apparently. “It’s simple, PaV, we’ve known about this for a long time….”

    Really. This ISN’T “frequency dependent selection.”

    “Alleles” are being INTRODUCED into an otherwise ‘identical’ line of organisms. If they introduce 5, or less, of the variant type worm into a population of 100 worms, then the ‘allele’ is ‘beneficial.’ If more than 5, then it’s ‘deleterious.’ Tell me, is NS math proficient?

    This isn’t “competition” between alleles—as is frequency dependent selection—this is, rather, a determination of “how” the newly introduced ‘alleles’ will be treated.

    When you react to something like this with the “we’ve known this all along” attitude, then how in the world will you ever get around to critically questioning the theory you embrace.

    Let’s look at the implications involved here. First, the use of the terms ‘beneficial’ and ‘deleterious’ probably just mean that the “frequency” of the alleles are either ‘increasing’ or ‘decreasing’ within the population as the generations proceed. Second, if ‘selection’ is at the level of the ‘individual’, then how in the world can ‘selection’ decide whether to treat the new alleles as ‘beneficial’ or ‘deleterious’? They’re the same ‘alleles’ whether they represent 10 individuals among 100, or only 2 individuals among 100. That’s why I asked if NS is math proficient. Third, the only reasonable and logical explanation is that the population—not the individual—is responsible for deciding whether or not the new allele should be treated as ‘beneficial’ or ‘deleterious.’ Fourth, this is only possible if there is some way in which the individuals in the population are somehow ‘signaling’ to one another. [We now know that horizontal gene transfer is not limited only to bacteria. Here we have a self-fertilizing (or asexually reproducing) population; so they’re NOT communicating via their the sharing of genes ‘directly,’ so, it shouldn’t be surprising that they do so ‘indirectly.’] If this is true, then, as I stated in the OP, this means that “selection” is dependent on the genome, and not the other way around; although here, we might say ‘selection’ is dependent on the ‘collective’ genome.

    IDists are accused of “stopping science.” And, yet, this absolute certainty in Darwinism stops you, wd400, from asking the appropriate questions; whereas, I move on to ponder the implications that might be involved.

    Elizabeth Liddle: this criticism might also apply to you.

    “To those who have ears, listen!” I’ve just pointed out what an enterprising young biologist might want to explore.

  34. 34
    PaV says:

    Elizabeth Liddle: [@6}

    PaV, absolutely nothing in that paper poses any problem for evolutionary theory at all! It’s a very elegant paper, and it demonstrates empirically a very important evolutionary principle.

    But, Elizabeth, the authors themselves say: “But our results show that further empirical work and more theoretical models are required to accurately predict the fate of that allele over long time spans”.

    So, “nothing in that paper poses problems for evolutionary theory,” and, yet, the authors tell us that “more theoretical models are needed”? Seems like they think something’s wrong.

    Evolutionary theory is about reproductive success in the current environment. That environment includes other populations in the habitat, as well as your own.

    From the article: “Taking advantage of C. elegans’ characteristics, Ivo Chelo and Judit Nédli used two lines of C. elegans to establish competition assays and see which individuals could survive and reproduce better.

    IOW, they took TWO populations. One population was MORE FIT than the other. When they introduced a high number of “more fit” alleles into the “less fit” population, they were treated as if they were “less fit.” Please explain this to me.

  35. 35
    lifepsy says:

    Elizabeth,

    This is exactly why crude models of population genetics don’t work – the allele frequency itself alters the environment that determines the selection coefficient of the allele.

    Elizabeth, can you kindly link to the “working” pop-gen experiments?

    (bonus: experiments that don’t involve maximum selection coefficients, where lack of trait leads to certain death)

  36. 36
    lifepsy says:

    Then there is this fruit-fly selection study from 2010

    http://www.nature.com/nature/j.....09352.html

    Genome-wide analysis of a long-term evolution experiment with Drosophila

    Burke et al. 2010

    Experimental evolution systems allow the genomic study of adaptation, and so far this has been done primarily in asexual systems with small genomes, such as bacteria and yeast. Here we present whole-genome resequencing data from Drosophila melanogaster populations that have experienced over 600 generations of laboratory selection for accelerated development. Flies in these selected populations develop from egg to adult ~20% faster than flies of ancestral control populations, and have evolved a number of other correlated phenotypes….

