Home » Intelligent Design » There are more things in heaven and earth, Paul, Than are dreamt of in your philosophy.

There are more things in heaven and earth, Paul, Than are dreamt of in your philosophy.

It’s funny how Paul Myers, Richard Dawkins, Eugenie Scott, et al say that evolution isn’t about religion yet you can’t swing a dead cat without hitting one of their rants on religion. But that’s not the point of this article.

I have a problem with these people in that they arbitrarily limit what science can potentially explain. The so called supernatural remains supernatural only as long as there’s no metric by which to measure it. Once a metric is discovered the supernatural becomes the natural.

Paul quotes someone on the virgin birth of Christ saying that it defies everything science has revealed in regard to mammalian reproduction. This is utter dreck. Even (especially!) Myers should know that meiosis is a two stage process wherein the first stage results in the production of two perfectly viable diploid cells. The second stage of meiosis then splits these two cells into four haploid gametes. Interrupting the process at the completion of the first stage results in parthenogenesis. Indeed, there are number of organisms in nature that have lost the second stage of meiosis and now reproduce parthenogenetically. See here for more detail. Moreover, it has also been scientifically established that an XX genome can produce phenotypical male offspring. Morever, while all observed XX males in humans are sterile, pathenogenetic populations can still reproduce sexually if sexual reproduction still exists in the species (Da Vinci Code fans will be happy to know this). While it was widely believed that mammals had completely lost the ability for parthenogenetic reproduction, in 2004 researchers in Tokyo managed to create viable parthenogenetic mice. So Paul, science now reveals that the virgin birth of a human male is quite possible. Put that in your pipe and smoke it. What I want to know now is whether ignorance or dishonesty explains why you’d quote someone who claims the virgin birth of Christ defies everything we know about mammalian reproduction. Neither explanation becomes you of course and it gives me immeasurable delight to put you in the proverbial position of choosing between a rock and a hard place. :lol:

The next thing I’d like to debunk in Paul’s latest diatribe is his assertion that matter and energy is all that exists in the universe and science can explain it all without reverting to anything else.

The latest findings in cosmology are that the universe is composed of 5% visible matter, 20% dark matter, and 75% dark energy. The theory of gravity applied to the visible matter and energy in our solar system and local region of the galaxy predicts with exquisite precision the motion of visible bodies. However, when applied to larger structures such as our galaxy and our local galactic cluster the predictions break down. In order to explain those motions there must be 5 times the amount of visible matter existing in some form of normal matter that is not visible. That’s not very incredible and many hypothesis based on known physics are on the table to characterize the dark matter component. See here for more detail. What’s more bizarre is that recently it was discovered that in the universe writ large (relative motions of galactic clusters) it is revealed that the universe is expanding at an accelerating rate. This was not predicted by the theory of gravity and the amount of matter and energy inferred from the motion of local galaxies. In point of fact there must be something completely unknown going on in the universe. 75% of the “stuff” which makes up the universe is an unknown coined dark energy that diffuses the universe.

So you see, Paul, matter and energy that we know about are only a small fraction of what makes the universe go ’round, so to speak. Who’s to say at this point in time that this huge amount of unknown “stuff” is incapable of organization that produces intelligence? Could God be lurking in the dark energy of the universe? Can science investigate the nature of dark energy? You bet it can. The jury is still out, Paul. You don’t know half what you think you know about the nature of nature nor of what you presume to be the bounds of science’s capacity to investigate it. Hence the subject line of this article.

Update: It has been suggested in the commentary from Professor of Biology Allen MacNeil of Cornell that I don’t know what I’m talking about regarding meiosis in that there is no stage wherein 2 diploid cells are present. I present to you The Phases of Meiosis from Biology 032 at Brown University.

Meiosis begins with Interphase I. During this phase there is a duplication genetic material, DNA replication. Cells go from being 2N, 2C (N= chromosome content, C = DNA content) to 2N, 4C.

further down

In Cytokinesis I, the cells finally split, with one copy of each chromosome in each one. Each of the two resulting cells is now 2N, 2C.

Now I don’t know exactly where the good Professor MacNeil learned his elementary cell biology but where I did a 2n,2c cell is a diploid cell with the normal diploid chromosome count (2n) and the normal amount of DNA (2c). But I’d like thank the professor for keeping on my toes. For a moment there I’d thought I’d had a senior moment and forgotten basic things I learned 30 years ago.

