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John Davison, Are You Listening?

I haven’t even read the entire article yet. But I just had to post this. From what little I’ve read, this Physorg.com article positively jives with Davison’s theory on evolution.

And this “old” theory has now proven to exist in nature because we now have “the ability to sequence whole genomes”. As has constantly been said on this blog, as science progresses, Darwinism will regress.

The finding, reported in today’s issue of Science, reveals that scientists must reassess the processes involved in the origin of species. The beginnings of speciation, suggests the paper, can be triggered by genes that change their locations in a genome.

“In the 1930s there was speculation that parts of chromosomes that switch from one location to another might cause a species to split into two different species,” says John Paul Masly, lead author of the paper and doctoral student at the University of Rochester. “Showing that it was more than an academic idea was difficult, and required a bit of luck. Other genetic causes of speciation are clearly documented in nature, and it wasn’t until we had the ability to sequence whole genomes that we could even attempt to investigate the question.”

Curiously, the hypothesis nearly died twice.

Theodosius Dobzhansky, a well-known evolutionary geneticist, studied fruit flies in the infant days of genetic research in 1930. He mapped out how it might be possible for sections of chromosomes to relocate themselves in a genome. Those mobile sections can cause sterility in inter-species hybrids, which can act as a speciation pressure.

In theory, the idea was sound, but scientists long debated whether it actually happened in nature. Eventually a competing theory involving the gradual accumulation of mutations was shown to occur in nature so often that geneticists largely dismissed the moving gene hypothesis.

So there you have it. Science can now confirm that Davison’s theory acutally exists, while there is no evidence that RM+NS has ever brought about macroevolution. I wonder what the NCSE is thinking right now.

Masly’s work shows a back door through which speciation can start. If the right genes jump around in the genome, a population can begin creating individuals that can’t successfully mate with the general population. If other speciation pressures, like geographic isolation, are added to the mix, the pressure may be enough to split one species into two new species.

Here’s the link to PhysOrg.com

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192 Responses to John Davison, Are You Listening?

  1. \”As science progresses, Darwinism will regress.\” Here\’s a link to an article at \”New Scientist\”:

    Here\’s the link: http://www.newscientist.com/ar.....books.html

    And here\’s the first paragraph:
    Molecular biology textbooks will need a little tweaking. Researchers have discovered a bizarre “Frankenstein protein” on the surface of leukaemia cells, with peptides stitched together in reverse order to that coded for by their DNA template.

  2. PaV, I don’t understand why you draw the conclusion you do about this study. Having parts of genes switch locations is a type of mutation, different than a point mutation but a mutation nonetheless. In plants it is well known that some speciation happens ofter, and reproducibly, through gene duplication, another form of mutation different than point mutation.

    Furthermore, the new species formed would be a new species primarily because of the inability to breed with the firmer species, but not because they were substantially different morphologically.

    And last, natural selection would still be operable in that if the new species was viable enough to grow as a separate population within the same environment as the original species, even small differences between the two could eventually lead to one (the original or the new) succeeding while the other failed.

  3. “Having parts of genes switch locations is a type of mutation, different than a point mutation but a mutation nonetheless.”

    But they aren’t _random_ mutations. Jumping genes are well-defined semantic units. They don’t split out arbitrarily, they split out across fairly well-defined boundaries. And, these jumping genes often just so happen to correspond to functional domains of proteins, or other such “functional unit”. So the “jumping unit” closely corresponds to the “jumping unit”. The question is, is this just a bizarre coincidence? Or is the genome made for specific acts of change?

    “In plants it is well known that some speciation happens ofter, and reproducibly, through gene duplication”

    Often and reproducibly. Why, that’s the opposite of random mutation! You have _reproduceable_ evolution. That indicates that the direction of the evolution is preprogrammed.

    I keep on having this nagging suspicion that Darwinists don’t really even know what the debate is about.

  4. The problem of the origin of novel genetic information persists. Genes jumping around might mix and match existing information, just as sexual reproduction does, but it can’t account for genuinely new information. Random mutation can’t account for it because of hopelessly monstrous combinatoric improbabilities. On this subject it should be admitted by evolutionary theorists that all they have is wild speculation, but they don’t. They speculate, declare the problem solved, and teach speculation as fact. That’s how science works.

  5. johnnyb said, “Often and reproducibly. Why, that’s the opposite of random mutation!”

    Are you suggesting that random phenomena are by definition completely unpredictable?

  6. They speculate, declare the problem solved, and teach speculation as fact. That’s how science works.

    For someone who seems to have a keen interest in intelligent design as science, you also seem to indicate tremendous contempt for science and for scientists.

    And then you wonder why ID critics think that ID supporters are anti-intellectual? Best get your own house in order, methinks.

  7. jonnyb wrote: “But they aren’t _random_ mutations. Jumping genes are well-defined semantic units. They don’t split out arbitrarily, they split out across fairly well-defined boundaries. And, these jumping genes often just so happen to correspond to functional domains of proteins, or other such “functional unit”.”

    I guess that settles it. They aren’t random (by your definition). And a purely naturalistic evolutionary theory has to, by definition, only use totally random mutations??? Is that what you are implying?

    I’m not entirely sure of what you’re alluding to when saying “And, these jumping genes often just so happen to correspond to functional domains of proteins, or other such “functional unit”.”. Should we be surprised if a jumping gene is “functional”? Mobile genetic elements such as transposons and insertion sequences contain genes whose protein products are able to catalyze the excision and insertion of themselves from one place to another (they are, thus, functional). For some of them, the place of insertion appears to be random, while others must insert into a certain sequence (=non-random).

  8. 8

    I’m listening but I won’t participate until my several papers are restored to the side board. I hope Uncmmon Descent can understand my position.

  9. But they aren’t _random_ mutations. Jumping genes are well-defined semantic units.

    Actually, then, by your definition point mutations aren’t random either. You will never get anything other than an A,T,G or C (pretty well-defined units). And aside from that, certain mutagens cause particular mutations and not other. UV light, for example, tends to fuse adenosine rings (I think, it’s been awhile since I’ve studied genetics). Long stretches of repeated nucleotides or short sequences are more frequently botched by the polymerase. Etc, etc, etc.

  10. “For someone who seems to have a keen interest in intelligent design as science, you also seem to indicate tremendous contempt for science and for scientists.” – Carlos

    I have a certain amount of contempt for the legal profession because of what the lawyer culture and lawyer organizations have become. That doesn’t mean I don’t hold many lawyers in high regard, and it certainly doesn’t mean I have contempt for the law!

    Scientists should not protect themselves from criticism by wrapping their biases, personal ambitions, and philosophical assumptions in “Science”.

  11. “And then you wonder why ID critics think that ID supporters are anti-intellectual? Best get your own house in order, methinks.”

    Comment by Carlos — September 8, 2006 @ 9:04 am

    Carlos, you apparently don’t read any of the critics of ID:

    * Intenional or negligent conflation of ID with Creationism;
    * Rejection of peer-review submissions, then criticism that “no ID papers are peer-reviewed”, even as those who actually publish such papers are hounded and persecuted;
    * Misrepresentations of ID in science journals in which rebutals are rejected;
    * Public workplace “shunning” of professors who support ID.
    * Suppression of ID so that students are not exposed to ID or even criticism of NDE.

    Methinks you need to dump your double standard before passing judgement on Gil or anyone else.

  12. Gil: “They speculate, declare the problem solved, and teach speculation as fact. That’s how science works.”

    Carlos: “For someone who seems to have a keen interest in intelligent design as science, you also seem to indicate tremendous contempt for science and for scientists.”

    Contempt for science? How on earth did you arrive at this conclusion from what I said? (Perhaps you didn’t detect the sarcasm in my comment regarding RM+NS speculation taught as fact: “That’s how science works.” Those who question the adequacy of orthodox Darwinian theory are always told that they don’t know how science works.)

    RM+NS is touted as an explanation for all of life’s diversity, complexity, information content and functionally integrated machinery, when it is nothing more than speculation. But it is presented, and taught, as a fact as certain as the fact that the earth orbits the sun. This is what I have contempt for.

    I do science every day. In aeronautical engineering we can actually test our hypotheses. If it flies, we were right. If it crashes, we were wrong. We never declare the problem solved until we perform the flight tests.

    ID proponents do not present their theses as established fact, as do Darwinists. ID proponents present their theses as inferences to the best explanation based on the known cause-and-effect structure of the world.

  13. UV light, for example, tends to fuse adenosine rings (I think, it’s been awhile since I’ve studied genetics)

    Thymidine, actually. So mutations induced by UV damage aren’t exactly “random,” as they only (as far as I know) occur when there are two consecutive thymidines.

  14. A summary of my critics:

    “Are you suggesting that random phenomena are by definition completely unpredictable?”

    “Actually, then, by your definition point mutations aren’t random either. You will never get anything other than an A,T,G or C (pretty well-defined units).”

    “I guess that settles it. They aren’t random (by your definition). And a purely naturalistic evolutionary theory has to, by definition, only use totally random mutations??? Is that what you are implying?”

    It seems you have all missed the point, but I think it is my fault for explaining it poorly. Let’s go to Berkeley’s definition of randomness with respect to genetics:

    In this respect, mutations are random—whether a particular mutation happens or not is generally unrelated to how useful that mutation would be.

    The point is that in all of these cases, the “jumpiness” of a gene is VERY related to how useful it is for that gene to be jumpy. MORE mutations occur in places that are likely to produce beneficial changes than in those places which are not. It’s not that the mutations have to be “random” in a mathematical sense in order to be ateleological, but that if the mutational bias is consistently in the direction of adaptation or even just “making biological sense” (as in the jumping of discrete protein domains), then it is clear evidence that this was engineered to be the case.

    Now, I actually believe that there also exists a certain degree of _constrained_ mathematical randomness in mutation, but that the constraints are set up so that it consistently gives you biologically sensical results. For an example of a mechanism to do that, see here.

  15. Also to point out, ALL phylogenies based on homology are based on the idea of random mutations (if organism X has the exact same pattern (tissue, bone structure, etc.) as organism Y it must be because of a shared common ancestor with that pattern. If random mutation is not correct, then it is very possible that two children could “evolve” the _exact same_ organ independently. Thus, if random mutations are found to be directed, then pretty much all phylogenetic trees need to be re-examined, and perhaps even the notion of morphological tree-building would be called into question.

  16. The point is that in all of these cases, the “jumpiness” of a gene is VERY related to how useful it is for that gene to be jumpy. MORE mutations occur in places that are likely to produce beneficial changes than in those places which are not.

    There is no support in the linked paper for either of those assertions.

  17. In regard to Dr. Davison’s papers on the sideboard, if someone else wants to gather them together and reformat for html (they are mostly pdf as I recall) and save them as drafts or mail them to me as attachments or otherwise provide them to me ready to cut & paste I’ll put them back on the sideboard. Some or most of them already exist in html format in the archived articles here. Doctor Davison also requested they be listed in chronological order. The WP software has no provision for that. It sorts them alphabetically. A little creative titling should solve that problem.

    Before I do this I need a promise from Doctor Davison that he’ll remain civil with everyone here including me, he’ll respect the beliefs of even the most profoundly religious members here, he’ll strictly avoid writing anything obscene or suggestive of something obscene (sex, bodily fluids, etcetera), and will otherwise not use language inappropriate for young ears. Bill, Denyse, and I all agree that we want a G-rated blog suitable for all audiences. No exceptions.

    I realize that I am guilty of breaking these rules in the past, especially in regard to respecting the beliefs of others, and for that I offer my humble apology. It was wrong of me.

  18. Gil,

    Although I’m something of a “Darwinist,” perhaps a very heterodox “Darwinist,” I would not want contemporary evolutionary theory taught as fact. (This is partly because of philosophical uneasiness I feel with respect to the very notion of a “fact.” The more I do philosophy, the more I understand Socrates’ remark in Meno that he does not undertake to resolve perplexity, but to infect others with the perplexity that he himself experiences.) But I would want it taught as an inference to the best explanation.

    So, in response to

    ID proponents do not present their theses as established fact, as do Darwinists. ID proponents present their theses as inferences to the best explanation based on the known cause-and-effect structure of the world.

    I don’t think that ID theorists have any claim on epistemic humility over and against evolutionary theorists, Dawkins bravado notwithstanding. ID theorists and evolutionists are competing on precisely the same terrain: the terrain of inference to the best explanation.

    Incidentally, this is where it seems very clear to me that creationism and intelligent design are different: intelligent design is a candidate for inference to the best explanation, whereas creationism is not even an explanation. It’s just that intelligent design is not a good inference to the best explanation. For while evolutionary theory doesn’t give us everything we want — as noted here many times, the origins of life and of complex structures are its Achilles heel — intelligent design gives us even less.

    En garde!

  19. “There is no support in the linked paper for either of those assertions.”

    I feel silly actually having to point this out, but there is more in biology than what is contained in this paper.

  20. I feel silly actually having to point this out, but there is more in biology than what is contained in this paper.

    Great. Please point me towards the “more in biology” that supports the assertions.

  21. Johnnyb:

    “there is more to biology than what is contained in this paper.”

    Agreed. So when you say:

    “in all of these cases, the ‘jumpiness’ of a gene is VERY related to how useful it is for that gene to be jumpy. MORE mutations occur in places that are likely to produce beneficial changes than in those places which are not.”

    Can you provide me with the source of that information? The reason I ask is the issue of speciation is of particular interest to me and mutations being more likely (or even much more likely) to have a positive direction would be a huge finding.

  22. Carlos:
    ID theorists and evolutionists are competing on precisely the same terrain: the terrain of inference to the best explanation.

    And design (ID) is a better explanation than “sheer-dumb-luck” (the materialistic alternative to ID).

    Carlos:
    It’s just that intelligent design is not a good inference to the best explanation.

    Considering the materialistic alternative you can’t be serious (and I didn’t call you Shirley).

  23. 23

    I will promise nothing to David Sprnger or anyone else [remainder deleted]

  24. Have it your way, John. Your papers will not be restored and you\’re back to having all your comments requiring approval by an editor before seeing the light of day.

  25. Joseph,

    Thanks for not calling me Shirley!

    You’re right to point out that evolutionary theory insists on the reality of contingency (“it could have gone down differently” and the reality of variation (there are no “kinds”). And that’s a barbed hook, for many.

    But intelligent design has plenty of barbed hooks of its own. The design inference, if it works, would only allow us to sort biological and physical structures into two categories: those that were designed, and those that weren’t. That might look like a lot right there, but it isn’t — because intelligent design does not, so far as I know, propose any further investigation or exploration besides classifying things into one of those two categories.

    One final point: I’ll defend a heterodox version of Darwinism, up to a point, but I’m not a materialist. Materialism has too many serious problems for me to find it worth defending.

    For example: if all properties are reducible to material properties — and it looks as though materialism would have to be committed to that — that would have to include at least:

    - aesthetic properties (the beauty or sublimity of a painting);
    - semantic properties (the meaning of a sentence or utterance);
    - moral properties (the rightness or wrongness of an action or intention);
    - aletheic properties (the truth or falsity of an assertion).

    These are all fundamentally normative concepts, and I don’t see how normativity can be accomodated within materialism, as materialism is usually construed. So I reject materialism, but not (some suitably heterodox version of) “Darwinism.”

    In this respect I’m a nice complement to John Davison, who is a materialist but not a Darwinist.

  26. First of all, will someone _please_ switch off magic_quotes_gpc from the server config? All those backslashes are starting to annoy me.

    As to jumping genes, I’ll give some review references at the end, but you may be interested in Shapiro’s talk (part 1, part 2) on the subject, where he states something to the effect of “in every case which has been studied, transposon insertion is a highly regulated process” (this quote, IIRC, is towards the end of part 2).

    A quick example of a very regulated jumping gene is Transposable elements as activators of cryptic genes in E. coli.

    Interestingly, this sort of an idea is actually what the original discoverer of transposable elements thought (I forget her name), and she called them “controlling elements”. This idea of elements controlling evolution was disturbing to Darwinists, who quickly relabelled them as parasites.

    Here are some reviews done by Shapiro and Sternberg:

    How Repeated Retroelements Format Genome Function

    Why Repetitive DNA is Essential to Genome Function

    Retrotransposons and Regulatory Suites

    Transposable Elements as a Key to a 21st Century View of Evolution

  27. I forgot to point out, the first two Shapiro and Sternberg papers have tables which show functions being found for every type of repetitive and mobile element.

    Also, we had an earlier review here on UD including information about some repetitive elements used as tuning knobs in the genome.

  28. PaV:

    After looking at the science paper and doing a genome search on the relevant gene in simulans, I don’t think that anyone can say with certainty that this particular relocation was caused by the classic retrotransposition mechanism. It may have been, particularly if it happened a long time ago, but the classic signs are no longer present. Typically, a transposition that is the result of the classic “jumping gene” reverse transcription mechanism will lack introns, and show other signs of having been copied from mRNA. In this case, the sequence doesn’t seem to show that. The D. simulans version seems to have introns of about the same size and in about the same positions as the D. melanogaster version. There are other mechanisms for movement of chunks of chromosomes, and some of these are fairly common in Drosophila – and known to be involved in species differences. This one seems to differ mostly in that it is a between-chromosome movement rather than the more common chromosome segment inversion.

    The physorg article really seems to be a lot more excited about this paper than it warrents. It’s a cool paper, and it demonstrates something that hasn’t been seen before, but it’s not going to radically change our understanding of speciation. We know, as the physorg article points out, that there is a great deal of evidence for the gradual accumulation of mutations model of separation – Coyne & Orr’s book Speciation provides an excellent review of several of those instances. Reproductive isolation is the key to understanding speciation, and there are already many different known mechanisms which can (and do) contribute to reproductive isolation. The Masly et al article identifies yet another mechanism for reproductive isolation, but it does not invalidate any of the other mechanisms.