    Signatures of selection are qualitatively different than what has been observed in asexual species; in our sexual populations, adaptation is not associated with ‘classic’ sweeps whereby newly arising, unconditionally advantageous mutations become fixed…

    We conclude that, at least for life history characters such as development time, unconditionally advantageous alleles rarely arise, are associated with small net fitness gains or cannot fix because selection coefficients change over time.

    In other words, reaching reproductive age 20% faster was not translated as enough of a gain in reproductive fitness for the trait to become fixated in a population. (classic sweep)

    Yet you guys believe a deer-like creature will be on its way to becoming a whale in comparable time-frames… so ridiculous.

  37. 37
    lifepsy says:

    wd400 [@5]:

    Dear me, frequency dependant selection is not a new discovery.

    PaV,
    Case closed, apparently. “It’s simple, PaV, we’ve known about this for a long time….”

    This is a very common evolutionist tactic. If something problematic is discovered, they will refer back to some unusual study done years ago and say “See? We already knew about this!” As if it is some kind of counter-argument.

    I guess they figure it provides the illusion that the problem has been dealt with… or since the problem’s been around so long and evolutionism is still getting published, then it must not be that bad.

  38. 38
    wd400 says:

    PaV,

    The reason I used the term Frequency Dependant Selection (FDS) was so that you might go off and read a little about this well researched phenomenon. If you do that, you’ll find the idea that “NS” (or, in fact, nematodes) have to be math-proficient for FDS to work is just not right.

  39. 39
    Mung says:

    So how is Elizabeth equivocating you ask? It’s simple. In one breath she speaks of diversity within a population, and then in the next speaks of diversity across taxa.

    Her initial “point” had to do with populations and the differences between individual members of the population, a “point” which she still has not defended.

    http://en.wikipedia.org/wiki/Genetic_variation

  40. 40
    PaV says:

    wd400:

    The reason I used the term Frequency Dependant Selection (FDS) was so that you might go off and read a little about this well researched phenomenon.

    Well, doesn’t this remark of yours imply that I HAVEN’T read about FDS? Well, of course, it does. But I have read about it. Kimura explains it quite nicely in his The Neutral Theory.

    But, again, this ISN’T FDS. This should be obvious. Why you have a need to pigeon-hole this experiment into FDS is puzzling. That you are incorrect in your assessment is made clear by asking this simple question: “If this were no more than FDS, then why are the authors quoted as saying: ‘But our results show that further empirical work and more theoretical models are required to accurately predict the fate of that allele over long time spans’?”

    Look at what I posted @34 in response to Elizabeth.

    Your implicit assumption in this matter is that ‘selection’ acts differently in different environments, or in different circumstances, and, that, given these ‘different environments’ either ‘allele A’ or ‘allele B’ is preferred, and that ‘selection’ simple acts accordingly. However, as I pointed out to Elizabeth, we’re dealing here with TWO populations that are then mixed together in various proportions. INDEPENDENTLY of the ‘mixing,’ ‘allele A’, let’s say, has been shown to be MORE FIT than ‘allele B’ in some given environment. Presumably (I don’t have full access to the original article), when the populations are ‘mixed,’ this SAME environment is the one being used.

    And, yet, ‘selection’ acts as though ‘allele A’ is ‘deleterious’, or LESS FIT, solely on the basis of whether or not it is being introduced into the larger population at, or above, a certain percentage (frequency). The very simple question then is this: “How in the world does ‘selection’ KNOW what the percentage (frequency) of ‘allele A’ IS [in the first place]—let alone, how MUCH it should be.?”

    Could you answer these questions for me?