Update 2: The preponderance of literature calls the intermediate cells 1N,2C. This appears to be just semantics. The cells contain 1n unique chromosomes but 2n total chromosomes. I can’t find a definition of “diploid” anywhere that says two identical paired chromosomes only counts as one chromosome. The situation is 23 paired chromosomes that are 100% homozygous. It’s still diploid except perhaps to a pedant.

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128 Responses to There are more things in heaven and earth, Paul, Than are dreamt of in your philosophy.

  1. Unfortunately, Dave, the first division of meiosis does NOT produce two “diploid” cells. It produces two HAPLOID cells (i.e. two cells that have a single set of chromosomes), in which the chromosomes are double stranded. The second division of meiosis simply divides the sister chromatids in these two cells, which doesn’t change the fact that they are already haploid at the end of the first division.

    This means that the products of the first division of meiosis are totally incapable of producing a fully functioning organism. This would be like producing a fully functioning organism from a sperm or egg cell; impossible, in other words.

    Those vertebrates that are parthenogenetic (a few species of whiptail lizards in the southwestern US and the Caucasus mountains in Russia) do not produce fully functioning offspring from first division daughter cells. They produce them from hybrids between several sets of chromosomes from different species (see http://en.wikipedia.org/wiki/Parthenogenesis for the details).

    This is freshman biology, Dave. If one of my students had made a statement this egregiously wrong, I would have flunked him or her on the exam.

  2. Sorry Dave,

    Yup Bio 101:

    Telephase I- the cytoplasm of the germ cell divides at some point. There are now two haploid (n) cells. Each cell has one of each type of chromosome that was present in the parent (2n) cell. However, all chromosomes are still in the duplicated state. (italics in original)

    Biology- concepts and applications Starr fifth edition page 142

  3. Allen,

    Would you flunk the student even if he/ she got everything else correct and that was only one of perhaps 100 questions they flubbed?

  4. DaveScot said:

    So Paul, science now reveals that the virgin birth of a human male is quite possible.

    From a phenotypically male human (which is what the discussion is about)?

  5. Whoops – looking more closely, you may be referring to the XX male as the offspring of the posited virgin birth. But that certainly hasn’t been shown possible. 80% of XX males are male because one X chromosome has acquired SRY from the father’s Y chromosome – and the reason for the other 20% isn’t yet known, so contribution from the father’s Y (or even any other) chromosome hasn’t been ruled out.

  6. Actually it takes a measure of faith for Prof. Myers to accept that even matter and energy exist independently of Mind. What is more real in our experience are conscious, first-person perceptions of matter and energy. I’d like to see him explain that in physicalistically acceptable terms. Good luck, Paul. (You’ll need all of it you can get.) ;)

  7. “It’s funny how Paul Myers, Richard Dawkins, Eugenie Scott, et al say that evolution isn’t about religion yet you can’t swing a dead cat without hitting one of their rants on religion.”

    I’m glad someone is calling these folks out on their anti-religious bias. Could it be a coincidence that the staunchest darwinians are also the staunchest atheists? Hmmm…

    “The so called supernatural remains supernatural only as long as there’s no metric by which to measure it. Once a metric is discovered the supernatural becomes the natural.”

    This has been my position on the matter for some time. But it raises an interesting question–is the ID movement really trying to expand science to include supernaturalism, or is it trying to expand science so that it might naturalise what is now considered to be ‘supernatural’. The former seems easier to support than the latter. After all, can’t something only remain supernatural if it can’t be explained? And doesn’t science purport to explain things? I consider these (at least somewhat) open questions.

    “Who’s to say at this point in time that this huge amount of unknown “stuff” is incapable of organization that produces intelligence? Could God be lurking in the dark energy of the universe?”

    I’m afraid this is where I must respectfully disagree. (I won’t comment on the section on parthenogenesis.) I’m more than a little bothered by the idea of a god that recedes into the far reaches of the universe where we have yet to probe–simply because we have yet to probe there. This is the ‘god-of-the-gaps’ par excellence. No god worth having should need to retreat into the darkness like that, and this position is simply not scientific.

    Apart from that, it seems a little absurd. Dark matter has a few things in common with familiar matter, and it differs in a few important details, but there’s no theoretical reason to posit something so radical as that it has intelligence! Not only is there no theoretical basis for such a prediction, but there’s also no theoretical framework in which it would make sense. That doesn’t rule it out by any means, but it makes such speculation unscientific–at least until we have more data about dark matter.