  29. Carlos:
    That might look like a lot right there, but it isn’t — because intelligent design does not, so far as I know, propose any further investigation or exploration besides classifying things into one of those two categories.

    Intelligent Design is the study of patterns in nature that are best explained as the result of intelligence. — William A. Dembski

    Got it? If not try this:

    Scott Minnich

    Biochemist Michael Behe used the flagella to illustrate the concept of irreducible complexity and Minnich takes the argument to the next level crediting the design paradigm to leading to new insights in his lab research at the University of Idaho.

    Detection and understanding. Understanding by studying. Studying to understand. Understood?

    Oh and as for contigency:

    Unified physics theory explains animals’ running, flying and swimming:

    The findings may have implications for understanding animal evolution, Marden said. One view of evolution holds that it is not a purely deterministic process; that history is full of chance and historical contingency. It is the idea purported by Steven Jay Gould and others that if you were to “rewind the tape” and run it again, evolution would proceed down a different path, Marden said.

    “Our finding that animal locomotion adheres to constructal theory tells us that — even though you couldn’t predict exactly what animals would look like if you started evolution over on earth, or it happened on another planet — with a given gravity and density of their tissues, the same basic patterns of their design would evolve again,” Marden said.

    For me that explains “convergence”…

  30. Carlos,

    You should take the UD challenge and be the first person to provide a coherent defense of neo Darwinism. So far no one has been able to do it so we are waiting for someone to step up to the plate and deliver.

    By the way over the last couple weeks I watched a complete course section (15 lectures) from a UC Berkeley biology class on evolution and they were not able to do it. In fact the professor falsified Darwin’s theory in his second lecture.

    Lots of accolades await the first person who can do it. You never see it in the popular press or even the scientific press. All you hear is that the evidence is so overwhelming that no one in biology doubts it but somehow they are hiding this overwhelming evidence. Maybe you could share it with us.

    You don’t have to defend materialism only Darwinism.

  31. carlos: “But I would want it taught as an inference to the best explanation.”

    I hope you mean best materialistic, anti-ID explanation.

  32. I hope you mean best materialistic, anti-ID explanation.

    I cam see why you’d hope for me to say that — because I’m such a nice and reasonable guy, you’d hate to have to disagree with me, right?

    Well, I’m sorry to disappoint, but by “best explanation” what I really meant was “best explanation”, i.e. the best explanation that we’ve been able to come up with so far.

    You should take the UD challenge and be the first person to provide a coherent defense of neo Darwinism. So far no one has been able to do it so we are waiting for someone to step up to the plate and deliver.

    And just who is supposed to determine what “the UD challenge” is? If you can justify to my satisfaction why “you” (the collective you of ID supporters and critical sympathizers) are even in the position to tell me where the bar is set at, I’ll consider your “challenge.”

    I realize that I’m playing in your sandbox, but I like to think I’ve been respectful so far. And I’ll happily point out that my points have found more fertile soil here than they have among militant atheists, especially in my interactions with “avocationist” and “BarryA.” But while I want to continue to be conciliatory, there’s a limit to how far I’ll go, and letting you set the standard for what I have to accomplish qua heterodox Darwinian is going too far. Am I being unfair?

  33. Carlos,

    I think ID uses standard scientific techniques to classify some events as very low probability and thus unlikely to have happened by chance. It makes inferences based on evidence and to me that is science. But I am not necessarily a big advocate of ID as an area of science or a separate discipline so am not personally interested in defending it as such. Some others here are. I happen to think defending ID gets in the way sometimes because it becomes a lightning rod and deflects the discussion from what I think is the real issue. But that is me and not everyone who visits here.

    What I am interested in is the adequacy or inadequacy of neo Darwinism as a theory. How robust is it. It is claimed to be a very robust theory but I have yet to see evidence for this provided by anyone. That is why I watched the whole Berkeley course to see if they could do it. It is always interesting to see how various people dodge the issue of defending it.

    Why am I interested? Because it is taught in our schools as dogma starting in some places in kindergarten and yet no one can provide evidence in support of it. Doesn’t that bother you?

    If you think I am wrong then make a fool out of me and provide the evidence. By the way if you were able to do so, you would shut down this site because it would have no more reason for being. If you believe in something then you should say why. You have said “So I reject materialism, but not (some suitably heterodox version of ‘Darwinism.’” Stand up for what you believe. If it is a science, then cite the findings to support it. If it is based on faith, then so be it but then that belief is not science.

  34. jonnyb used this definition: “In this respect, mutations are random—whether a particular mutation happens or not is generally unrelated to how useful that mutation would be. “, and also wrote earlier:

    “Often and reproducibly. Why, that’s the opposite of random mutation! You have _reproduceable_ evolution. That indicates that the direction of the evolution is preprogrammed.”

    I’m wondering why you seem to be so hung up on the notion that there is a need for mutations to be random (in order to support evolutionary theory). You even mention in post 26 what is more or less said in Shapiros “Transposable Elements as a Key to a 21st Century View of Evolution”: “Since there is no reason to suppose that biochemical systems working on DNA are less subject to regulation than any other cellular functions, biological information-processing has the potential to play a major role
    in genome change during the course of organismal evolution.”

  35. johnnyb: “It’s not that the mutations have to be “random” in a mathematical sense in order to be ateleological, but that if the mutational bias is consistently in the direction of adaptation or even just “making biological sense” (as in the jumping of discrete protein domains), then it is clear evidence that this was engineered to be the case.”

    The operative part of your argument is “consistently in the direction of adaptation or even just making biological sense.” They are not; that view is simply not consistent with the data. You are being misled because the reports that you read about and find interesting are those infrequent cases where particular mutations do turn out to be beneficial. If you were to look at the literature more closely, look into existing and de-novo genomic variation as it appears in human or any other population, you’d find no systematic advantage to the commonplace mutations that arise. More often than not, *if* they do anything, it’s bad. That includes jumping genes. For every once incident of a jumping gene doing something positive, I can show you several more where it’s done something awful. If you objectively review what we know about mutations–look at *any* literature where a population’s dna has been sequenced at a given loci–the changes you find are best described as random.

  36. But they aren’t _random_ mutations. Jumping genes are well-defined semantic units.

    There are many kinds of statistical distributions. You seem to be thinking of “random” as being limited to a uniform probability distribution. This is not how scientists use the term. For example, if there are multiple possible locations to which a particular gene can translocate, and exactly where it will go is not predictable, then it will qualify as random in the sense used by scientists. Point mutations also do not have a uniform distribution. Some sequences mutate considerably more frequently than others. There is, of course, absolutely nothing in the theory of evolution that requires a uniform probability distribution. Darwin, of course, did not know about genes, and the original theory was quite vague as to the basis of mutation, and certainly did not propose any kind of statistical distribution. In developing more specific versions of the theory of natural selection, the relative contributions of different types of mutations have been extensively debated, with some favoring point mutations as occupying the major role and others more large scale rearrangements. Everybody agrees that both types of mutations have occurred in evolution, so the debate is entirely over which mechanism is more frequently important.

  37. jonnyb,

    I’m happy to see that you seem to be actually reading the literature that you cite. It’s a good first step. The problem remains, however, that your characterization of randomness, or your understanding of it, seems to be a little misbegotten. There’s also the problem of mechanisms, of course. It’s not enough to say “This thing appears to have jumped for a reason, so it must have jumped for a reason.” But therein lies the entire problem with ID, no?

  38. Jim Wynne,

    ID has no problem with mutations or randomness no matter what the definition or probability distribution. It has no problem with natural selection, genetic drift or whatever else causes differences in the allele distribution of populations. All it says is “that certain features of the universe and of living things are best explained by an intelligent cause rather than an undirected process such as natural selection.”

    The implication of this is that ID says that there are certain things that are so complex and so intricately inter-related that they could not happen by chance. We can argue over what events or phenomena fit that description.

  39. jerry: “ID has no problem with mutations or randomness no matter what the definition or probability distribution. It has no problem with natural selection, genetic drift or whatever else causes differences in the allele distribution of populations. All it says is “that certain features of the universe and of living things are best explained by an intelligent cause rather than an undirected process such as natural selection.”

    The implication of this is that ID says that there are certain things that are so complex and so intricately inter-related that they could not happen by chance. We can argue over what events or phenomena fit that description. just to make it clear to myself: don’t you have the order of arguments reversed?

    I thought the primary statement of ID was that certain things are so complex that they couldn’t happen by chance. And secondarily only, things are best explained by an intelligent cause rather that by an undirected process.

    Starting with an intelligent agent and then looking for a complex system to fit that notion: That is just what ID is accused of by many, and an impression that the ID camp is working mightily to avoid.

  40. Ofro,

    I have read your comment 4-5 times and haven’t a clue what you are talking about. The definition of ID used on this site is at

    http://www.uncommondescent.com/index.php

    from which I partially quoted in my first paragraph (comment #38). If my second paragraph is not consistent with that, then let me know.

  41. Jerry,
    sorry, my bad. I misunderstood your original statements. I agree, the two statements can be seen equivalent as opposed to a being logical sequence.

  42. Mike Dunford wrote: “This one seems to differ mostly in that it is a between-chromosome movement rather than the more common chromosome segment inversion.”

    I think this might qualify for the understatement of the year.

    ‘It’s a cool paper, and it demonstrates something that hasn’t been seen before, but it’s not going to radically change our understanding of speciation. “

    Then why are they invoking 70 year-old theories?

  43. It’s a cool paper, and it demonstrates something that hasn’t been seen before, but it’s not going to radically change our understanding of speciation. “

    Then why are they invoking 70 year-old theories?

    Mostly because it’s a 70-year-old hypothesis that until quite recently has been very, very difficult to test. I seem to recall seing some speculation in some papers from the 1970s and 1980s that chromosomal rearrangements might be implicated in speciation within the Hawaiian Drosophila (that’s the group I’m working with), but the most that they were able to do there was note the correspondence of different chromosomal banding patterns with different patterns of hybrid viability and fertility in different species. The ability to look at these sorts of things simply wasn’t there. At the same time, there was another hypothesis out there which involved the accumulation of mutations. That hypothesis was easier to test, was tested, and continues to look very, very solid. (Again, the new paper doesn’t argue against that mechanism, and we’ve known for quite a while that there isn’t a single mechanism involved in speciation, but rather several different mechanisms.)

    Genomics made it easier to test the chromosomal rearrangement hypothesis, and that is just what this grad student did. (Perhaps ironically, genomics didn’t stand still while he worked his ass off, so I was able to run a few searches on the computer and note the different chromosomal position of the gene in about 15 minutes, while it took him six years to find it working in the lab.)

    Again, this is absolutely fantastic work. It’s absolutely a science article, and I will definitely be taking some time in the very near future to think about how these results might apply to the system that I’m studying. This paper is very good science, and it definitely does very neatly resurrect a 70-year old hypothesis that was previously extremely difficult to test. However, this is not a paper that is going to fundamentally alter our understanding of speciation. It has added another mechanism to consider when looking at cases of speciation, and it has demonstrated another means of generating reproductive isolation. That’s very cool, it’s definitly very good work, and the guy that wrote it is going to go places. But it’s not a radical shift in our understanding of the field.

  44. PaV: “Then why are they invoking 70 year-old theories?”

    Because now there is empirical evidence to back up this particular type of mutation as being important. Conceptually, however, there is nothing fundamentally different from what is posited in current theory. Current theory holds that a mutation or series of mutations occur that make the offspring of the separated populations inviable or infertile. Perhaps the biggest question in speciation is, “how exactly can populations become reproductively isolated such that they embark on different evolutionary trajectories?”. Ironically enough, Darwin does not really address this in “Origin of species.” Although to be fair, it was only with advances in population genetics that we came to understand the homogenizing forces of gene-flow.
    This study provides one biological speciation genetic scenario, perhaps a much more important one than was commonly thought. But it doesn’t help ID in any way shape or form. It simply makes standard evolutionary explanations of speciation all the more plausible. This mutation most likely wasn’t advantageous to either proto-species population. Those flies that attempted to breed across populations had lower overall fitness in terms of fertile offspring. It probably took additional mutations in one or both populations, so-called “reinforcement”, to help them discriminate and not make the mistake of breeding with incompatible mates. This just illustrates that mating compatibility will ultimately break down with enough time. While this does nothing to rule out “prescribed” or “front-loaded” explanations in evolution, it is at least a small link in the chain of explaining why such proposals are superfluous. Once two populations start to go on independent evolutionary trajectories (i.e. they can no longer share genetic information) additional differences inevitably arise. This is the tiniest step on the road to explaining macroevolution.

  45. 46

    Here is a partial list of organelles that never had any precursors and appeared full blown as we see them now.
    1. centriole.
    2. centromere.
    3. bacterial flagellum.
    4. Eukaryotic flagellum.
    5. cell membrane.
    6. nuclear membrane.
    7. mitochondria and they are not transformed bacteria.
    8. bacteria in their several non-transformable types.
    9. every one of the animal phyla and the plant divisions, none of which can be comvincingly derived one from one another.
    10. many more structures and groups too numerous to mention.

  46. 47

    Population genetics has now and never had anything to do with creative evolution. It is just more Darwinian pablum.

  47. 48

    I am not only listening, I am trying to respond to those who question my Prescribed Evolutionary Hypothesis. I guess Uncommon Descent doesn’t need any help from the author of the PEH and the subject of this thread.

  48. I am not only listening, I am trying to respond to those who question my Prescribed Evolutionary Hypothesis. I guess Uncommon Descent doesn’t need any help from the author of the PEH and the subject of this thread.

    Sorry about that, John. Your comments were stuck in moderation.

  49. 50

    That’s fine. Just don’t let it happen again. What of course is unknown is what would have been done had I not complained both here and elsewhere, notably at “brainstorms.” And where is my other comment or is it comments. I can’t remember? They were far more significant than these. I am old you know and my short term memory is not what it used to be. What I do remenber is something my mother once told me. John, she said, it is only the squeeky wheel that gets the grease. Apparently this is an example of my mothers wisdom. Thank you mom!

    Oh I remember now. It was the one where I accused the Darwinians of being so weak minded as to believe that population genetics ever had anything whatsoever to do with creative evolution. See if you can’t cough that one up. As I recall it was one of my better efforts.

    If I can’t be treated as a peer here at Uncommon Descent I would prefer that you deny me the opportunity to submit messages. I don’t care to be treated as a second class citizen anywhere, anytime or anyplace and I am likely to make that widely known whenever and wherever it occurs, as I just did.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  50. 51

    Okay, much as I hate to ever have to say this, I now give my solemn promise in advance that will never make any lewd or vulgar remarks here at Uncommon Descent and humbly beg the blogczar to be granted the same priveleges as other contributors have here. If this is not sufficient, please have the common decency to outright ban me from wasting my time posting messages that may never appear.

    Maybe you could do what they did over at Panda’s Thumb. No matter where I said it, it immediately appeared on “The Bathroom Wall.” Or perhaps you could do what they did at EvC where it was “Boot Camp.” Heck, I will take whatever I can get. It is a cruel world out there don’t you know. But seriously, it is no fun for a published scientist to be treated as a second class citizen anywhere. I am sure you can understand.

    “I get no respect.”
    Rodney Dangerfield

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  51. “I’m wondering why you seem to be so hung up on the notion that there is a need for mutations to be random (in order to support evolutionary theory)”

    I think the issue is that you don’t understand Intelligent Design. Intelligent Design does _not_ say that evolution did not happen. It does _not_ even say that evolution did not proceed via purely naturalistic mechanisms. What it _does_ say, however, is that functional complexity does not evolve from undesigned sources. If evolution proceeds according to a directed process, there must have been a director somewhere in the causal chain. See for instance Dembski’s No Free Lunch, Searching Large Spaces or this paper.

    “It’s not enough to say “This thing appears to have jumped for a reason, so it must have jumped for a reason.” But therein lies the entire problem with ID, no?”

    Why is it that ID cannot make reasoned inferences, when the entire structure of evolution is based on inferences?

    “They are not; that view is simply not consistent with the data. You are being misled because the reports that you read about and find interesting are those infrequent cases where particular mutations do turn out to be beneficial. If you were to look at the literature more closely, look into existing and de-novo genomic variation as it appears in human or any other population, you’d find no systematic advantage to the commonplace mutations that arise.”

    Ahhh, but I think you do. I think the commonplace mutations are are hedges against future change, as I described here. They may be, in large part, neutral or degrading in the current context, but I think that the purpose of these things is to establish diversity to prevent total wipe-outs. This isn’t to say that degrading mutations don’t happen — I’m convinced that they do. But I think that the ones that are important to significant biological change are the regulated ones, not the haphazard ones.

  52. “Here is a partial list of organelles that never had any precursors and appeared full blown as we see them now…” J.D.

    Never had any precursors? That’s a very strong claim. No doubt the product of your having combed through libraries of fossilized microorganisms spanning the last 3.5 billion years or so. Must have been hell on the eyes.

  53. 54

    Before this thread disappears into the sunset, as all threads here do, let me offer a few challenges to those from “Camp Chance” also know as “Elsberry’s Alamo,” the last major surviving bastion of Darwinian mysticism.

    1. Name any two species, living or dead, for which convincing evidence can be presented that one is ancestral to the other.

    2, Name a mammalian species known to have arisen since Homo sapiens or a genus known to be younger than Homo.

    3. Name a genus of any organism that can be proven to have arisen within the last 2 million years.

    4. Name a species that can be physiologcally proven to have arisen in historical times.

    5. Present a physiological proof that any new true species can be produced by artificial selection.

    6. Present concrete evidence that sexual reproduction can support creative evolution now or ever could for that matter.

    7. Present a physiological proof that allelic mutations have ever played a role in creative evolution beyond that of promoting ultimate extinction, if something else didn’t cause it first.

    After you fail to answer these challenges, I will have some more for you to digest and then be quite unable to answer as well.