  41. 41
    wd400 says:

    nd, yet, ‘selection’ acts as though ‘allele A’ is ‘deleterious’, or LESS FIT, solely on the basis of whether or not it is being introduced into the larger population at, or above, a certain percentage (frequency)

    Yeah – it’s fitness is dependent on it’s frequency, which is called frequency dependent selection. A balanced polymorphism like this presumable arises when the alleles under selection compete at some level. If I had to guess, and given the set up of the experiment, I’d say the alleles under selection are involved in metabolism. With one allele letting nematodes make use of scarce resource. One that allele is common the benefit dissipates as the resource is competed for (i.e. selection is density-dependent) so the allele’s fitness is determined in part by how many nematodes carry it.

    As I say, the specifics are a guess. But that doesn’t require math-ability of the behalf of nematodes of a mystical thing called “Selection”. I hope the researchers are sequencing there strains, as it will be exciting to see how is underlying the processes they describe.

  42. 42
    Mung says:

    Wikipedia:

    Frequency-dependent selection is the term given to an evolutionary process where the fitness of a phenotype is dependent on its frequency relative to other phenotypes in a given population.

    Ridley:

    Frequency-dependent selection occurs when the fitness of a genotype depends on its frequency.

    lol

  43. 43
    wd400 says:

    Though it does tell you something about Ridley’s approach to biology, I don’t think that’s a particularly difference is it Mung?

    A genotype’s fitness is determined by it phenotype, after all.

  44. 44
    PaV says:

    Apprently the article is open access. Here’s the link.

    wd400:f I had to guess, and given the set up of the experiment, I’d say the alleles under selection are involved in metabolism. With one allele letting nematodes make use of scarce resource. One that allele is common the benefit dissipates as the resource is competed for (i.e. selection is density-dependent) so the allele’s fitness is determined in part by how many nematodes carry it.

    It turns out that they used inbred lines as ‘surrogates’ for an allele.

    The reason this is NOT FDS is due to the fact that a particular ‘allele’ is NOT being selected for, or kept in balance. Instead, it is the organism itself, the lineage. The GFP (introgrossed Green Flourescent Protein line) is beneficial below 5% and above 93%. The only ‘stable’ equilibrium point (between lineages!) is at 5%.

    When between 5 and 93%, however, selection will be against the GFP allele. In other words, there was frequency-dependent selection among the two inbred lines.

    (N.B. The GFP ‘allele’ is no more than a ‘proxy’ for the lineage.)

    This is completely in line with what I wrote @33: Here we have a self-fertilizing (or asexually reproducing) population; so they’re NOT communicating via their the sharing of genes ‘directly,’ so, it shouldn’t be surprising that they do so ‘indirectly.’] If this is true, then, as I stated in the OP, this means that “selection” is dependent on the genome, and not the other way around; although here, we might say ‘selection’ is dependent on the ‘collective’ genome.

    Let’s remember that the GFP is ‘more fit’ than the other, ‘wildtype’, lineage. This then means that SELECTION somehow determines that the GFP are ‘more fit’ up to 5% of the population, then ‘less fit’ from 6% to 92%, and then, at 93% decides that it is ‘more fit’ again. Remember, SELECTION is none other than either ‘death,’ or ‘sterility.’ They say that the effects they see are the same at the L1 ‘larval stage’ as it is for adults. This means that ‘death’ is likely not involved; i.e., ‘selection’ is not making a distinction from the time the worm was at the larval stage up to the time of its being an adult. And, presumably as an adult, being ‘more fit’ the GFP’s should have an advantage; but we don’t see this. Thus, it is most likely that something happens before the L1 stage, including some kind of limitation in the number of offspring being produced; i,.e., a loss of fertility (outright ‘sterility’ was not reported).

    The authors say: “It is possible that underlying frequency-dependent selection are differences in the reproductive behaviour of the two inbred lines, as they seem to differ in embryo laying and embryo retention rates, as well as in successfully propagating themselves in our speci?c culture protocol . . ..