  8. Allen

    Excuse my ignorance. Pedantry in the definition of “diploid” and “haploid” in describing meiosis is beyond me. I was under the impression that haploid and diploid refer to no more than the the normal number of chromosomes (haploid = n = 23 and diploid = 2n = 46 for humans) . The second stage of meiosis involves no DNA replication so I’m wondering how two cells with haploid number can become four cells with haploid number without DNA replication. Is there some sort of magic involved here or do the two daughter cells from the first stage of meiosis each contain 46 chromosomes arranged in 2 duplicate sets of 23 where they can then divide into four unpaired groups of 23 chromosomes each in another slightly modified mitotic division?

    Meiosis is described as two mitotic divisions with a little bit of modification to normal mitosis such that the first division instead of producing two heterozygous daughters identical to the mother cell produces two homozygous daughters, one with a pair of 23 chromosomes from the maternal side and the other with 23 chromosomes from the paternal side (with a little bit of crossover between maternal and paternal sides to make a novel result instead of an identical copy).

    If this is not correct then the literature is very misleading.

    This makes all kinds of sense in an evolutionary POV. Mitosis ostensibly evolved long before meiosis. The first stage of this evolution would simply be a modification of mitosis that resulted in two homozygous but perfectly viable cells. Then the second stage evolved where the homozygous cells divide again in a slightly modified mitosis into two haploid cells.

    This then handily explains why formerly meiotic organisms could devolve into parthenogenetic reproducers and also why the Tokyo researchers could coax a mouse into producing viable parthenogenetic offspring.

    Of coures I didn’t come up with the semi-meiotic theory of evolution. That credit goes to J.A. Davison who published it in 1984 in the peer reviewed Journal of Theoretical Biology.

    http://hkusua.hku.hk/~cdbeling/Semi-Meiosis.pdf

    Why don’t you be a maverick and be the first to find fault in Davison’s work. I sure can’t. It’s as much as I can do to count up the chromosomes at the end of prophase 2 and arrive at a number of 46 in each of the daughter cells.

    Barring that maybe it’s really you that should flunk out of Biology 101 for failing to count up the number of chromosomes at the end of prophase 2 and not coming up with the 2n number for humans.

  9. Reed

    You confused dark matter with dark energy.

    Given the typically transcendant portrayals of God existing outside the physical universe as we know it, and dark energy existing outside the physical universe as we know it… I’m just connecting some hypothetical dots there.

  10. Robin

    Yes, Christ would ostensibly be an XX male through parthenogenesis. The fact remains that 20% of the XX males have no SRY so while it remains to be explained how that happens the fact that it DOES somehow still happen is still there.

  11. Frank Tipler writes about the Virgin Birth of Jesus as follows (I’m not sure how much to buy here, but it’s in the same ballpark as DaveScot’s post):

    We first have to understand how a virgin birth of a human male can be accomplished using only known molecular biological mechanisms. There is now an extensive scientific literature on virgin birth in vertebrates. Virgin births have been extensively studied in Caucasian rock lizards [34], and also in turkeys ([35], [36]). There is one strain of turkeys ([35], [36]) in which more than 40% of all births are virgin births. What happens in these turkeys is that often a haploid egg cell begins to divide without being fertilized by a sperm cell. If at some point early in the cell division process, the chromosomes duplicate so that a diploid cell is formed, a normal turkey is born. This parthenogenetic turkey is always a male, because in birds, a male results if the two sex chromosomes are the same (a male bird has two Z chromosomes and a female is WZ.).

    It is easy to induce a human oocyte (egg cell) to begin cell division without first being fertilized by a sperm ([37]-[40]). The oocytes thus induced to begin division can be either haploid or diploid. This human oocyte cell division is so easy to induce in the laboratory that many researchers in this field have suggested that virgin births may be quite common in humans, perhaps as common as identical twins, which on the average occur 1 out of every 300 births (Encyclopaedia Britannica, “Multiple Births”, 1967 and 2003 edition). This conjecture on the rate of virgin births could be easily tested. One would merely conduct a DNA identity test on female children who are observed to closely resemble their mothers. (Almost all virgin birth children would be expected to be females. The extremely rare exception I shall discuss below.) To date, no such investigation has been carried out, probably because of ethical objections. With human oocytes, again for ethical reasons, no attempt has yet been made to implant these virginally conceived fetuses into a womb. An attempt was made a few years ago to complete a virgin birth in a marmoset monkey [37], but it was unsuccessful. Because of a peculiarity in the centromeres of primate cells (they are inherited from the father), I myself suspect a primate virgin birth could result only if a diploid oocyte started to divide. Of course, in every case of a virgin birth, all the genetic information has to be already present the mother. There are at least three ways to generate a male human being from genetic information which comes entirely from the mother. I shall discuss only one such method here (for another, see [18], p. 44, and below.).