    While you are at it, explain why the Darwinians never bothered to test Darwin’s finches for hybrid sterility, which is the only reliable criterion for true speciation. After all, finches are among the easiest birds to demesticate. The canary is a finch!

    “How sweet it is”
    Jackie Gleason

    “War, God help me. I love it so!
    General George S. Patton

    “Ask not for whom the bell tolls. It tolls for Darwinian mysticism.”

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  54. To both Mike Dunford and great ape:

    In the PhysOrg article, they make the following statement:
    “In theory, the idea was sound, but scientists long debated whether it actually happened in nature. Eventually a competing theory involving the gradual accumulation of mutations was shown to occur in nature so often that geneticists largely dismissed the moving gene hypothesis.”

    Another way of saying this is: The Modern Synthesis, relying as it does on the gradual accumulation of mutations, displace any notion that moving genes can explain what we see in nature. Well, if nature is now showing that moving genes do indeed occur, then this is a direct challenge to the Modern Synthesis. How can that be ignored? Further, given the fact that–as John Davison has demonstrated in his last few posts–gradual accumulations of mutations have not been demonstrated to bring about speciation, it would seem nature is certainly favoring ‘moving genes’ as an explanatory mechanism.

  55. John Davison: Nice to have you making posts. I hope it continues. I, for one, certainly appreciate the depth of your knowledge.

  56. 57

    If I promise to continue to be good boy (79 next June), do you suppose my papers might be restored? If they were it would make it much easier to respond to many of the questions that I have provoked. The answers would be a touch of the mouse away don’t you know. I just realized that I have not kept my word when I promised that I would not participate until they were. I guess my word isn’t worth a nickel is it? Oh well, that is just old senile John again. He can’t remember anything any more.

    I know I am senile because I get the senile citizen’s discount (10%) every Tuesday at Ben Franklins, one of the few virtues of getting old. They used to have it at KMart but it stopped when Martha Stewart went into stir.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. davison

  57. PaV – I think you’re making a few separate mistakes here. The largest, I think, is that you seem to be assuming that a theory that states that the gradual accumulation of mutations is responsible for reproductive isolation would be shown to be entirely incorrect if it is shown that something else is sometimes responsible.

    We’d have to discard the idea that the gradual accumulation of mutations is responsible for reproductive isolation if it had been shown that gradual accumulation of mutations couldn’t or hasn’t done the job. We’d certainly have to at least consider discarding the idea if we discovered that something else was causing reproductive isolation and did not have good evidence that the gradual accumulation of mutations can cause reproductive isolation. Neither of those conditions applies here. There is plenty of evidence that the gradual accumulation of mutations can, has, and does cause reproductive isolation. Again, see Coyne and Orr’s book Speciation for a good review of case studies on that. In this case, it’s been shown that something else besides the gradual accumulation of point mutations can also cause reproductive isolation.

    This isn’t the first time that something like this has happened. For example, we’ve known for quite some time now that karyotype changes – changes in numbers of chromosomes – can act to cause reproductive isolation. Those cases differ from the current one in that large portions of chromosomes move rather than a single gene.

    Gradual accumulation of mutations works to cause reproductive isolation. Karyotype changes work to cause reproductive isolation. Other things work to cause reproductive isolation. Now we know that movement of single genes can cause reproductive isolation.

    For the record, there is nothing about the Modern Synthesis that would mandate that only gradual accumulation of mutations can cause reproductive isolation. The focus on gradual accumulation of mutations came about because they were a prediction, and one that was clearly shown to work. The idea that movement of genes might cause reproductive isolation wasn’t discarded because there was any theoretical reason to think it wouldn’t work. It got left behind because it wasn’t testable at that time.

  58. John, here’s a quick stab at answering your questions. Hopefully someone more knowledgeable than I will be able to fill in more detail.

    1. Name any two species, living or dead, for which convincing evidence can be presented that one is ancestral to the other.

    Common ancestry is more than enough to demonstrate, as it shows that two living species derived from a previous species, which is either living or dead. I posit humans, chimps, and gorillas as more than adequate evidence of common ancestry. Each of these share viral, endogenous retroviral, and transposon insertions in shared loci (at precisely the same genomic location) in a manner that is only coherrently explained by common ancestry. Common ancestry, by its very definition, meets your requirement, and common ancestry is accepted by IMO all reasonable people who look into the matter.

    2. 2, Name a mammalian species known to have arisen since Homo sapiens or a genus known to be younger than Homo.

    Why mammals? How about vertebrates… Cichlid fish in Africa, for instance. I will have to look up my mammals, but I’d wager I can stir up a rodent or two to meet your challenge more adequately.

    3. Name a genus of any organism that can be proven to have arisen within the last 2 million years.

    All of them. The Genus is an abritrary naming construct imposed by humans. I don’t want to rehash this tiresome argument yet again, but a genus formed within the last 2 myrs would only be recognizable as such (i.e. invoked as a label), in retrospect, in the distant future.

    4. Name a species that can be physiologcally proven to have arisen in historical times.

    Historical times. Let’s say 12,000 years or so since agriculture got a foothold. That’s a smallish window evolutionarily speaking, but this challenge will be answerable when we examine–we are in the process now–more genomic data from tiny crustaceans, etc that have much shorter generation times. Of course, I’m not exactly sure what a “physiological proof” for a historical event consists in, perhaps you can elaborate a bit?

    5. Present a physiological proof that any new true species can be produced by artificial selection.
    Consider the great dane and the pug. Sure, maybe no one has proclaimed them separate species, but they’ve about reach the point of physically precluding mating. This has been done through selective breeding. If they can accomplish this, it shouldn’t take much more tweaking to make it completely impossible for them to mate. Selectively remove any intermediate dogs that might mediate gene-flow between them, and there you have it.

    6. Present concrete evidence that sexual reproduction can support creative evolution now or ever could for that matter.
    I don’t understand this question exactly, but I will say that sexual reproduction, because it allows the reconstitution of otherwise doomed genotypes, helps the efficiency of the positive selection process. This has been shown quite conclusively in drosophila experiments (see, for example, Bill Rice’s work (2001)). (i.e. mitigates mullers ratchet).

    7. Present a physiological proof that allelic mutations have ever played a role in creative evolution beyond that of promoting ultimate extinction, if something else didn’t cause it first.
    Let’s start by saying “creativity” is somewhat subjective. There is fairly strong evidence that a group of monkeys, via key mutations in their lysozyme gene, gained the ability to digest leaves. That’s creative evolution in my book. Is it a new body plan? No. Is it a flagellum? Hardly. But examples like this are slowly but steadily cropping up, to the point where it will become increasingly difficult to dismiss them as trivial. (for a couple examples, see:
    Trends Genet. 2002 Sep;18(9):433-4. “Adaptive evolution after gene duplication.”
    As well as:
    Nature. 1987 Nov 26-Dec 2;330(6146):401-4. “Adaptive evolution in the stomach lysozymes of foregut fermenters.” Stewart CB,Schilling JW, Wilson AC.)

  59. John, the self deprecation is unbecoming. Won’t you just please be the professional scientist with the great ideas about organic evolution that we all know you can be when you want to be? The scientist with your name writing on brainstorms, for instance, before I came along to set you off. That’s the guy we’re looking for here. If I beg, will you please be the same here? I’m begging!

    About your papers. I’m unwilling to find and reformat them all for proper display in a web browser (HTML) a second time and I regret not saving the reformatted versions. It represented about a day (8 hours of work) for me. It requires a level 10 admin to mess with the sidebar and since there’s only a few of us I’m willing to be the one to mess with it in order to get your papers back up and to figure out a way to make them appear in chronological instead of alphabetical order. Some of them I believe are reformatted and appeared as a regular article so should be lurking in the archives. I’ll look for those and email all the UD authors looking for a volunteer reformat the remainder.

    Sal and PaV seem to be the most likely candidates to do the reformatting. I’ll email all the authors and see who’s willing to take it on.

  60. 61

    This is my response to great_ape, whoever that is in message 53. Before I begin, why is that nearly every Darwinian I encounter on the internet insists on using an alias?

    The reason I can make the claim to which great_ape refers is because I am now convinced that absolutely nothing in evolution ever took place gadually. In reaching this conclusion I have been profoundly influenced by the evidence presented by Otto Schindewolf, without question the greatest paleontologist since Cuvier. This is the same Schindewolf whose views were dismissed by Stephen Jay Gould as “spectacularly flawed,” in one of the most cowardly comments ever presented in the evolutionary literature. Gould made that statement as part of the Foreword he wrote to the 1993 English translation of Schindewolf’s great 1950 book with the English title “Basic Questions in Paleontology.” Incidentally, Schindewolf had been dead for 20 years.

    Schindewolf, like Richard B. Goldschmidt was a convinced saltationist because he recognized that the fossil record doesn’t support any aspect of the gradualist Darwinian myth. He summarized his pespective with his famous but neglected comment which I paraphrase as follows.

    “We might as well stop looking for the missing links as they never existed.”

    One of the most remarkable relationships that ever existed in the evolutionary literature was that between Goldschmidt and Schindewolf. Goldschmidt, an experimental geneticist and Schindewolf, a paleontologist, reached identical conclusions coming from entirely different disciplines. They each cited the other with whom they had complete ageement. I document that relationship in my Manifesto. I don’t believe they ever met. Both have been largely ignored by the evolutionary establishment. I join with both of them as a convinced saltationist and am happy to extend their conclusions a step further with the following summary.

    No genetic change ever took place gradulally, not one. All such changes are now and always have been instantaneous events. Those instantanious events include all of the following. The creation of each and every phylum, class, order, family, genus and every true species. None of these taxa were produced gradually which is what makes the Linnaean system so obviously valid.

    The Darwinian myth is based on a faulty original assumption which is that phylogeny was the result of the action of the environment on a plastic responsive evolving system. THAT IS NOT TRUE. Every aspect of phylogeny emerged from within those relatively few organisms who were able to produce progeny drastically different from themselves in a series of discrete and progressively ascending steps. The number of such creatures has steadily decreased as evolution has finally wound down to the point where even speciation is no longer in progress.

    Exactly the same can be said for ontogeny where the environment also has played a minor role, if any role whatsowever. All that can be documented as a role for the environment is that of a stimulus for an endogenous potential.

    Leo Berg put it this way when referring to ontogeny and phylogeny -

    “Neither in the one nor in the other is there room for chance.”
    Nomogenesis, page 406.

    These considerations, of which I am very confident, have served as the basis for the Prescribed Evolutionary Hypothesis. These facts have been before us for a very long time and have been ignored by an atheist Darwinian mentality that is congenitally incapable of realizing that there was a purpose in every aspect of a completely designed and predetermined universe.

    “Everything is determined… by forces over which we have no control.”
    Albert Einstein

    Darwinism is dead and always was. It was never anything but an illusion created by the imagination of a couple of Victorian naturalists, one of whom, Alfred Russel Wallace, had the good sense to abandon later in life. The complete title of his last book published in 1911 says it all –

    “THE WORLD OF LIFE: A MANIFESTATION OF CREATIVE POWER, DIRECTIVE MIND AND ULTIMATE PURPOSE”

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  61. 62

    I missed DaveScot’s message as I was busy composing my own when it appeared.

    Thanks.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  62. John, check the sidebar and your email.

  63. John,

    (The alias, by the way, is because of the precariousness of my only recently embarking on an academic career, one where even conversing with this crowd is not looked kindly upon, much less my occassional sympathetic remark about the philosophical underpinnings of certain darwinian positions.)

    The problem I see with the extreme saltationist approach, as represented by Goldshmidt, is what happens once the “hopeful monster” is produced from a population genetics perspective. Are there other such monsters among its peers to breed with? If not, it does not persist in time as it is a singleton event. If it breeds with its progenitor population, it is reabsorbed into that population. The progenitor population, for saltationism to be plausible, must therefore be producing an abundant number of similar and reproductively compatible “fundamentally different” organisms to constitute a viable population. There are certainly no organisms today, as you yourself indicate, that demonstrate this generative capacity. Why would you then conclude there were such organisms in the past? Is it not more likely that change occurred more gradually, at a rate somewhere between the canonical darwinian rate and Gould’s punctuated equilibrium? If biological systems in the past were poised to make these saltational jumps, we should find remnants of the orchestrating systems, those that made these leaps possible. I know of no such systems. All we see is random genetic variation that sometimes has phenotypic consequences. I see no reason, at least at this juncture, to postulate there was ever anything else involved in evolution.

  64. For the record, there is nothing about the Modern Synthesis that would mandate that only gradual accumulation of mutations can cause reproductive isolation.

    When the Modern Synthesis was forged, it relied on Fisher’s model of gradual accumulation of small mutations. Orr calls it an infinitesimal model. If you want to include other effects, then you’re not dealing with the Modern Synthesisl. There’s also the Neutral Theory of Kimura. But that has problems as well. Currently–per Orr himself, there is no real theory of evolution that account for the various known mechanisms of genetic change. The Modern Synthesis was completely unconcerned about reproductive isolation–that is a concern that Wright stressed, and, I believe Dobzhansky and others. But it’s not part of the mathematical basis of the Modern Synthesis.

  65. apedude

    John must get asked that question a lot – it was the first question I asked.

    The answer is that semi-meiosis is a gynogenetic mechanism – only one female producing gynogenetic offspring (of both sexes) is required. I think it’s talked about in the manifesto which is on the right sidebar here.

    Is that about right, Dr. Davison?

  66. PaV:

    I’m honestly not sure what you are trying to get at here. As far as I can tell, I can see absolutely nothing about the newly reported situation that does not fit in well with the basic population genetics that serve as the foundation for the modern synthesis – the presence of the chromosome on a different chromosome is not very hard to model as a different allele of the gene. (Actually, now that I think about it, it would be much easier to model as two genes, each with two alleles, with infertility resulting in any offspring that has the null allele at both loci. In any event, the mechanism involved in this case might not be a point mutation, but it’s still a simple fit with basic population genetics. In fact, the basic principles of population genetics were used in setting up the experiment in question and in interpreting the results. To the best of my knowledge, we’re talking about the same population genetics that serves as the mathematical foundation for the modern synthesis.

  67. 68

    A single virgin female frog, with no contribution from the male, has already been demonstrated to be able to produce both male and female fertile offspring. That has been known for 40 years and actually, come to think of it, for almost a century, and is documented in the Manifesto. It is not speculation but a demonstrated fact and requires no further explanation. What has not been seriously attempted is to see if this can be repeated with higher vertebrates including humans. Also, many creatures routinely produce males gynogenetically from vigin mothers, rotifers, bees, wasps, cladocerans etc, etc. Many animals and most plants are hermaphroditic (monoecious) as well.

    It is perfectly conceivable that both the virgin origin of Christ and the Immaculate Conception of his mother, Mary, have a firm biological basis. Like it or not there is no question that all the information necessary to produce both functional sexes is contained in the female genome alone. That is not a matter of conjecture for those forms where it has already been demonstrated and it will remain in the realm of possibility until it has been found to be experimentally disproven in every living creature that reproduces sexually.

    Biology is after all an experimental science athough you won’t find Darwinians doing much of that these days. They got tired of constant failure and finally gave it up entirely.

    Even if it is impossible to gynogenetically produce males, that is of no concequence anyway. Once the new chromosome homozygote is produced semi-meiotically, those females can now mate with males of the species from which they were derived and a new species could be produced in a single step as some of her offspring would eventually be of the same chromosomal configuration as herself, in principle a new species. This follows directly from the crossing of two heterozygotes. In other words, l/4 will be homozygotes like the original new mother. While Mendelian sexual reproduction is probably incompetent to produce a new species all by itself, it can play a role in establishing the new species once it has been produced gynogenetically as proposed by the Semi-meiotc Hypothesis (SMH). Goldschmidt was acutely aware of the critical step in evolution which is the creation of the new chromosome structural homozygote, and semi-meiosis provides the mechanism for this step. Once established, Mendelian bisexual inheritance can finish the job. Unfortunately as near as can be determined, semi-meiotic reproduction is no longer in progress in higher animals but then neither is creative evolution. It does occur in certain flagellate protozoa in the genus Spirotrichosoma and also can be demonstrated in certain strains of poultry as I document in the Manifesto. I am convinced that the immediate ancestor of Homo sapiens was Neanderthal for the simple reason that there was no other hominid around at the time we appeared. We most certainly were not created de novo as some would have us believe. While I am a Creationist, I will not accept Divine intervention for the origin of man when there is a perfectly sound material alternative explanation available. I am confident that we will some day be able to experimentally create our ancestors step by step when we can experimentally control the restructuring of our own chromosomes. Everything we know about primate evolution can be explained through the remodeling of an original chromosomal structural complex. That in no way denies a role for a Creator. It simply means the Creator worked in the past to ensure that the final product would be Homo sapiens, who I still maintain is the youngest mammalian species and probably the last one to ever appear on this planet. All we see now is extinction, the evolutionary counterpart to the death of the indivdual. There is an element of truth in Ernst Haeckel’s Biogenetic law, “Ontogeny recapitulates phylogeny.” I wish people would stop picking on him. He a was a great zoologist and a talented artist. Unfortunately, he was also a Darwinian!

    I hope this clarifies my position.

  68. 69

    DaveScot

    I am behaving and you known it. It is very true as you just admitted that you “set me off.” You sure have, big time and many times. That is a matter of record. I recommend that should be put in the past. What says DaveScot?

  69. 70

    great_ape

    You have failed to answer a single one of my challenges with specific exmples which is what I asked for, You have changed the subject and even denied the validity of the genus as a valid taxon. Dogs are nothing but intraspecific varieties. If you think otherwise just observe the behavior of a male Great Dane when he gets a whiff of a Chihauhua in heat. It is a sight to be seen. I have been over this before and I am convinced that a cross between these two breeds would be successful in either direction but probably would only require the help of a vet or an enterprising amateur like yourself maybe? I would do it in a flash if the owners would let me. Trust me. A spontaneous cross between a male St Bernard and a female Dachshund resulted in a fertile female named “Rollmops.” Her belly dragged on the floor and had to be protected by towels during her own succesful pregnancy. You would know all this had you read my Manifesto. You would also realize that I am convinced that macroevolution is a thing of the past and have presented plenty of evidence for that conclusion along with citing the same conclusion from Julian Huxley, the man who coined the term “Modern Synthesis.” Figure that one out for me. I can’t.