    From this vantage point, what I said @33 also applies:

    Third, the only reasonable and logical explanation is that the population—not the individual—is responsible for deciding whether or not the new allele should be treated as ‘beneficial’ or ‘deleterious.’ Fourth, this is only possible if there is some way in which the individuals in the population are somehow ‘signaling’ to one another. [We now know that horizontal gene transfer is not limited only to bacteria.

    Indeed, this “signaling” could easily take the form of some specific protein directly affecting fertility. It could be the case that the ‘wild type’ population (less fit) produces some ‘signaling’ protein with the ability to diminish the number of offspring produced, but which, in the case of the ‘wild type’s, is counteracted by another protein, or by some regulatory network that negates its effect.

    This is NOT FDS. And it points to chemical signaling by the population as a whole. IOW, ‘selection’ is but a phantom here—as it very well could be in many other places as well. There is, we know, the whole new world of ‘epigenetics’ that is opening up. NS, and Darwinism, are unlikely survivors.

    But that doesn’t require math-ability of the behalf of nematodes of a mystical thing called “Selection”.

    Would you have us believe that a lineage that is known to be ‘more fit’ than another lineage, when introduced at a frequency between 6% and 92%, will be treated by ‘selection’ as ‘less fit.’ On what basis? Remember, they’re reproducing asexually via hemaprodites. The lineages are not changing; they’re simply competing. And yet we’re to believe that ‘selection’ can decide: “Oh, it’s too high; let me eliminate some. Oh. its frequency is not high enough. Let me eliminate some.” What’s your explanation?

  45. 45
    wd400 says:

    I really have no idea what you insist all calling this something other that what it is (and what the authors call it, for that matter).

    Yes the GFP is a marker for many different alleles at which the two isogenic lines will differ. I don’t see how that changes anything but for the fact we dont’ know which alleles are giving rise to the pattern of frequency dependance.

  46. 46
    PaV says:

    I really have no idea why you think using a term used for ‘one’ allele can now just magically be applied to the entire genome.

    It’s as if having a term to describe the phenomena is all you need. It gives you a sense of knowing what’s going on.

    But, of course, you don’t know at all. And, so, SCIENCE STOPS. “Oh, this is just FDS.” End of story. Case closed.

    That the GFP lineage is ‘more fit’ than the ‘wild type’ is a FACT.

    And, yet, supposedly, SELECTION treats it as ‘more fit’ or ‘less fit’. How in the world can “selection,’ which is, of course, operative when it is determined that the GFP line is ‘more fit’, turn around and now decide it is ‘less fit’? This REQUIRES AN EXPLANATION; NOT A NAME.

    I have argued more than once that EVENTUALLY Darwinism will be put to the one side; but in the meantime so much valuable time is wasted. Why? Because Darwinism is completely misguided and has scientists asking the wrong questions. But in this case, it has scientists asking NO questions.

    What a pity.

    Don’t bother responding. We’re now arguing over the obvious. You choose to deny it. I don’t. Let’s leave it at that.

  47. 47
    wd400 says:

    And, yet, supposedly, SELECTION treats it as ‘more fit’ or ‘less fit’. How in the world can “selection,’ which is, of course, operative when it is determined that the GFP line is ‘more fit’, turn around and now decide it is ‘less fit’?

    Because genes and other nematodes are part of the environment. The environment changed, so did the fitness function for each of these lines.

    But, of course, you don’t know at all. And, so, SCIENCE STOPS. “Oh, this is just FDS. End of story. Case closed.And, yet, supposedly, SELECTION treats it as ‘more fit’ or ‘less fit’. How in the world can “selection,’ which is, of course, operative when it is determined that the GFP line is ‘more fit’, turn around and now decide it is ‘less fit’?

    I described a simple model – a density-dependent process. As for stopping science – about three comments I go I said I hope those guys are sequencing their lines, because it would exciting to see how the the frequency-dependence they demonstrate arises. So, I’d like them to keep doing science.

    I’m very happy to leave it here, but I can’t agree it’s at all obvious that this pattern can’t arise from frequency-dependent selection

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