    I propose that Jesus was a special type of XX male ([44]-[49]). Approximately one out of every 20,000 males is an XX male. Such males are normal in behavior and intelligence, but have smaller teeth, shorter statue, and smaller testis than normal males. They are usually identified as XX males because they cannot have children, and ask doctors to cure the infertility. Normal males are XY, but there are only 28 genes on the Y chromosome, as opposed to thousands on the X chromosome. Of these 28 genes, 15 are unique to the Y chromosome, and 13 have counterparts on the X chromosome [41]. The gene with counterparts on both the X and the Y chromosomes are called “homologous genes.” An XX male results when a single key gene for maleness on the Y chromosome (the SRY gene) is inserted into an X chromosome. I propose that ALL (or at least many) of the Y chromosome genes were inserted into one of Mary’s X chromosomes, and that in Mary, one of the standard mechanisms used to turn off genes were active on these inserted Y genes. (There is an RNA process that can turn off an entire X chromosome. This is the most elegant turn-off mechanism.) Jesus would then result when one of Mary’s eggs cells started to divide before it became haploid and with the Y-genes activated. (And of course with the extra X genes deactivated.) If a sample of Jesus’ blood and/or flesh could be obtained, my proposal could easily be tested by carrying out two distinct DNA tests for sex: (1) test for the Y genes and (2) test for two alleles (different gene forms) of X chromosome genes. In other words, a male born of a virgin would have two X chromosome genes for each of its counterpart Y gene. Normal males would have only one X chromosome gene for each of its Y counterpart gene. This pairing would apply to each of the 13 genes on the Y chromosome that has an X counterpart.

    Such a Virgin Birth would be improbable. If the measured probability that a single Y gene is inserted into an X chromosome is 1 in 20,000, then the probability that all Y genes are inserted into an X chromosome is (1/20,000) raised to 28 power, the power corresponding to the number of Y genes. (Assuming that the insertion of each Y gene has equal probability, and these insertions are independent.) There have been only about 100 billion humans born since behaviorally modern Homo sapiens evolved between 55,000 and 80,000 years ago ([74], p. 704). The number of humans that have ever lived is roughly computed as follows. In the first 60,000 years of modern human existence, there were roughly 10 million humans living world wide, with complete replacement every generation, roughly every 30 years. With 2,000 generations in 60,000 years, this means 20 billion people lived in this period. Over the next 6,000 years, humans had agriculture, which allowed the support of a population of roughly 300 million. With 200 generations in 6,000 years, this means that 30 billion people lived in this period. Finally we come to the modern period, essentially the period of the people now living. There are now 6 billion people in the world. Adding all these numbers gives about 60 billion people as the total number of people who have ever lived.

    Thus, the virgin birth of such an XX male would be unique in human history even if there were only 2 such Y genes inserted into an X chromosome. (I assume an upper bound to the rate of virgin birth is 1/300. Then the probability of a virgin birth of a male with 2 Y genes is 1/(300)(20,000)(20,000) = 1/120 billion.)

    SOURCE: http://home.worldonline.nl/~sttdc/tipler.htm

  12. Allen

    This would be like producing a fully functioning organism from a sperm or egg cell; impossible, in other words.

    Allen, are you familiar with automictic parthenogenesis by any chance? Clearly females of sexually reproducing species in most of the plant and animal taxa are capable of virgin birth. Mammals and gymosperms are the sole exceptions but maybe it just hasn’t been observed in those yet and it can indeed happen.

    Davison in the paper I referenced refers to experiments with frog eggs that were induced into producing offspring both with needle pricks to simulate sperm entering the egg and by using sperm that had been irradiated to destroy their DNA.