    I am afraid you have failed to effectively discredit or disprove my challenges. Sorry about that.

    Now don’t get all exercised which is what Darwinians almost always do when I am around. I’ll just get banned again or worse. Not that it really matters, as I do this sort of thing for amusement mostly. I promise not to lose my temper and I expect everyone else to do the same. As DaveScot often says. Got that? Write that down. Okay? – Okay!

    Who is next?

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  70. Doctor Davison

    It’s all water under the bridge. Let’s focus on our common belief that chance never had anything significant to do with organic evolution.

  71. 72

    Let’s do just that. Set them up in the other alley. So far I am bowling a perfect game!

    Who is next?

    I love it so!

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. davison

  72. 73

    It is not a mere belief that chance had nothing to do with evolution. It is a proven reality. Why don’t you get some of the troops from Panda’s Pathetic Pollex (PPP) over here. I hope they haven’t all been banned already as I feel like exposing them don’t you know. It is great sport. Invite Wesley.

    I love it so!

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  73. I already did invite them. Unbanned whoever asked if they were banned. Even our old friend Alan Fox is commenting here again. If you ask me, they’re yella. Wesley to this day has refused to unban either one of us at any of his websites. Even over a year later. Asked why, he still says it’s because I made a vague remark about poor security on Panda’s Thumb and not make me angry lest I take advantage of it. All I ever meant by that was getting around the ban – which I’ve done on a few rare occasions since then. It’s a pretty lame excuse over a year later. He makes out like I threatened to hack his server and cause considerable harm. Wesley’s a weasel.

  74. Hello, John,

    Perhaps you would like to discuss your 12 convictions?

  75. 76

    All I ever do any more is laugh at them. They can’t handle that at all. Of course I also called Wesley Elsberry Der Fuhrer, Herr Doktor Professor Esley Welsberry, pronounced Velsberry.

    I never met a Darwinian with a sense of humor which is what making fun of them so very enjoyable don’t you know.

    Who is next?

    I love it so!

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  76. 77

    GilDodgen in message #4

    I am not at all sure that there was any new information required. I am also not sure that evolution hasn’t proceeded in part through a loss of information either. Higher vertebrates for example have lost the powers of regeneration which are still retained by urodele amphibians and to a lesser extent by reptiles. It is also implicit in the PEH that the information was front-loaded long before it was expressed. We don’t even know how many front-loaders there were or even how many times, when, or where they did the front-loading. I am confident however of the basic validity of the PEH or I would never have published it. I see no compelling reason to postulate new information to account for the evolution within the Primates order to which we belong. If it was required, then where did it come from becomes a important issue and I am not prepared to accept direct Divine Intervention. I don’t think it is required. The old saying is –

    “God works in mysterious ways.”

    I would modify that to read-

    “God worked in mysterious ways.”

    Also I am not at all certain there was a single God. When I look at the world around us I am inclined toward at least two Gods, one benevolent, the other malevolent. But that is just me. I am using God as synonymous with the less personal BFL which stands for Big Front Loader.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  77. 78

    I see that Alan Fox, Welsberry’s chihuahua, has surfaced once again trying desperately to cause trouble and failing miserably as always. He is pathetic, an uneducated ex biochemist who, by his own admission, abandoned a career in science to devote his remaining life to the biggest myth in the history of science. To make matters worse he is a proudly declared fan of Richard Dawkins.

    It is hard to believe isn’t it?

    I love it so!

    Who is next?

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  78. I see that Alan Fox, Welsberry’s chihuahua, has surfaced once again trying desperately to cause trouble and failing miserably as always.

    Aw, come on, John. I can play nice and I know you can.

  79. D.S., John Davidson: I shall refrain from commenting on Dr. Davidson’s ideas until I have read and digested his manifesto. I thank Dr. Davidson for his patience and willingness to reiterate what he has written previously. I am headed to the old world for a few weeks, partly on scientific business, and hopefully I will be able to return with new and relevant information.

  80. 81

    Sure you can Alan. That is why you were banned at “brainstorms” for acting as you did on the thread where I was presenting some of my usual Antidarwiniana. You have never had an original idea in your entire life you have publicly admitted that you were afraid to mention my name at Panda’s Pathetic Pollex for fear that Der Fuhrer would ban you for life. You remind of Harry Truman’s comment about Harold Ickes I believe it was.

    “He is a living miracle with neither brains nor guts.”

    Go play with your hero, that genetically selfish blind watchmaker and internationally famous mountaneeer, Richard Dawkins,B.S., Ph.D.,F.R.S., O.B.E. etc.,etc. Have a nice climb and don’t forget your oxygen tank.

    greast_ape

    It is John Davison as in John Davison Rockefeller, a relative, not John Davidson. He is the singer and actor. I am the most loathed evolutionist in cyberdom. If you happen to drop by Oxford, give my regards to Dicky Dawkins. Thanks.

    I love it so!

    Who is next?

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  81. #68 John A. Davison: Like it or not there is no question that all the information necessary to produce both functional sexes is contained in the female genome alone.

    You are not correct with your statement that a human female can give rise to a male (by non-supernatural means, that is). The X chromosomes contains several genes that are not present on the Y chromosome and therefore not in the female genome, the most prominent being male sex-determining gene, SRY.

  82. correction: X-chromosome (singular)

  83. #68 John A. Davison: “I am convinced that the immediate ancestor of Homo sapiens was Neanderthal for the simple reason that there was no other hominid around at the time we appeared.”

    One more clarification: It is my impression that there is paleontological evidence that the closest precursor to present-day humans overlapped chronologically and geographically with the Neanderthals. The implication is that one is not a descendent of the other.

  84. Mike Dunford:

    I’m honestly not sure what you are trying to get at here. As far as I can tell, I can see absolutely nothing about the newly reported situation that does not fit in well with the basic population genetics that serve as the foundation for the modern synthesis – the presence of the chromosome on a different chromosome is not very hard to model as a different allele of the gene.

    There’s population genetics, and then there’s the Modern Synthesis. It’s built largely on Fisher’s “The Genetical Basis of Natural Selection.” Notice it doesn’t say the Population Genetical Basis….. In deriving his equations, equations that he said proved that the gradual accumulation of extremely small mutational changes could lead to what we call “macroevolution”. That’s why Orr calls it an “infinitesimal” model: it has to do with Fisher’s derivation involving a correlation to mutation size and fitness effects. The bottom line is that large mutational effects don’t fit into Fisher’s model. Chromosomal rearrangements are simply too large a mutational change to fit into his model. That’s why evolutionary biologists are still looking for a model that corresponds to the types of mutational changes we now know take place. Q.E.D.=this means I’m a little tired of the subject, and likely won’t make any more responses. We’ve covered the ground more than sufficiently.

  85. 86

    The model is already here. I proposed it 22 years ago and it was offered in principle by Richard B. Goldschmidt long before that. The unit of evolutionary change is not the gene. It is the chromosome. One can select for all the allelic mutants in the world and one will not transcend the species barrier, and you probably won’t even introduce any real barrier to fertility. Imagine all the Mendelian factors that separate a Chiuahua from a St Bernard yet they are still dogs or, if you prefer, wolves because dogs are wolves and produce fertile hybrids with them as they do with coyotes, the latter being known as coy dogs.

    Here is what I propose. Do some of you out there in cyberspace have a Chihuahua and others either a St Bernard or a Great Dane and happen also to live close enough to arrange the experiment? I am sure you know the experiment I have in mind. Check with your Vet and if you want, have him get in contact with me. I want one of the pups as payment for helping to prove that neither natural nor artificial selection have anything to do with creative evolution and never did.

    The barriers to speciation are not Mendelian but are structural incompatibilities between the members of each chromosome pair. These prevent the normal production of balanced gametes with resulting sterility. Such structural rearrangements are the primary if not often the sole cause of hybrid sterility between members of related known species which produce viable but sterile hybrids. The greater the differences the lower the fertility. The mule is a strong animal but virtually totally sterile and can never be estblished as a true breeding species. If that were possible, the army would have done it eons ago because the mule is stronger than either of its parents athough frightfully stubborn as we all know. Hybrids are often stronger than their parents. Is is known as “hybrid vigor” and has been known for centuries by plant and animal breeders.

    Goldschmidt realized this 66 years ago.

    “Species and the higher categories originate in single macroevolutionary steps as completely new genetic systems. The genetical process which is involved consists of a REPATTERNING OF THE CHROMOSOMES. which result in a new genetic system.”
    The Material Basis of Evolution, page 396, my emphasis.

    This immediately explains why distantly related species can be virtually identical at the DNA level yet separate true species nevertheless. I thought everyone had accepted this by now but apparently not, something I fail to understand because this basis for both speciation and hybrid sterility has been known ever since the analysis of chromosome morphology has been possible. It also lies at the heart of the semi-meiotic hypothesis (SMH) because the first meiotic division is the CAUSE of speciation. When the second division occurs, which makes the union of haploid nuclei mandatory, all evolution comes to a screeching halt. That is why I can safely offer the challenge – show me a new species known to have been produced by a known ancestor through sexual means. It simply can’t be done, because Mendelian, sexually mediated, genetics never had anything whatever to do with creative evolution. Quite the contrary, it prevents it. Bateson knew that over 80 years ago as I have demonstrated here and in published hard copy.

    “You can lead a man to the literature but you cannot make him read it.”
    John A. Davison

    It is hard to believe isn’t it?

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  86. 87

    Surely there must be a Darwinian somewhere here at Uncommon Descent that would take exception to my remarks isn’t there? I hope so because I am bored and, being bored, spoiling for a fight. Come out, come out, wherever you are!

    “War, God help me, I love it so!
    General George S. Patton

    “I’m an old campaigner and I love a good fight.”
    Franklin Delano Roosevelt.

    “A past evolution is undeniable, a present evoluton undemonstrable.”
    John A. Davison

  87. John Davison:
    1. Name any two species, living or dead, for which convincing evidence can be presented that one is ancestral to the other.

    What about teosinte and domesticated corn?

  88. Hohn Davison:
    And while you are at it, would you agree with my comment #82?

  89. John Davison,
    Sorry, I didn’t mean to mis-spell your name.

  90. PaV:

    1: RA Fisher did not call what he did “population genetics,” but his work (along with that of Sewall Wright and J.B.S. Haldane) provides the foundation for the field.

    2: Fisher did demonstrate that the larger the effect of a mutation, the less likely it is that a particular mutation will be beneficial. The key word here, which you seem to be missing, is “effect.”

    The effect of this particular mutation – the relocation of the gene from one chromosome to another – is not particularly large. Nor, for that matter, is it belived to be particularly beneficial. If anything, the mutation probably falls into the category of “slightly deleterious mutations” that Ohta discussed back in the late 1970s. Both species have functional copies of this gene. All F1 hybrids should have functional copies of the gene. The problems don’t arise until the F2 and/or backcross generations. The fact that the mechanical basis for this mutation appears (in your judgement) to be large is entirely irrelevant – the only thing that matters is the magnitude of the effect of the mutation. As Orr put it, “The population genetic fate of a mutation is determined by the magnitude of its effect on characters affecting fitness, whatever its mechanical basis.” (Orr, 2001).

    Remember, Fisher published his work five years before the chromosome was first identified as a possible unit of inheritance. He had no ideas about point mutations, insertions, deletions, relocations, translocations, or any of the other terms that we use to describe mutations. He did not – could not – formulate his theory based on the magnitude of the change in terms of what happened to the DNA. He formulated his theory entirely around the phenotypic effects of mutations. The phenotypic effects of this gene changing chromosomes are relatively minor.

  91. jonnyb,
    “I think the issue is that you don’t understand Intelligent Design.”
    Could be.
    “Intelligent Design does _not_ say that evolution did not happen. It does _not_ even say that evolution did not proceed via purely naturalistic mechanisms.”
    I never said it did.
    “What it _does_ say, however, is that functional complexity does not evolve from undesigned sources. If evolution proceeds according to a directed process, there must have been a director somewhere in the causal chain. See for instance Dembski’s No Free Lunch, Searching Large Spaces or this paper.”"
    If these assertions were true, then how do these mutations support them?

  92. 93

    ofro

    Your message 82 is irrlevant to the matter becuse no experiment has been successfully performed (that I know of) to see if the human female can even produce offspring gynogenetically, not to mention what sex the progeny might be. It is perfectly possible and even likely that humans cannot reproduce other than sexually NOW. That says nothing about our origin. Also I am not surprised that Neanderthal and ourselves overlapped chronologically. What would be very surprising, and would very definitely favor a Divine origin for modern man, would be if we HADN’T overlapped in time. The one thing that the fossil record clearly supports is reproductive continuity, a continuity were it ever to be broken entirely would mean the end of life. Any viable hypothesis for evolution must be based on the continuity of the living sequence. There is neither place nor need for Divine intervention until we reach back to the farthest reaches of our origins where I feel it is unavoidable. To that extent only, I am a Creationist.

    Where genes are now found in the genome does not mean they were always there by any means. If new genes have been added along the evolutionary pathway their origin must be verified. Maybe they have. My position is that we see only that part of the genome that is activated or “derepressed” which is my preferred term, which implies they were already present but masked somehow.

    Schindewolf claimed that evolution cannot be studied experimentally. I am not yet convinced he was right about that. I think everything here on earth, past and present, will eventually be explained in the experimentally laboratory. One thing is certain. One cannot dismiss an idea until the critical experiments are performed to test it. All the armchair speculation and discussion is of no consequence until a proposed mechanism has been tested under controlled conditions which is all that the Semi-meiotic Hypothesis (SMH) is, a potential mechanism which has not yet been proven to be WRONG. The Darwinian proposed mechanism has never been proven to be RIGHT. They don’t even try any more because they know it won’t work. They even dignify it by calling it a THEORY of evolution which it most certainly is not. We don’t even have a theory of evolution yet. I published a paper to that effect.

    “Small minds are easy to find and hard to change.”
    John A. Davison

    “No sadder proof can be given by a man of his own littleness than disbelief in great men.”
    Thomas Carlyle

    Preeminent among the great men of evolutionary science are the six to whom I have dedicated my own work. Those who have ignored them have established Carlyle’s aphorism beyond any doubt. They are widely known as Darwinians. There are tens of thousands of them. You can’t turn over a rock but there is another Darwinian.

    It is hard to believe isn’t it?

    I love it so.

    Who is next?

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  93. 94

    In further support for my previous comment I refer to the side bar and my paper “Do we have an evolutionary theory?,” which I believe is in the current issue of Rivista although I can’t be sure because I don’t get the journal. Also I don’t think they like me any more because they used to send me copies of the issues in which my papers were published. They don’t any more. One of my papers was not even indicated on the cover but was tucked away inside the issue. That one was “The case for instant evolution,” in my opinion, one my most important ones. It was as a Letter to the Editor in
    Rivista di Biologia 96: 203-206, 2003. I believe ISCID reprinted it but I may be wrong about that. My short term memory is shot but I can assure you that my long term one isn’t. I am an elephant in that regard and just as unforgiving. Trust me. Elephants are dangerous animals you know. I love stomping Darwinians and ideologues generally. It is great sport.

    A past evolution is undeniable, a present evolution undemonstrable.\”
    John A. Davison

  94. 95

    Yes it is.

    I believe that all of my evolutionary papers, except the 84 and 87 ones in J.Theor.Biol., are available in the “brainstorms” Archives. Thank goodness for “brainstorms,” one of my favorite forums. They tolerate me don’t you know.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  95. jonnyb said:

    Why is it that ID cannot make reasoned inferences, when the entire structure of evolution is based on inferences?

    Well, evolutionary theory proposes mechanisms, while ID offers naught but arguments from incredulity. Even Dembski himself has indicated that the level of detail proposed by IDers doesn’t approach the “pathetic” level. You can make all of the reasoned inferences you want, but until you eliminate “poof!” as your primary mechanism, you aren’t doing science.

  96. John Davison:
    “1. Name any two species, living or dead, for which convincing evidence can be presented that one is ancestral to the other.”

    You forgot to respond to this suggestion to your question: What about teosinte and domesticated corn?

  97. Dr. Davison wrote:

    That is why you were banned at “brainstorms” for acting as you did on the thread where I was presenting some of my usual Antidarwiniana.

    I was banned because you requested it, John. However Micah has not responded to your latest request which I forwarded a few days ago, and I quote (from your post on my blog)

    “Okay you cowardly, ignorant little twerp. You are cordially invited to come back to braimstorms and repeat your comments there. You tell Micah Sparacio that I have said you are welcome there you ignorant half wit.”

    It seems odd in view of your complaint:

    “It seems that the “Darwimps,” as I affectionately call them, are going to continue their long tradition of assuming that their adversaries do not now and never have existed. I have, here as elsewhere, given them plenty of opportunities to counter my claims and convictions. Their silence speaks volumes as to their insecurity. Perhaps they have other excuses. I would love to hear them.”
    Link

  98. Mike:

    He did not – could not – formulate his theory based on the magnitude of the change in terms of what happened to the DNA. He formulated his theory entirely around the phenotypic effects of mutations. The phenotypic effects of this gene changing chromosomes are relatively minor.

    There’s plenty to quibble about in your post, but I’ll just address this point. Fisher could not address in his theory what was only later discovered, but others could have, and they haven’t. That’s the point. As of right now, there really isn’t a Modern Synthesis any longer. And though Fisher was working with phenotypic effects, nonetheless, his mathematical model did not allow the presence of “point-mutations” that have large-scale effects, which is what science has recently discovered to be the case. You can confer Allen Orr’s recent papers on all of this.

  99. Ofro:

    You forgot to respond to this suggestion to your question: What about teosinte and domesticated corn?

    And we know that domesticated wolves–dogs–come from wolves. But what does this prove? To me this simply proves that before human beings came along to intelligently select for certain features, neither corn nor domesticated dogs had been produced by nature. Where does this get us?

  100. PaV
    You have a strong argument. However, the challenge John Davison threw out was fairly broad, and I don’t know whether he excluded the possibility of human-mediated selection. In addition, I would have liked to hear it (any answer) from him, because I wanted to understand how this fit into his scheme of current non-evolution.

  101. PaV:

    And though Fisher was working with phenotypic effects, nonetheless, his mathematical model did not allow the presence of “point-mutations” that have large-scale effects, which is what science has recently discovered to be the case. You can confer Allen Orr’s recent papers on all of this.

    I work on speciation, and I am quite familiar with Orr’s recent work. I also understand it well enough to recognize cases where it does not apply – such as this one.

    As I have pointed out several times already, the phenotypic effects of this mutation are not large scale. The phenotypic effects of this mutation are something between none and very, very little when in the background of the native population. The only time that this particular mutation has any effect at all is when the two species are crossed, and then the effects don’t show up until the backcross or F2 generations. That is an extremely minor effect.

    The fact that the cause of the mutation is (in your opinion) major is entirely irrelevant when looking at this particular case from the perspective of any Fisher-type phenotypic effects model. This particular type of mutation is difficult to treat from the perspective of a Gillespie-type mutational landscape model because it doesn’t fit the categories of mutation that this model was designed to handle. (Here, I think you need to remember the difference between a “theory” and a “model.” Finally, Orr’s recent work has been focused on the treatment of adaptive evolution, but this particular case does not seem to fit into that category, either. This is a situation where the mutation is, if it occurred via duplication and subsequent loss as the authors of the paper hypothesize, neutral or nearly neutral within the population. It really has no effect unless the two species are crossed.

  102. Mike Dunford: In your answer to my post you kept repeating the words, “this mutation”. I don’t know what you’re refering to when you say, “this mutation”, so I just can’t follow your argument. Can you specify what you mean by “this mutation” a little bit more. Thanks.

  103. In this case, I am referring to the relocation of the JYAlpha gene from chr4 to chr3, which is the speciation mechanism identified in the paper that kicked off this whole thread.

  104. 105

    This thread is about to disappear south and I predict that when that happens all interest in it will end as well. The old expression is –

    “out of sight, out of mind”

    and this forum format virtually ensures that result. The endless cyclic battle of fixed “prescribed” ideologies will then commence again, proving as it always has that the one thing we learn from history is that we don’t learn from history. Pardon my cynicism born of long experience.

    “Nothing is so firmly believed as what we least know.”
    Montaigne

    “Men are most apt to believe what they least understand.”
    ibid

    I love it so!

    As for ofro’s question about selection, I don’t believe artificial selection of allelic mutations will produce new species but I am confident that rearrangement of existing chromosome information might very well do just that. And yes, I believe that creative natural evolution is finished and has been for a long time. Why doesn’t everyone?

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  105. Comments are open on the sidebar topics under your name and they don’t drift off into the sunset. I’m not sure what to do to get commentary going there. Any suggestions?

  106. Mike Dunford:

    The fact that the cause of the mutation is (in your opinion) major is entirely irrelevant when looking at this particular case from the perspective of any Fisher-type phenotypic effects model.

    This isn’t a position I think you want to maintain. Although the ‘phenotypic’ effects are almost nil, the effects to the animal (fly) are enormous. They become sterile, incapable of passing on their genes. I don’t think that’s a subtle change.

    And the fact that this discovery is unsettling to what had been considered settled theory is seen in this statement from the article:

    “The reigning theory of speciation says that the genes causing hybrid sterility must have diverged slowly by normal evolutionary changes. To determine if this was true, Masly had only to look at chromosome #4 and find the gene on it that caused the hybrid sterility.”

    Isn’t it obvious from this quote that they consider their results to fly in the face of the ‘reigning theory’ (Fisherian) which assumes that divergence to sterility happens “slowly”?

  107. 108

    Sir Ronald Fisher was a Darwimp through and through and nothing he ever wrote ever had anything to do with creative evolution, absolutely nothing. The same can be said for J.B.S. Haldane, Ernst Mayr, Stephen J. Gould, William Provine, Richard Dawkins and all the rest of the armchair theoreticians with which we have been so blessed, not a scientist in the lot. Every one of them was glued to an endowed chair somewhere. The surviving two still are. It is disgusting!

    How do you like them apples?

    I love it so!

    “We seek and offer ourselves to be gulled.”
    Montaigne

    “A past evolution is undeniable, a present evolution undemonstrable”
    John A. Davison

  108. #100 Pav: ”And we know that domesticated wolves–dogs–come from wolves. But what does this prove? To me this simply proves that before human beings came along to intelligently select for certain features, neither corn nor domesticated dogs had been produced by nature”.

    I agree that breeding by humans this does not formally qualify for “natural” selection, even though for me it makes not difference in principle in terms of evolutionary mechanisms. However, I wonder how that affects your position that you described in your thread on random mutations. In it you mentioned some sort of designed control mechanism built into the genome that is somehow able to predict or adapt to a changed environment.

    Would you postulate the same directed control mechanism for the process of breeding when humans are selecting for “freak” mutants (a dachshund with crippled legs, an orange tree with seedless fruit, a decorative goldfish with exorbitant fins etc.) that would clearly not be viable in nature? I can’t see how this kind of artificial human interference could be anticipated during the postulated design of the genome.

  109. 110

    DaveScot on #106

    I don’t either but don’t worry about it as I am sure I can still stir up a mess almost anywhere I am allowed. It means a lot to me don’t you know.

    I love it so!

    Who is next?

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  110. 111

    ofro

    I beg your pardon about my Dachshund Otto (named for Otto Schindewolf) having “crippled legs.” That was uncalled for and I demand a public apology. Otto is like greased lightning as he “does laps” around my apartment when I ask him to. He loves to perform because he gets “dog yummies” afterwards. Also I recommend you visit the “Animal Planet” channel on the tube where they frequently hold Dachshund races. You ought to be ashamed of yourself.

    I love it so!

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  111. Doctor Davison

    Well now. So much for drifting off into the sunset this week. I changed the timestamp on the article to today. Perhaps you could invite commenters to a discussion on the sidebar so there’s no need to keep floating this up to the top which seems unfair to the other authors and thus makes me uncomfortable in so doing. Maybe even ask Alan Fox or some other kind soul who hasn’t been banned by Herr Docktor Vesley to direct your undying fans on PT forums in that direction.

  112. John Davison
    My apologies to Otto. Please don’t let him read this post. But the reality is that this breed came about because of a mutation that prevented the legs from growing to full length. As a consequence, it was developed further into a recklessly brave (in my mind) breed that would (and could!) crawl into badger holes and fight the beasts therein. I presume that you know some German since you read Schindewolf, so you know that “Dachs” is German for “badger”.

    If the people who discovered this mutation several hundred years ago had been out to get a dog that chases foxes or boars, they would have discarded this puppy.

    Sorry Otto, but as my grandmother used to say:

    “If it is true, you can say it”

  113. Do you think Otto is a mutant, per se, or a natural variant whose emergence was inevitable?

    I ask because it seems to me that nature constantly and purposely varies the relative scale of body parts and indeed the size of the entire organism. It also seems to vary cosmetics such as coloration and length of fur. It does it on a sort of trial balloon basis regularly producing small variations and giving them a chance to become widespread and larger variations. In lean times a smaller animal requires less food thus nature providing a path for drastically reducing body size in a short amount of time confers a big survival advantage. In times of abundance a larger body size helps ward off smaller predators and widens the range of available prey. Coloration and fur length variation makes for quick adaptation to changing climate patterns and optimum camouflage.

    Little or no creative evolution is needed for adjustments in scale and cosmetics. So this leads me to wonder whether Otto is really a mutation or just a natural, planned variant whose time had arrived.

  114. Consider a wolf living on a prairie covered by short grasses where there’s an abudance of prarie dogs. Because the prairie dogs stay near to their burrows and stand up with their head above the grass to scan for predators they are a difficult target for a full size wolf. A wolf that makes a simple adaptation of shortened legs gets two tremendous advantages. First of all he can charge at full speed through the grass without rising above it. Secondly he can pursue his prey into the burrow. Moreover he can also adapt the color of his coat to better blend in with the prairie grass. The short legs mean she can even take over the burrow as a den for her own young. Even better, a reduction in overall body weight means he can survive on the same number of prey that are smaller than his larger cousin requires.

    If you presume that nature can somehow accidently generate a ribosome and the digital code on a DNA molecule that drives it, it should be no problem for you to accept a mechanism that responds to environmental pressures and generates variation in a purposeful manner to better cope with those pressures. I put forward that all the variation seen in dogs in the short span of time that humans have been selecting for unusual traits is evidence that this mechanism exists. Note that in the same span of time no creative evolution has taken place. Not a single retractible claw, for instance, has ever been seen in a dog, and all dogs are still the same species with any true breeding variant able to produce fertile hybrids with any other variant. Furthermore, I posit that if you were to mix all the true breeding variants back together into the natural environment you’ll eventually end up with just three variants – a wolf, a jackal, and a coyote. Nothing was gained or lost, just temporarily modified in a non-creative manner for expediency.

  115. Gildogen: “They speculate, declare the problem solved, and teach speculation as fact. That’s how science works.”

    No, that’s how ideology works.

  116. DaveScot: “Do you think Otto is a mutant, per se, or a natural variant whose emergence was inevitable?
    I wonder if there are historical documents that describe the generation of a (any) dog breed over the years. They should tell us if the shortening of the dachshund legs or the feature development of other breeds occurred gradually or in large steps. So that would be a way to distinguish between what you call adjustment and true mutation.

    From what we know about human dwarfism, I would classify Otto as having a mutation somewhere in the growth hormone signaling pathway controlling bone growth.

    Having said that, in my mind what brings about all these breeds are good, old-fashioned (random) mutations, differing in the severity of phenotype. I just don’t see the need for a purpose in mutations other than this being the mechanism by which life was able to radiate and spread into just about all niches on Earth. Do you require in your scheme of things that an organism or genome “knows” that it needs to modify its code to meet potential environmental challenges, and how? You mention the word “trial balloon” which I would interpret as “random search”, unless you restrict the trial to a limited list of available or prescribed mutations. In the latter case, some environmental challenges may not be met as readily or not at all. A truly random mutation paradigm has a better chance of meeting a greater range such challenges.

  117. ofro

    Evolution via random mutation isn’t supposed to work so quickly that it can produce variations ranging from chihuahua to great dane and everything in between in a few thousand years. I seriously doubt there’s anything random about the variation in dogs. These are preprogrammed limits to variation that we’ve quickly bumped into via unnatural selection. No dog has emerged over a certain size (why don’t they just keep getting bigger until elephant size if the size mutation is random?) and none under a certain size (why don’t they keep getting smaller until shrew size if the size mutation is random?). The range in size of dogs is clearly a built-in limit in the canine genome as sure I’m sitting here describing it to you. I really don’t understand how things so obvious can escape notice in really bright people.

  118. Do you require in your scheme of things that an organism or genome “knows” that it needs to modify its code to meet potential environmental challenges, and how?

    Nope. I just figure that I shouldn’t deny such a simple mechanism as directed changes in response to the environment when such a mechanism is so simple in comparison to really complex mechanism found in living things. I’m repeating myself here but you don’t seem to grasp the complexity of ribosomes and DNA. If you can believe that this hideously complex machinery can be generated by random mutation & natural selection then something simple like directed mutations in response the environment which would obviously confer tremendous survival advantate would be something you deny to the same mother nature that created the ribosome/DNA machinery through the same mechanism of descent with modification. Your position makes no sense at all.

  119. 120

    Otto has exactly the same condition and exactly the same genes that produce that condition as those that create the human achondroplstic dwarf. Both are caused by the premature cessation of the growth of the long bones and leave the axial skeleton largely unaffected. Both in the Dachshund and dwarf human anatomy the hind legs are straight while the forelegs, our arms, are somewhat twisted.

    All living things are remarkably similar at the gene level. It is the regulation of the manner and rates at which genes are expressed or silenced that produces most of what we see in the living world. My God we are 50% identical with bananas at the DNA level and probably 99% identical with chimpanzees, our closest living relative. Allelic Mendelian segregating and recombining genes probably had little or nothing to do with organic evolution. Bateson realized that, Grasse did and so do I. It is the chromosome, not the gene, that is the unit of organic evolution just as Goldschmidt claimed 66 years ago. The primary role for sexual reproduction is to bring creative evolution to a complete halt and to allow, at best, only minor adjustments in an otherwise immutable species. Referring to evolution -

    “The genetical process which is involved consists of a repatterning of the chromosomes, which results in a completely new genetic system. The theory of the genes and the accumulation of micromutations by selection has to be ruled out of this picture.”
    Richard B. Goldschmidt, The Material Basis of Evolution, page 396.

    Another indispensable role for sexual reproduction was to ensure extinction without which evolution could never have progressed.

    How wrong can an hypothesis possibly be? Nothing, absolutely nothing, in the Darwinian model ever had anything to do with creative evolution, a phenomeonon I am convinced is no longer in progress and hasn’t been for a very long time.

    Trust me but of course you can’t unless you are lucky enough to have been “prescribed” to be able to hear Einstein’s “music of the spheres.” Darwinists, like nearly all pure white cats, are congenitally deaf don’t you know.

    It is hard to believe isn’t it?

    I love it so!

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  120. 121

    Otto’s condition, like every other genetic change, was the result of an instaneous event, a Mendelian dominant mutation which probably originated in a single individual ancestor and was propagated by dog fanciers who were interested in producing a breed that could and would go down the holes of European badgers. They developed the Fox Terrier for flushing foxes or killing them outright also. Most dog breeds were produced for practical purposes. There was even a breed produced to power squirrel cages for the purpose of rotating roasting pigs on a spit. They just loved to run! I’m not sure they are still around although I think they are. It would be a shame if they weren’t wouldn’t it? There was a pointer breed which would hold point for 8 hours which is probably why it is now extinct. Dogs are wonderful.

    It is hard to believe isn’t it?

    I love it so!

    Who is next?

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  121. ofro

    I’m just spitballing here but consider:

    A rapid method of producing heritable change is epigenetic gene induction through methlylation of the DNA molecule. Undoing the methylated change can be just as rapid. A model organism for this is colonial fungi which are able to adapt quickly to different nutrient sources by regulating their digestive enzyme suite through methylation. The mechanism is rapid (days or weeks), reversible, and heritable. However, it also seems that eventually they completely “forget” how to digest substrates that have not been present for too long a time. Commercial labs maintaining mushroom strains in pure tissue culture with charateristics of high commercial value know this and thus they periodically switch off agar recipes to vary the nutrient source to ward off inevitable senescence and include a small fraction of the fruiting substrate in the agar so the fungi doesn’t “forget” how to digest it.

    Let’s call the rapid adaptation “acute” methylation. Now let us hypothesize that “chronic” methylation is a state of persistent acute methylization and that that the cell has a mechanism for distinguishing between acute and chronic. Furthermore that when chronic methylization is detected there is a mechanism that causes a genetic change in the regulatory mechanism for that gene such that the epigenetic change, having proven its worth over an extended period of time, becomes a more permanent genetic change that is more difficult to lose.

    For things as complex as we’ve found even the simplest cells in nature to be I sure won’t deny them such a simple mechanism and indeed would be very surprised if something of that nature DOES NOT exist.

  122. Doctor Davison

    Why didn’t dogs, under unnatural selection, just keep mutating bigger and bigger varieties until we had dogs the size of elephants or in the other direction until we had dogs as small mice? It seems to me there are preprogrammed limits in the size of the animal that the dog genome is allowed to traverse. It hits those limits and there is no more variation possible. That’s why we don’t have dogs the size of mice or elephants – the mutations are not random at all but operate within strictly defined limits with nature constantly and purposely producing incremental change within those limits such that you can’t go from chihuahua to great dane in one generation but you can in hundreds of generations.

  123. 124

    ofro

    Do you know what happens to dogs when they are too big? They die early just like people do. Tiny dogs have short life spans also. There is not a dog breed on earth that could not be produced by breeders in 200 years or less. 100 generations would be plenty long enough especially when one is going to get a lot of help from random undirected mutations such as those that control hair color, and quality, body size, temperament, and every other Mendelian character not one of which ever had anything to do with evolution anyway. Dog breeders have to do a lot of culling of back mutations to maintain the desired characteristics of the various breeds. Horticulturists have the same problem with plants.

    The only reason we do not have as many cat varieties as we dog varieties is because cats are no good for anything anyway. Stuffed, they make great doorstops or bookends maybe. That is about it.

    A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  124. John Davison,
    :The only reason we do not have as many cat varieties as we dog varieties is because cats are no good for anything anyway. Stuffed, they make great doorstops or bookends maybe. That is about it.”

    Now I may need to ask you for an apology to Miss Kitty (we already apologized to her for giving her that atrocious name; she understands that Charles doesn’t work well for a female) ;)

  125. PaV:

    “This isn’t a position I think you want to maintain. Although the ‘phenotypic’ effects are almost nil, the effects to the animal (fly) are enormous. They become sterile, incapable of passing on their genes. I don’t think that’s a subtle change.”

    Actually, I’m totally comfortable maintaining the position that the effects of this mutation are relatively minor. If you look at the actual Masly et al. article in Science rather than the physorg.com summary, you will see that. Sterility did occur, but only under certain special circumstances. First, there was a hell of a lot of playing around that had to happen to get the crosses to work. The F1 (first generation) hybrids from Drosophila simulans x D. melanogaster crosses are typically not viable or are sterile. (That’s because the JYAlpha shift is far from the only postzygotic barrier separating these species.) After going through the necessary contortions, Masly was able to create a hybrid line where most of the genetic material was from D. melanogaster, but the fourth chromosome was from D. simulans.

    What he then found was that males in this hybrid line were sterile if they were homozygous for the Drosophila simulans fourth chromosome. They were sterile because they only had D. melanogaster versions of chromosome 3 (where the gene is located in D. simulans) and only D. simulans versions of chromosome 4 (where the gene is located in D. melanogaster). This is one of those relatively rare cases that can actually be modeled as a classical dominant-recessive problem — it’s the 2-gene, 2-allele model from basic biology. In this instance, it was the double recessive males (those flies lacking either a D. melanogaster or D. simulans version of JYAlpha) that were sterile.

    In sum, the phenotypic effect of JYAlpha’s shift from chr-4 to chr-3 is to reduce the percentage of fertile male offspring resulting from matings between two hybrid individuals or between a hybrid and an individual from one of the parental species. Theoretically, this reduction should be just about 6.25% (1/16). That’s worth repeating, I think. If this was the only mechanism for reproductive isolation between these two species, all hybrids would be fertile, all of the female offspring of the hybrids would be fertile, and almost 95% of the male offspring of the hybrids would be fertile.

    That is a minor phenotypic effect.

  126. Carlos: “Well, I’m sorry to disappoint, but by “best explanation” what I really meant was “best explanation”, i.e. the best explanation that we’ve been able to come up with so far.”

    How is a committedly anti-ID explanation of that sort that “best explanation that we’ve been able to come up with so far” ? Given what we know about the possibility of intelligent designers (given ourselves, beings with intent and insight), positing an intelligent desiger is just as good, given the evidence.

  127. 128

    DaveScot post # 112

    I am just a guest here and have nothing to say about how this forum is being run. I wouldn’t anyway. That is not my style. I have noticed this though. Items on the side bar attract very little sustained attention. Everyone seems to be caught up in the moment as threads come and go never to be heard from again. Also I doubt very much if the denizens of Panda’s Pathetic Pollex (PPP) are going to take me on because Der Fuhrer, Herr Doktor Professor Esley Welsberry (pronounced Velsberry) has told them not to invade other forums and they tend to do as they are told, something I am not very good at myself. They are even afraid to mention my hideous name in their own domain for fear of instant bannishment. Falan Ox has already admitted that. Isn’t that just precious? PPP is a sewer and its denizens are the effluent if you don’t mind my saying so or even if you do.

    I love it so!

    Besides I think I will soon run of of gas here anyway. It is like talking to a wall everywhere I go don’t you know. The main problem is I’m not dead yet but I’m working on it. It helps a lot if you’re dead as the history of science clearly testifies.

    It is hard to believe isn’t it?

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  128. DaveScot,
    ”A rapid method of producing heritable change is epigenetic gene induction through methlylation of the DNA molecule”.

    Methylation is, as far I understand, a method that cells can use to silence genes. In micro-organisms such as your fungi, it is a mechanism to adapt to an altered environment and tell the offspring to do the same. Methylation is also found in mammalian cells and can result in turning off individual genes or whole blocks of genes, especially when it occurs in conjunction with a similar modification of histone proteins. However, I doubt very much that this is the reason for the processes happening when breeding. In plant breeding, you will find a fair amount of transposon movements that activate or inactivate genes; I don’t know how important that is in dog breeding.

    Overall, I can virtually guarantee you that the genomic changes made during breeding are not epigenetic phenomena such as methylation. As you mentioned for your cells, epigenetic phenotypes have a tendency to disappear after a number of generations. In contrast breeders are out to get stable breeds through many generations and will discard any individuals (animals or plants) whose feature disappears with time.

  129. DaveScot,
    ”Evolution via random mutation isn’t supposed to work so quickly that it can produce variations ranging from chihuahua to great dane and everything in between in a few thousand years.”

    You are underestimating how much is constantly going “wrong” with a complex genome with each generation. Just look at the number of inheritable diseases in humans. What gave the appearance of accelerated evolution in the dog breed is the human interference. When a breeder pulls out a pup with an interesting trait, he immediately tries to breed offspring, and through back-crossing ends up with a pure-bred phenotype, and many copies of it. The emphasis is on population size: the more of the newly formed mutant animals there are, the better is the breeder’s chance to get another mutant with a still stronger phenotype. The rate-limiting step in evolution is natural selection. NS acts much more slowly in its action because, first of all, it will only give beneficial mutations a reasonable chance to expand, and in addition will produce a pool of mutated offspring at a much slower rate (back-crossing involves a lot of specific pairings for reproduction, which are rather unlikely in a natural population).

    ”The range in size of dogs is clearly a built-in limit in the canine genome as sure I’m sitting here describing it to you.”

    You are forgetting that external features are not everything that needs to change if a canine species is to grow to the size of an elephant. Just one problem is the heart, whose growth-controlling genes need to be mutated as well. Without this kind of background mutations there are severe physical limitations on a rapid change. One of the reasons large dogs such as the St. Bernard or great dane die faster is that their heart can’t keep up and develops cardiac myopathy. Additional limitations will come from joint strength etc.

    ”I really don’t understand how things so obvious can escape notice in really bright people.”

    Things are not as obvious as they may appear to you. In fact, your statement sounds to me like a weakly veiled ad hominem, which is a no-no here. What happened to the pledge to be Mr. Nice Guy?

  130. 131

    That is another thing. Like ontogeny IS now, phylogeny WAS irreversible. So much for allelic mutations, all of which are freely reversible. In fact you can’t maintain a pure strain of any animal or plant without constantly culling out the back mutations. That is why feral animals and plants soon revert to the ancestral form when artificial selection is terminated.

    Natural selection is entirely conservative just as Reginld C. Punnett (1915) and Leo Berg (1922) independently concluded. Darwinians continue to deny that which horticulturists and animal breeders have known for centuries. They have the whole thing bass ackwards.

    It is hard to believe isn’t it?

    I love it so!

    “A past evolution is undeniable, a present evolution undemonstrable.”

  131. Doctor Davison

    My cats are quite devoted to the capture and subsequent dispatch of small animals that tend to invade stored foods. My dogs have a similar interest but far less talent at it. Moreover, the cats don’t slobber and act in a shameless emotionally needy manner as the dogs do. The cats do their jobs with quiet competence and don’t sulk if they aren’t fawned over for doing their job well. In fact the cats will even try to teach us to hunt for ourselves by presenting us with samples of vermin in various stages of disassembly ranging from quite alive to completely dissected with with edible parts in one pile and inedible parts in another (this is according to the individual cat’s taste in what’s edible and what isn’t – usually feet, tail, and gall bladder are deemed inedible but some cats will eat those too). The level of aliveness is based on an individualized assessment of how well the human has learned his hunting lessons so far. Evidently I really suck at it because the vermin presented to me are almost always quite dead but some of my cats have had more faith in me and regularly brought them home unharmed for me to practice with. One of my cats used to bring home birds that would fly away as soon as she opened her mouth. I never saw that one harm a bird. She was also the one that fastidiously and without exception left a neat pile of uneaten rodent parts consisting of feet, tail, and gall bladder.

    I think you owe all my cats an apology for calling them useless.

  132. Darwinians continue to deny that which horticulturists and animal breeders have known for centuries. They have the whole thing bass ackwards.

    It is hard to believe isn’t it?

    Incredibly hard to believe.

  133. You are forgetting that external features are not everything that needs to change if a canine species is to grow to the size of an elephant. Just one problem is the heart, whose growth-controlling genes need to be mutated as well.

    Piffle. The same genes that control overall size control the size of individual organs. There aren’t great danes born with chihuahua size hearts or vice versa. Breeders don’t have to discard puppies with shrunken or oversize organs. I suggest you put a little more thought into what you write for I have little tolerance for unreasoned outbursts such as that pitiful piece.

    The rest of your argument about limitations in joint strength and other things that reduce fitness make some sense in a natural environment but not in an unnatural environment. In the breeding world if you got a dog that weighed 500 pounds, needed a wheelchair, and lived only 3 years they’d breed that puppy and get rich doing it. Aside from that, you completely failed to address the flip side of the coin – why dogs don’t mutate to the size of mice. No problems with joints or anything like that there now is there?

  134. DaveScot: “Piffle”

    And you may need to slow down a bit with your assumptions about biology. It is likely (generally assumed but probably pulled out of a hat by you for the sake of arguing) that the coordinate organ size regulation with animal size is subject to the same sets of mutated genes. However, this is only a general rule, and additional organ-specific growth factors are very likely involved, too, which need to be modified for _excessive_ animal size. The evidence that the heart plays a limiting role can be seen from the much higher prevalence of cardiovascular problems in giant and large dogs (see http://www.gcvs.com/imaging/ul.....opathy.htm) compared to smaller breeds. This is too much to be a coincidence.

    As to the argument about mini- or micro-dogs, you need to exclude first the strong possibility that breeders don’t see a market in selling rats on a leash. Who would be interested in that for longer than 10 minutes? Dogs are kept by humans as a companion they can interact with and touch and feel, not to observe them in a hamster wheel. Just think how easy it would be to step on a creature like that by accident.

  135. ofro

    additional organ-specific growth factors are very likely involved

    There ya go. In true Darwinian chance worshipping fashion when you run out of facts just start making them up [my emphasis] to support your preconceived conclusions. Bravo. I love it.

    Who would be interested in that [rat size dog] for longer than 10 minutes?

    You gotta be kidding me. A tiny dog that should live (according to your lifespen extrapolations) for about 50 years, consume about 10 fifty-pound sacks of dogfood in its entire life, bark at just the right volume to be an effective alarm against home intrusion but no loud enough to be a nuisance, big enough inflict a nasty bite but not big enough to tear a child’s face off. Good God man, if some breeder could isolate that and sell only neutered/spayed animals he’d be a multi-millionaire virtually overnight.

  136. These are not my lifespan estimates or extrapolations. There are small animals such as rodents that life 2 max 3 years.

  137. ofro

    You were happy enough to speculate that a very large dog would have a vastly reduced lifespan based on the curve in existing dogs. I didn’t even bother mentioning that elephants average 70 years but let you have your extrapolation and said that even at 3 year lifespan and can’t walk a dog the size of a horse would sell as a curiosity for a very high price. Then I pointed out that according to your lifespan extrapolation of the actual curve a tiny dog should live much longer. But you reject that. Nice double standard there. Then in an even more desperate attempt to make a point you said “who’d want a tiny dog anyway?” and I gave the reasons why. And just now, as a quick test of my tiny dog marketability hypothesis I dashed into the living room all excited and told my teenage daughter that a breeder had just announced a dog that weighs less than a pound full grown and would she like me to buy one for her. Guess what the instant response was? :razz:

    Are we having fun yet? I sure am!

  138. 139

    You guys obviously don’t need me here. I will go find another thread or maybe another forum even. Enjoy!

    A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  139. DaveScot:
    ”Are we having fun yet? I sure am!”

    You sure appear to have fun, twisting around what I said and putting words in my mouth, cranking up the intensity dial on the conversation meter.

    You accused me of making up facts. I only downplayed the contributions of the cardiac-specific factors because I wanted to avoid getting too detailed about the factors that influence heart muscle development and growth. Check out http://www.sciencemag.org/cgi/...../5317/1404, and http://www.nature.com/emboj/jo.....0543a.html, just to name two recent reports. The American Heart Association, the National Heart, Lung and Blood Institute and the pharmaceutical industry are putting in big dollars to learn all the details of cardiac development and growth because of its health relevance.

    You accused me of a double standard even though I never made any age estimate for dogs of any kind. Any numbers you may imagine you read elsewhere. I said, and gave you veterinary evidence, that the very large breed dogs are having cardiomyopathy problems. This implies that they may not live as long, but I never indicated by how much. I never made any comment about the marketability of horse-sized dogs, only about rat-sized dogs. Would a mouse- or rat-sized dog initially sell because of its novelty? Long enough to make the breeder rich before the fad disappears? Who knows. However, I would like to see how long your daughter would hold on to a dog the size of a rat or smaller after the curiosity factor has worn off or she stepped on it by accident.

    You are making mis-informed comments about the sound volume a dog the size of a rat could produce. The high-pitched yip of such a small creature will at best be loud enough to barely penetrate a solid wooden door doors, much less scare away a potential intruder. Just about any engineer with basic mechanical training can tell you that the resonance frequency of such a small animal will be quite high, as you would know if you ever heard a rat squeal, and a rat squeal has the advantage over a dog yip that it is continuous. ”I really don’t understand how things so obvious can escape notice in really bright people.”

  140. 141

    Small mammals have a much higher metabolic requirement than larger ones because they have a relatively greater surface per unit volume and heat is lost from the surface of an animal. Small mammals accordingly burn out sooner and die sooner. There is a shrew which weighs less than a gram. It has to eat every few minutes or it will starve to death in a couple of hours and it dies of old age at about 9 months. Larger mammalian species live longer but abnormally large or small members of a particular species have shortened life spans. It is not unusual for mid-sized dogs to reach twenty years but I don’t believe there is a St Bernard that ever exceeded ten. Any attempt to depart from the species norm results in problems no matter what kind of animal it is. The same can be said for many plants.

    Life span is clearly correlated with metabolic rate. The Galapagos tortoise that Darwin brought back to Engand just recently died. Big sluggish reptiles like that live much longer than small metabolically active ones. I have a Russian tortoise that never does a darn thing and I am sure he will outlive me. The same is true of birds. Big parrots live a long time probably because they never do much of anything either. Sloths do too and probably for the same reasons. Man is unusual as he lives much longer than other mammals of similar size. I think this is because he takes much longer to reach maturity taking 18 years or so compared to a little more than a year for a sheep of similar size. His resting metabolic rate is about the same as any other mammal the same size. The equation which describes the relationship between body weight and metabolic rate for mammals is

    Cal/kg = K(Wt in Kgs) raised to the minus 1/4 power. The bigger the animal the lower the metabolic rate. In other words if you plot the log of (Cal/kg) versus the log of (Wt in Kgs) from mice to horses you get a straight line with a negative slope of 1/4. K is the metabolic rate of a 1 Kg animal. Man fits right next to a sheep of the same size. Those are resting metabolic rates. A well conditioned athlete can manage ten times the resting rate for short periods of time.

    The whole business about animals struggling for existence is a lot of nonsense.

    “Animals are not always struggling for existence. Most of the time they are sitting around doing nothing at all.”
    I can’t remember who said it but it is right on. Well adapted creatures don’t need to struggle.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  141. John Davison,
    sorry, I got carried away. I’ll stop.

  142. 143

    comment #98 by Falan Ox

    It is not true that I requested that you be banned at “brainstorms.” I simply explained that I wouldn’t further interact with you and I didn’t. Somebody else asked you to leave. It wasn’t I that is for sure. The important thing is that you did leave because I have never known you to contribute a single constructive comment anywhere.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  143. 144

    What happened to the very long comment I just sent off just before this last one? Am on the list again?

  144. 145

    That commment which still has not appeared had a great deal to do with exactly what DaveScot and ofro have been talking about. What happened to it? It was comopletely innocuous and it took me a long time to compose. Don’t tell me I am to be monitored over that because I won’t buy it. How about an answer Dave or whoever is tending the store.

  145. John, I can get to your post in the “comment” section, but I don’t know how to get it onto this post. Maybe Dave can get it down. The post isn’t terribly long–I hope it’s the one you’re interested in. If it is, then it hasn’t been lost. So hang on.

  146. John, if the post you’re after starts like this, then it’s awaiting someone to “moderate” it. Apparently I don’t have the authority to do that, so someone else will have to. But it’s there. Here’s the beginning of your post that’s stuck awaiting moderationL

    “Small mammals have a much higher metabolic requirement than larger ones because they have a relatively greater surface per unit volume and heat is lost from the surface of an animal. Small mammals accordingly burn out sooner and die sooner.

    P.S. I even saw posts from Gil Dodgen sitting there in the “comment” section; so who knows what gives with these computers and their software?!

  147. Mike: This is from the latest issue of Nature:

    The developmental and evolutionary mechanisms behind the emergence of human-specific brain features remain largely unknown. However, the recent ability to compare our genome to that of our closest relative, the chimpanzee, provides new avenues to link genetic and phenotypic changes in the evolution of the human brain. We devised a ranking of regions in the human genome that show significant evolutionary acceleration. Here we report that the most dramatic of these ‘human accelerated regions’, HAR1, is part of a novel RNA gene (HAR1F) that is expressed specifically in Cajal–Retzius neurons in the developing human neocortex from 7 to 19 gestational weeks, a crucial period for cortical neuron specification and migration. HAR1F is co-expressed with reelin, a product of Cajal–Retzius neurons that is of fundamental importance in specifying the six-layer structure of the human cortex. HAR1 and the other human accelerated regions provide new candidates in the search for uniquely human biology.

    This seems virtually certain to destroy the central dogma molecular biology. And how does Fisher’s mathematics apply to RNA genes? And, of course, this was found in “junk-DNA”, which, it seems, they now want to call the “dark matter” of the genome.

    As to your comment, if you can’t admit that the abrupt appearance of sterility in an individual fly is not a large-scale effect for the fly, then what’s the point of discussing this issue? John Davison, following a line of biologists including Richard Goldschmidt, who have said that “macroevolution” is likely the by-product of chromosomal rearrangements. In this instance, we see chromosomal rearrangement, and we see a large-scale effect resulting. You seem to be overly concerned about this individual effect on the overall population. Well, if a fly, in one generation goes from being a fly to being a hummingbird, if the population of flies is 10,000, this effects the overall gene pool almost negligibly. Does that make it a small effect?

  148. PaV:

    I read the Nature paper earlier – it’s absolutely fascinating. It doesn’t do anything to the central dogma that hasn’t already been done. We’ve known for decades now that DNA -> RNA -> Protein isn’t the only thing in play. In fact, if you look at Crick’s 1970 paper on the central dogma (http://www.euchromatin.org/Crick01.htm), you’ll see that RNA genes fit in just fine with what he was saying then. In terms of the application of Fisher’s mathematics, or, for that matter, the mathematics of any other sort of population genetics that I can think of, a gene is a gene whether it codes for DNA, or for RNA, or for nothing at all. (In fact, most of the markers that I’ve been using in my own work are introns.) As long as we’re working with heritable material, there’s no real problem for population genetics. As far as “junk DNA” goes, that’s definitely not a phrase I’m particularly fond of. There are chunks of non-protein-coding DNA that have functions, chunks that don’t, but there’s way too much going on there to lump it all together with a single term.

    As far as the fly goes:

    (1) I was not talking about the population genetic effects. I was talking about the phenotypic effect of the mutation on the F1 generation hybrids. That effect is a 1/16th chance that a male offspring will be sterile, and it is a phenotypic effect, not a population effect.

    (2) I chose to examine the phenotypic effect at the F1 hybrid level because that is the effect that is relevant for evolutionary modeling. The effect on the sterile offspring is not, and the presense of those individuals in the population has already been accounted for by addressing the reduced F1 production of fertile offspring.

    (3) It is also important to note that the shift of the gene from chr4 to chr3 has no phenotypic effects in cases where the mating takes place within species. It creates a relatively weak postzygotic reproductive barrier (one of several that are known to exist between these two species) that acts to reduce the possibility of gene flow between the species. It does not do anything to within-species mating success.

  149. Doctor Davison

    Occasionally a comment from an unmoderated commenter will be held up automatically. There is a list of words that trigger this. The word list is composed so that it stops unwanted commercial advertisements. To date it has blocked 30,000 comments that were advertisements for online casinos, pornography sites, insurance companies, loans, prescription medications, etcetera. Once in a while it blocks a legitimate comment. Periodically a human goes through the list of blocked comments to make the final decision. The longer the comment you write the greater the chance that one of the red-flagged words will be used in it. That was the case here. I’m not sure what word it was.

  150. ofro

    If you had the first clue about pets people keep you’d know how popular small mammals are. Hamsters, guinea pigs, dwarf rabbits, hedgehogs, sugar gliders, chinchillas, and ferrets are a few that come to mind that my kids have had. One of my daughters had a chihuahua the weighed about 3 pounds full grown. You can take it to the bank that an even smaller dog would be very popular. All you have to do is google teacup puppies and you’ll get hundreds of thousands of hits.

    I never said anything about scaring away an intruder. I said a tiny dog would function as a home intrusion alarm while not being loud enough to be a nuisance to neighbors. It doesn’t have to be any louder or lower pitched than a wrist watch alarm to perform that function. Pitch is dependent on the length of the vocal cords not the size of the animal. A young girl that masses as much as a large dog has a very high pitched scream in comparison. But that’s beside the point as small mammals that have no practical use at all sell well as pets.

    Given your proclivity for making up facts out of thin air in a desperate attempt to defend your dogmatic chance worshipping worldview and wasting everyone’s time in the continual process of correcting you, you’re going to have to find another forum for it. Goodbye.

  151. 152

    Thank you.

    Pardon my well earned paranoid tendencies. I have more enemies than Carter has little liver pills.

    “Even a paranoid can have enemies.”
    Henry Kissinger

    Pav

    All that I am claiming as far as chromosome rearrangement is concerned is that it seems to be sufficient to explain evolution within the scope of the mammalian Order Primates to which we belong. Huge problems arise when we attempt to extend it further. Evolution has been a continuous production of unexplained gaps. Even within the Urodele amphibians there exist enormous differences between genera with respect to the amount of DNA per cell. Amphiuma has the highest DNA per cell and accordingly the largest animal cells while there are other urodeles with only modest levels of DNA per cell and proportionally smaller cells. DNA per cell seems to be best correlated with cell size and metabolic activity with those with high amounts of DNA/cell being rather sluggish animals. Mammals, birds and flying insects all have small cells, small DNA/cell and high metabolic requirements. There is no simple answer to these matters. The fact that the most advanced animals have so little DNA/cell is one of the reasons that I believe evolution may have involved a loss rather than a gain of information. I know of no highly evolved and recent creatures with large concentrations of DNA per cell. Humans have about the same relatively low amount as any other mammal. Birds too have small cells with low DNA per cell as one would expect with their high metabolic rates as well. Certainly these large differences were never produced gradually and must also have been instantaneous transformations. I believe that absolutely nothing in evolution of any real significance ever came about other than instantaneously.

    One can experimentally change the DNA per cell and cell size in amphibians by producing triploid frogs in which each cell is 3/2 times larger than in a diploid control, yet the animal remains perfectly normal in all regards except it is sterile because it is impossible to pair three of a kind so meiosis fails. All triploid frogs (Rana pipiens) become sterile males although as tadpoles they may be either male or female.

    The whole matter of the effect of cell size on animal organization is a fascinating one at least to me. Several years ago I contributed an essay to a book, “Form and Strategy in Science: Studies dedicated to Joseph Henry Woodger on the Occasion of his Seventieth Birthday.” John R. Gregg and F.T.C. Harris edtors, D. Reidel Publishing Company, Dordrecht, Holland, 1964. My essay was “Animal organization as a problem in cell form.” It turns out that the number and size of cells has very ltitle to do with the way animals are put together because you can experimentally alter cell size and number and still get a perfectly normal creature out of it. It doesn’t seem possible that was 42 years ago but it was. That was before I lost my marbles and got interested in evolution.

    “He used to be a decent scientist but something happened to him in the 1980s.”

    I don’t remember which Darwimp it was that came up with that one. It was someone over at “After the Bar Closes.” It may have been Alan Fox. Was it Alan?

    I am also not at all sure that all the reported concentrations of DNA per cell are accurate. That is not always an easy determination.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  152. 153

    Tiny dogs are ibvariably nasty. My thought for the day.

  153. On second thought I’m not going to restrict ofro but rather point out that he is an Associate Professor of Physiology at a well known U.S. medical college and obtained his PhD over 30 years ago in Germany. It’s enlightening that I was able to box him into an indefensible position regarding the built-in size/weight limitations in the dog genome so easily and such that I had him making up things up like there being no market for tiny dogs and thus no one had tried to breach the 1 kilogram barrier. A simple google that takes just seconds reveals the huge market for the smallest possible dogs and anyone with any exposure to much of the real world knows how popular small mammals are as pets for children. Yet this esteemed professor couldn’t be bothered to check the validity of the assertions underpinning his arguments. Why would an otherwise respectable professor do this? Hubris? Unaccustomed to being defied? I don’t know. But I do no one thing, it’s people like Ofro that have caused me, over the decades, to have no intellectual respect for any professor until they’ve demonstrated to me they deserve it. Titles unfortunately have come to mean nothing. Ofro has demonstrated just the opposite of deserving respect. His inability to concede a point and the lengths he went to to avoid doing so earned nothing but contempt. I’ll let him stick around just so I can make an example of him again in the future. A bit of down home American advice, Ofro: “People who get too big for their britches get exposed in the end.” Is there a German equivalent to that meme?

  154. 155

    I have another long one incubating in the oven there. I hope it appears soon as I put a lot of thought into it. At least I think I did.

    “I get no respect.”
    Rodney Dangerfield

  155. Doctor Davison

    :-) I had to pull that last long one out of the spam bin too and I happened to notice which word it was that triggered it.

    P I L L

    That word, whether by itself or as part of another word like “P I L L O W” will trip it. So will D I E T.

    I put spaces between the letters to fool the filter lest I have to fish my own comment out of the spam bucket.

  156. Doctor Davison

    As I was reviewing Ofro’s previous commentary to see if there was a good reason for letting him continue here, I chanced upon his comment to you that human female genome is incapable of gynogenetic production of a male because of the SRY (sex determining gene) only being found on the Y chromosome.

    For obvious reasons I had to check that out for myself as Ofro has demonstrated an easy capacity for making things up to support his arguments.

    It appears he’s correct about SRY but I’d like to hear your rejoinder as I might’ve easily missed something or you may be aware of other ways a human male can be produced absent this SRY gene.

    An interesting tidbit I chanced upon while reading about SRY is how it works. The protein it produces attaches itself to preferred points on the DNA molecule and causes the molecule to bend sharply at those points. The different SHAPE of the molecule causes the expression of masculine traits! So in this way SRY lends great support to your assertions on “position effect”. Perhaps you could give us the Reader’s Digest version of position effect to stimulate further discussion?

  157. Speaking of how SRY works I guess this means that we males are literally and scientifically proven to be bent-out-of-shape versions of the female. My wife has been telling me that for years. It also doesn’t lend much support to Genesis where it says that woman came from man.

  158. 159

    Dave

    I already explained that it is of no consequence whether or not males are produced through semi-meiosis. The key step is the formation of the new chromosome structural homozygote. Goldschmidt was the first to recognize that and the SMH provides the mechanism. Scan back a few posts and you will discover my message that explains that whole business. I have no intention of repeating that whole message again. You will find the full explanation in message 68 of this thread.

    I will also add that until an experiment has been performed, the results can never be known. Whether male humans can be produced gynogemetically will remain completely unknown until the experiment I outlined has been performed. Science is like that don’t you know. No one expected male frogs to be produced gynogenetically either but they were and they were fertile.

    “You can lead a man to the literature but you can’t make him read it.”
    John A. Davison “or comprehend it either.”

    “Hypotheses have to be reasonable, facts don’t.”
    Anonymous

    “An hypothesis does not cease to be an hypothesis when a lot of people believe it.”
    Boris Ephrussi

    “A past evolution is undeniable, a present evolution undemonstrable.”

  159. I reread #68 and see where you explain. I’m confused in that I don’t understand how a female of the new species could successfully mate with males of the prior species. Wouldn’t the rearranged chromosomes of the gynogenetically produced female of the new species be incompatible with the chromosomal arrangement of the male of the old species?

  160. P.S. XX human males (phenotypically male, genotypically female) have been identified. In all cases the SRY gene was present on the X chromosome and arrived there via chromosomal translocation. In all cases the XX males were sterile.

    I’d still like to hear you talk about position effect some more as the SRY gene in any case generates a functional male by simply bending the female DNA molecule into a different shape. Presumably a different shape can be attained in any number of ways. If the shape of the DNA molecule is the difference between male and female I wonder what other phenotypical changes can be made by merely changing the shape of the molecule without altering its sequence.

  161. 162

    They don’t call her Mother Nature for nothing.

    Another one of my several unanswered challenges is – just exactly when did the Creator (or Creators) hand over the reins to Nature that which had, by then, been created? My answer is a resounding -

    NEVER

    Natural selection never had anything to do with evolution except to temporarily allow that which had emerged to survive long enough to become extinct and thereby make way for the next step in the ascending process of evolution, a process no longer in progress. The entire business was determined from the beginning to the end. We are now in that stage of evolution Schindewolf called “typolysis.” From here on it is all down hill. Trust me but of course you won’t because you don’t like the idea. That is the main reason most things aren’t accepted. It is not a valid reason.

    “Everything is determined… by forces over which we have no control.”
    Albert Einstein

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  162. 163

    DaveScot

    The answer to your question is that a single or even a few chromosome rearrangements in hererozygous form will not materially reduce fertility. It is only when several are present that fertility is adversely affected. No more than a dozen major rearrangements separate us from chimpanzees. I believe that exactly that same number of discrete intermediate species existed in our lineage since we separated from chimps millions of year ago. That is based on the reasonable assumption that each rearrangement produced, when homozygous, a new intermediate species which could succesfully breed with the preceeding form which had semi-meiotically produced it. I feel that that number, 12, is extremely reasonable in view of what we really know from the fossil record. There could actually be fewer than that if more than one new chromosome pair was produced at each step. In any event I see no need for the introduction of novel new information to account for any such transformations in the orthogenetic sequence which I regard the human lineage to be. If it did occur where did the information come from? It is implicit in the PEH that it was already there and simply was derepressed one step at a time. This also explains why it is very difficult to identify known ancestral forms with certainty becase when a chromosome is rearranged many characters are bound to be affected simultaneously. Both the horse and the human lineages demonstrate these expected features very nicely.

    It is appropriate to remember Henry Fairfield Osborn’s 1909 appraisal on this matter.

    “In all the research since 1869 on the transformations observed in closely successive phyletic series no evidence whatever, to my knowledge, has been brought forward by any paleontologist, either of the vertebrated or the invertebrated animals, that the fit originates by selection from the fortuitous.”
    Quoted by Leo Berg, Nomogenesis, page 127

    Every orthogenetic sequence of which I am aware indicates a goal that was reached with a terminal ideal form that either then became extinct or is now still extant. The horse. running around on its single finger nails is an obvious terminal form which could not possibly be further improved. So is the elephant and the sequences of both are well documented in the fossil record. Chance never had anything to do with either phylogeny or ontogeny. Of that I am certain.

    If not due to chance and natural selection then what? I propose that the Prescribed Evolutionary Hypothesis (PEH)and the Semi-meiotic Hypothesis (SMH) provide the mechanism.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  163. 164

    I can’t add much to your post 161. Ask someone else, The factors that determine phenotypes are undoubtedly complex and not simply Mendelian and allelic in nature.

  164. 165

    DaveScot

    Here is a little down home advice from me. I don’t care for the way you treated ofro in # 154. You threatened to ban him because he didn’t agree with you, and you questioned his intelligence also. You start treating me that way and I will be out of here in a heart beat. You won’t have to ban me. Your overt contempt for others is unacceptable. It makes my participation here strained to say the least.

    ofro apologized to me for some of the things he said about me and about Otto and I think you should apologize to ofro for some of the things you said about him. It is as simple as that.

    A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  165. 166

    PaV introduced this thread and I would prefer that Pav moderate it.

  166. DaveScot:

    Re comment 161: It’s interesting to note that about 10-20% of XX Male syndrome male cases actually don’t seem to involve a SRY translocation. (see http://www.priory.com/med/xx.htm for a case report of one such instance). The current hypothesis is that SRY is a regulatory gene that controls the expression of another gene on one of the autosomes that actually controls sex determination. In cases where there is an XX male who lacks the SRY gene, it is believed that the autosomal gene has mutated directly, and is no longer appropriately responding to the SRY control.

  167. 168

    Where did each X chromosome come from? I recall a case a long time ago in which it was claimed that both of a male’s X chromosomes came from his mother. Nothing in that paper precluded that all of his chromosomes came from his mother. Incidentally, if an animal of any sort was gynogenetically produced, its mother should be able to accept a skin transplant from that individual but the individual would not be able to accept a skin transplant from its mother. The reason is because the gynogen (offspring) has only her genes all of which the mother accepts as self, but the gynogen has only one-half of its mothers genes so it will reject a skin transplant from its mother. I believe this has already been established in frogs and should be applied to any XX male that pops up provided of course that his mother is still alive. Who knows, we may have a new Christ among us and not even know it! (I am only kidding folks so don’t go ballistic please). As a matter of fact it has been verified in frogs and I document that in “IV-6, Semi-meiosis and genetic variability” in my Manifesto, available on the side board right here at Uncommon Descent. I had temporarily forgotten about it. Isn’t that pathetic? Getting old is like that.

    As a matter of fact semi-meiosis can generate more genetic variabiity than sexual reproduction for genes located at some distance from the centromere which I also document in the Manifesto, based on some experiments I published 45 years ago. The theoretical limit in crossing two heteozygotes is of course 50% That has been substantially exceeded in experiments performed by others and myself and published in the paper below.

    Davison, J.A. 1961, A study of spotting patterns in the leopard frog 1. Effect of gene dosage. J.Hered, 52: 301-304.

    Of course that was back when I was still a decent scientist and hadn’t yet lost my mind. Right Alan?

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  168. Mike Dunford:

    I read the Nature paper earlier – it’s absolutely fascinating. It doesn’t do anything to the central dogma that hasn’t already been done. We’ve known for decades now that DNA -> RNA -> Protein isn’t the only thing in play.

    Yes, reverse transcriptase shook up the central dogma. But a pathway from RNA to DNA is not the same thing as a “RNA gene”. Is there any other known “RNA gene”? This is the first I’ve heard of it.

    Mike:

    I chose to examine the phenotypic effect at the F1 hybrid level because that is the effect that is relevant for evolutionary modeling.

    But this is so because we’re dealing with the particular effect of sterility. A novel chromosomal mechanism has been experimentally demonstrated. If this mechanism involves something other than sterility, it’s effect on the population will be more pronounced. The point we’ve been haggling about is the Fisherian mathematical underpinnings to evolutionary theory and its ‘infinitesimal’ assumption regarding mutational effects. In theory, this newly discovered mechanism can lead to large-scale mutational effects–of which plenty are already known–which contradict Fisher’s underlying assumption. Again, the question remains: what is the mathematical underpinning of the Modern Synthesis?

  169. 170

    The primary cause for sterility in hybrids between related species is purely mechanical and results from any cross-over that occurs in the region of synapsis where one of the chromosomes has undergone a rearrangement with respect to its homologue. No viable gametes can be produced when this has occurred. The two parent species could be identical at the DNA and allelic level and the result would be the same. Mendelian mutation never had anything to do with creative evolution in the past and has nothing to do with it now either. All creative evolution was essentially a position effect phenomenon. Allelic mutation had absolutely nothing to do with any of it, except to possibly be instrumental in ultimate extinction.

    I don’t expect this to be acceptable but will welcome any formal proof that it is wrong. In short, show how the accumulation of micromutations can result in either true speciation or the formation of any of the other taxonomic categories. You will be the first to do so. Have fun.

    “A past evolution is undeniable, a present evolution undemonstrable.”

  170. PaV:

    There are plenty of other RNA genes that are known – this is far from the first. I’m not sure which was the first, but it was probably either the ribosomal RNA genes or the transfer RNA genes – I’m pretty sure both of those were known by the time Crick wrote the 1970 paper linked above. Since then, there have been a number of others found. Most, including the one outlined in the Nature paper, are involved in gene regulation. In these cases, a gene codes for a segment of RNA. That RNA, in turn, binds to the DNA at another site in the genome, affecting the regulation of whatever gene is found there. This is evo-devo territory, and I’m not as knowledgable there as I am in my own area, but from what I’ve picked up talking to other grad students who are involved in evo-devo, the specific gene discussed in the nature paper is a new discovery, but the basic mechanism and the class of gene are not new.

    Going back to the chromosomal rearrangement stuff, my expectation based on the way the mechanism works is that F2/backcross sterility (or reduced fertility) and F2/backcross inviability (or reduced viability) are going to be by far the most common effects for this type of genomic change. That is because having the same gene on different chromosomes in different species means that, depending on the gene, you may see both over- and underdose issues in some of the offspring (5/16th of the offspring will have more than 2 copies of the gene, and 5/16th will have fewer than 2 [2-gene, 2-allele Mendellian prediction]), and you will always have 1/16th with no copies of the gene. The only time you will see any other kind of effect is if the translocation also results in one or more genes being mutated at the same time that they are moved. In those cases, I would expect that the evolutionary behavior would basically fit the classic model.

    Relocating a gene from one chromosome to another looks to be a good mechanism for increasing the reproductive isolation between two populations, but it doesn’t look to me like it’s any more (or less) likely to result in major phenotyic changes than most other sorts of mutation.

    I’m not sure what your question about the mathematical underpinnings is getting at. As best as I can tell, it’ll depend a lot on what you mean by “modern synthesis.” If you are using the phrase in the classic sense, then I’d refer you back to Fisher, Wright, etc. If you are asking if our current understanding of evolution has different mathematical underpinnings, I guess it will depend a lot on what you mean by “different.” The modern synthesis is still very much a part of our current understanding of evolution, but we’ve filled in a lot of the gaps, shown what happens under slightly different assumptions, etc. I’d expect that you’d get the same sort of answer if you asked a theoretical physicist about relativity today compared with relativity as originally described by Einstein.

    If you’re looking for specific names, the first two that pop to mind are Joe Felsenstein (UW) and Sergey Gavrilets (U Tenn.). The theoretical work of both is thought well enough of that I’ve been spending a lot of time reading them in preparation for my comps.

  171. Mike Dunford:

    Thanks for the references. I found this commentary about Gavrilets’ 2004 book to the point:

    John A. Endler, University of California, Santa Barbara : This is the first book I have read about speciation that actually presents the topic in an objective way, rather than carrying on the fifty-year tradition of strong opinions without critical evidence. Gavrilets does a splendid job of building all of the models and discussing their implications.

    This is basically the point I’ve been making on this post. I’m going to see what I can do about securing a copy of his book.

    As to the chromosome translocation, again, for the fly that is sterile, the phenotypic effect is enormous. (And, incidentally, Darwin argued the reality of sterility. And now a gene for it has been identified.) Fisher envisioned–per Orr–that a very large number of genes acted in an interconnected way in organisms. Hence, any mutation in one of the genes would be effectively “watered-down”, let us say, by the effects of the other genes. This mechanism, newly verified, just does not fit this model–no matter what you say, nor how many times you say it. Now, I can possibly look at Gavrilets’ book and find that he has, indeed, come up with a model that is consistent with currently known genetic mechanisms of change (mutations), but I surely haven’t seen any proposed model as yet that is able to do this.

    As I say, I’ll see what I can do about getting a copy of it.

  172. Fitness Landscapes and the Origin of Species definitely does do a very thorough job at constructing and discussing mathematical models for speciation. His treatment of parapatric speciation, in particular, is quite good, and goes a long way toward addressing and area that was overly neglected for way too long. He does also cover chromosomal rearrangements, by the way, and reviews some of the prior theoretical work in that area.

    I would have a much easier time accepting your views on the newly-identified fly translocation if the translocation in question (JYAlpha) created a more substantial level of reproductive isolation between the species, or if it were the only postzygotic barrier separating them. At present, however, it appears that the JYAlpha chromosome jump reduces interfertility by not a lot more than 5%. We also know that it is not the only postzygotic isolating mechanism separating the species – if it was, Masly wouldn’t have had to spend nearly as much time on the experiment, and he wouldn’t have had to utilize so many complex breeding strategies to establish the hybrid line.

  173. 174

    Mike Dunford

    It is far more than “relocating a gene from one chromosome to another” that is involved when whole chromosome segments are relocated. Such events have multiple effects, often so dramatic that the offspring may be drastcally different from the parent species that produced them. I repeat that genes have had very little to do with evolution because at that level we animals are very much alike and so are the plants. I know of not a single instance where a mutated gene can be demonstrated to play any role even in speciation and I welcome a demonstration by anyone else that it has.

    I also note that there has been no response to the challenge I presented in my last message here. It is as if it had never been presented. That is standard procedure when the particulate genetic model is challenged, just as it was when Goldschmidt first presented it sixty-six years ago. We saltationists are not allowed to exist by an establishment still dominated by the devout advocates of the most failed hypothesis in the history of science. They are finally finished, kaput, washed-up, thoroughly exposed and hung out to dry. After i47 years of what can only be described as a continuous mass hysteria, they are beginning to realize it as their stony silence these days so eloquently displays.

    I love it so!

    The particulate gene cannot be demonstrated to have played any role whatsoever in the origin of any taxonomic unit from species to phylum. The entire basis for the gradualist, accumulatory version of evolution is an illusion based on a faulty original assumption. That assumption is that evolution can be explained by the action of the environment. Does the environment in any way affect the development of any organism from its beginning whether that be an egg or a vegetative cutting or any other source of a new organism? The answer is a deafening NO! All that the environment can do or ever has done is to serve as a suitable milieu for the continuity of life and as a stimulus for the release of an endogenous, preprogrammed potentiality. Even extinction has probably been preprogrammed for many and perhaps all life forms, including ourselves. Without extinction there could never have been evolution.

    As nearly as I can determine, the innate capacity for the present flora and fauna to evolve into new life forms has been exhausted. Others may choose to imagine otherwise. I will continue to join with Grasse until we are proven to be wrong which I do not anticipate as even a remote possibility.

    “The period of great fecundity is over: present evolution appears as a weakened process, declining or near its end. Aren’t we witnessing the remains of an immense phenomenon close to extinction? Aren’t the small variations which are being recorded everywhere the tail end, the last oscillations of the evolutionary movement? Aren’t our plants, our animals lacking some mechanisms which were present in the early flora and fauna?
    Pierre Grasse, The Evolution of Living Organisms, page 71.

    Like the real scientist he was, Grasse asked questions. He questioned the entire Uniformitarian foundation on which the Darwinian model is based, a model which has proven to be absolutely useless as an explanation for either ontogeny or phylogeny.

    “Neither in the one nor in the other is there room for chance.”
    Leo Berg, Nomogenesis page 134

    What is the only conceivable alternative to chance? Einstein gave us the answer -

    “Everything is determined… by forces over which we have no control.”

    Allelic mutations, natural selection, sexual reproduction, population genetics – none of these ever had anything to do with either ontogeny or phylogeny. Both were preprogrammed eons ago and the phylogeny program has terminated with the production of Homo sapiens the last mammal, in my opinion, that will ever appear on this planet. Evolution is apparently finished and to blindly assume otherwise, as the Darwinians so obviously do, is intellectually dishonest, driven entirely by an ideology, probably largely innate, that refuses to recognize that there was purpose in every aspect of the living world, a purpose that has finally been achieved.

    A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  174. 175

    Just to make my position a litte more interesting, I will put it in the form of a challlege as I have done many times before. Not one of my several challeneges have ever adequately answered. Most of them have not even been recognized. Let me see if this one can be added to the long list of those which either cannot be effectively answered or will not even be acknowledged.

    Demonstrate, with as many examples as you want, how any number of allelic (Mendelian) mutations have ever resulted in the production of any new life form, prokaryote or eukaryoyte, that would satisfy the criterion of being recognized as a new true breeding species.

    To demonstrate my generosity, I will give you 24 hours or until about noon tomorrow, the 16th of September. I have another one pending over at “brainstorms ” so excuse me while tend to that one.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  175. Mike Dunford,

    I’ve located a library where I can get “Fitness Landscapes…”. I’ll be interested to see what models he proposes.

    I agree with John Davison. What Masly’s paper demonstrates is the mobility of gene segments from chromosome to chromosome. I consider that to be of some significance. But, of course, the “gene” content of the human genome is what, less than 10%. I’m convinced (meaning I predict) that this 90% of the genome is where all the significant regulatory systems controlling development and repair, will be found–in other words, “design”. The RNA “gene” we talked about earlier is just one example of what I predict they’ll be finding more and more of (since now they’ll start looking!) Anyways, enjoyed the give and take.

  176. 177

    Mike Dunford or anyone else for that matter.

    Time is up. Yesterday I asked for evidence that any number of allelic mutations ever played any role in the life of any organism enabling it to produce a new species. As is typical, this challenge, like all my others, goes both unanswered and unacknowledged. This is an old story, one to which I have grown accustomed. This is just for the record. Naturally I am pleased.

    Thanks, by your silence, for providing more evidence for my conviction that Mendelian, allelic mutations never had anything to do with creative evolution. I really appreciate that.

    It is hard to believe isn’t it?

    I love it so!

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  177. John asks:

    Of course that was back when I was still a decent scientist and hadn’t yet lost my mind. Right Alan?

    Remember the film “Tootsie”, where Tootsie is rebuffing the eldrly actor who has just serenaded her and said “Of course I am just an old has-been”. Tootsie asks, “were you ever famous?” :P

  178. From John’s Evolutionary Manifesto:

    It is not the genes but the chromosomes that do the evolving

    A serious question. What is a gene if not a nucleotide sequence with alleles contained in a chromosome, and what is a chromosome if not a longer sequence of nucleotides associated with supporting protein?

  179. 180

    Alan Fox

    If that is your concept of a chromosome, nothing but a string of genes, good for you. Write a paper to that effect and try to get it published, something you have never done and probably never will do. As usual, you contribute nothing of substance and never have. You are nothing but a “prescribed” feckless, clueless, troublemaker and one man goon squad for Der Fuhrer Herr Doktor Professor Esley Welsberry (pronounced Velsberry). The gossip mongers over at “After The Bar Closes” still are afraid to mention my name. You even admitted as much. That was good enough for me to reject you once and for all. Give your “groupthinking” cronies over at the Darwinian “Alamo” my best. Get lost.

    “A past evolution is undeniable, a present evolution undemonstrable.”

  180. If that is your concept of a chromosome, nothing but a string of genes, good for you.

    The commonly accepted view of a chromosome is of a continuous linear polymer of nucleotides with associated support protein. One of the fastest moving areas of biology is evo-devo, which is trying to unravel how encoded grnomic information is translated into phenotypic structure. I suspect there are already many papers on this subject.

    You seem to imply this is incorrect, but you neglected to mention in what way in post n° 180. Would it be possible for you to give a brief explanation of how a chromosome is not a sequence of nuceotides, some sections of which being described as genes. Alternatively, a link to an existing reference would be fine.

    Thanks in advance

  181. 182

    Not a chance. I do not suffer fools of which you are a perfect example.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  182. John, are you listening? From your “flowery” language the last couple of posts, I can see why you’ve gotten the boot. We’re going to have to find a way to keep you calm!!!:)

    John Davison:
    “Thanks, by your silence, for providing more evidence for my conviction that Mendelian, allelic mutations never had anything to do with creative evolution. I really appreciate that.”

    That’s what had Bateson scratching his head for so long. And no one has really come up with an answer. You gave Alan 24 hours; but it’s been 100 years since Bateson, and still no sensible answer to the question, “Whence alleles”?

  183. It is a shame John does not choose to elaborate on his assertion: “It is not the genes but the chromosomes that do the evolving”. I suspect the reason John’s challenges remain unanswered (though I have seen responses to him; most get the treatment similar to #181 and 182 and depending on the moderation policy of the particular thread, either John or his critics are booted) is that they are not taken seriously.

    I doubt anyone would disagree that Bateson was a fine scientist (he coined the word “genetics” and promoted the work of Mendel), but he died in 1926. Had he been working today, after the discoveries of DNA, the genetic code, advances in molecular and developmental biology and embryology, would he still have reached the same concusions that John claims he espoused in his published work?

    My question to John was intended to see what common ground exists between his ideas and mainstream science, so that the differences could be brought into focus. I chose the “gene” question because biochemistry is a subject I have studied. Would John prefer another or will his response be the same to any query?

  184. 185

    At “brainstorm’ I refused to interact with Alan Fox and I will do the same here thank you very much. At “brainstorms” he was finally banned because of his behavior. If you choose to tolerate him here that is fine with me but as far as I am concerned the man does not exist. If you choose to give me “the boot” that is also fine with me. It will simply become, like every thing else that transpires on internet forums and blogs, a matter of record, a record I am happy to recount and preserve.

    As for my several unanswered, unacknowledged challenges, they too are now a matter of record and I am growing weary of repeating them for the benefit of a stone deaf audience, a reality I now regard as firmly established both here as elsewhere wherever I have been allowed.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  185. John, I’m not giving you the boot. (I don’t even think I have the ability, by the way–or, at least, I haven’t figure out the way yet.) I would just say to you to lay off the 2 x 4 approach. I know that when I get worked up I try, figuratively, to take a few deep breaths. I also know (‘sense’, really) that the farther I move beyond Darwinism, the less anything Darwinists say makes sense anymore–and it gets frustrating. For me, this has been going on for about 10 years. I imagine for you it’s been quite a bit longer than that. So I can understand (from a personal perspective) your frustration at times. As I say, I have no intention to “boot” you; but I’m thinking of other places that might. And it would be a shame not to have your thoughtful, professional input.

    Alan Fox: I believe I agree with John. I think the overall “information structure” (I’m sort of coining a term here) of the chromosome is something that needs to be ‘rearranged’ if you’re going to have a new “development” program established for the new embryo. I think we can all agree that if we and chimps share 97% of the same genes then it’s not the genes that makes us different.

    Yet, for all the advances in molecular biology and such, there is still no Darwinistic mechanism that satisfies me intellectually. It just doesn’t add up. I’m near, or at, the genius IQ level, so it ain’t that. It just doesn’t add up.

  186. 187

    Pav

    It is the advances that are being made by molecular biology that are the most devastating to the Darwinian fairy tale. Absolutely nothing revealed by the experimental approach can ever be reconciled with the Darwinian hoax, absolutely nothing. Nothing ever has and nothing ever will. It remains today what it always was, the product of the overactive imagination of a pair of Victorian naturalists, one of whom had the common sense to abandon it entirely later in life.

    “in accordance with the views expounded in a former work, Man’s Place in the Universe, I have fully discussed the evidences in plant and animal life indicating a PREVISION AND DEFINITE PREPARATION of the earth for Man – an old doctrine, supposed to be exploded, but which, to all who accept the view that the universe is not a chance product, will, I hope, no longer seem to be outside the realm of scientific inquiry.”
    Henry Russel Wallace, The World of Life: A Manifestation of Creative Power, Directive Mind and Ultimate Purpose, page 399, my emphasis.

    If evolution was not to prepare the earth for man, then why is Homo sapiens the youngest mammal on the planet? He is you know or so I will continue to claim until I am proved to be in error. Trust me.

    To continue to ascribe to chance a role in either ontogeny or phylogeny is absurd. It always was.

    “Neither in the one nor in the other is there room for chance.”
    Leo Berg, Nomogenesis, page 134.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  187. For anyone interested, here is the thread page where David Hagen suspended my posting priviledges for exceeding three per day. Prior to that, I can’t see where I was off-topic or abusive, although admittedly, I was disagreeing with other posters.

    PaV wrote:

    I think we can all agree that if we and chimps share 97% of the same genes then it’s not the genes that makes us different.

    I’m sorry but, no, I can’t agree. The information stored in a chimp or human oocyte necessary for that oocyte to develop into an individual capapble of reproducing is stored in the DNA sequences of the chromosomes, plus that inherited via the maternal egg cytoplasm, such as mitochondria (which have their own DNA) and the other cytoplasmic machinery needed for protein synthesis, etc.

    Maybe we misunderstand each other, but “It is not the genes but the chromosomes that do the evolving” would seem to be either a tautology, or John is suggesting genetic information resides in some other part of the chromosome than the DNA. As he seems unwilling to clarify, it is difficult to know what meaning this sentence is meant to convey.

  188. 189

    Alan Fox lies.

    Incidentally this thread is about to disappear again and if it is going to be constantly interrupted by Alan Fox, I recommend it be terminated. The man contributes absolutely nothing to any subject. His sole purpose is to discredit me whatever the cost. That is all he has ever done. Why Uncommon Descent tolerates him escapes me.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  189. Alan Fox lies.

    Please be a little more specific. I may have made an incorrect statement, and if you can point out the error, I shall be happy to admit the error and apologise. I have not said anything here that I know to be untrue.

  190. 191

    As this thread slowly sinks in the south I bid you all a fond farewell. I think from here on in I will just be a kibitzer. After all, my work is published and doesn’t need to be either defended or repeated here or on any other internet forum for that matter.

    “A past evolution is undeniable, a present evolution undemonstrable.”
    Joh A. Davison

  191. Dr. Davison, I for one look forward to your perspective on the various topics that arise here. It’s my assumption that if someone posting here makes a good point, that you will acknowledge it as such. I trust your expertise. So I think you serve a valuable function in keeping both sides honest here.

    I hope you keep up the posting.

    As to this thread, I think I know how to pull it, so officially, it’s closed. No more comments. Thanks to all who contributed.