    Going back to Kayuga, the parthenogenetic mouse… I quote from the article:

    In parthenogenesis, the egg becomes the sole source of genetic material for the creation of an embryo. It is a mode of reproduction in some species, though not in mammals. In mammals parthenogenesis can begin if an egg is accidentally or experimentally activated as if it had been fertilised – but this parthenote never grows past a few days.

    This is because of there a biological phenomenon known as imprinting. During sperm and egg formation in mammals, certain genes necessary for embryo development are shut down with a series of chemical marks, or imprints, some in the sperm, other in the egg. Only when sperm and egg meet are all of the key genes available, allowing proper development.

    http://www.newscientist.com/article.ns?id=dn4909

    This basically says that you’re all wet about reproduction being impossible from just an egg. Not only does it occur in many species the process can even begin in mammals with cell division proceeding for a few days. I note you don’t qualify your statement that reproduction from just an egg is impossible only in mammals. Would you take this opportunity to qualify the statement and then we can proceed to discuss why it might not be possible in mammals.

  13. Allen

    Maybe you can correct this description of meiosis I found at Brown University.

    http://www.brown.edu/Courses/B.....seIB1.html

    Meiosis begins with Interphase I. During this phase there is a duplication genetic material, DNA replication. Cells go from being 2N, 2C (N= chromosome content, C = DNA content) to 2N, 4C.

    In Cytokinesis I, the cells finally split, with one copy of each chromosome in each one. Each of the two resulting cells is now 2N, 2C.

    Again, forgive my ignorance but isn’t a cell that is 2N, 2C a cell with the diploid number of chromsomes (2n) and the normal amount of DNA (2c) whereas haploid cells are 1n, 1c?

    Help me out here, Allen. Either Brown University’s Biology 032 course is mistaken regarding meiosis or you are.

    Maybe you might have flunked me but methinks Brown would flunk YOU.

  14. DaveScot said:

    Yes, Christ would ostensibly be an XX male through parthenogenesis. The fact remains that 20% of the XX males have no SRY so while it remains to be explained how that happens the fact that it DOES somehow still happen is still there.

    But until it has been explained, and involvement of the father’s Y chromosome or its effects discounted, it’s not correct to claim that this phenomenon demonstrates that the virgin birth of a human male (without the involvement of a male) is possible.

    The other point to note is that the XX males without the SRY gene are more likely to have “ambiguous genitalia, hypospadias, and/or undescended testicles” inter alia; that is, physically to show their condition. Both types of XX male are also shorter than the average human male.

  15. This appears to be a semantic issue. At the end of cytokinesis there are two daughter cells each with 46 chromosomes. However, it has only 23 unique chromosomes in two 100% homozygous pairs. I can’t find anywhere in the literature where the diploid number is defined as 2n unique chromosomes. In humans, 23 unique chromosomes paired up as 46 total chromosomes is still a diploid number. If someone can point me point me to a defintion of diploid that says identical pairs of chromosomes only count as one chromosome then I’ll concede I made a mistake in semantics (but still no mistake in principle). Good luck.

  16. I deleted a previous response to Robin as it was unnecessarily offensive. I found a non-offensive rebuttal.

    Robin writes:

    The other point to note is that the XX males without the SRY gene are more likely to have “ambiguous genitalia, hypospadias, and/or undescended testicles” inter alia; that is, physically to show their condition. Both types of XX male are also shorter than the average human male.

    http://www.springerlink.com/co.....c402w3k6n/

    From the journal “Human Genetics”

    We report a Mexican family in which two sibs were identified as “classic” XX males without genital ambiguities. Molecular studies revealed that both patients were negative for several Y sequences, including SRY. A review of familial cases disclosed that this is the first family where a complete male phenotype was observed in Y-negative XX male non-twin brothers. These data suggest that an inherited loss-of-function mutation, in a gene participating in the sex-determining cascade, can induce normal male sexual differentiation in the absence of SRY.

    Furthermore, parthenogenesis has been observed in all taxa except gymnosperms and mammals. This makes the capability a rule and mammals a rare exception. Now you have have to ask yourself why the exception. Unless you can explain why it’s impossible in mammals it is reasonable to conclude the capability is present but not yet observed (not observed if you don’t count Christ).

  17. If someone can point me point me to a defintion of diploid that says identical pairs of chromosomes only count as one chromosome then I’ll concede I made a mistake in semantics (but still no mistake in principle). Good luck.

    Chromatid
    From Wikipedia, the free encyclopedia
    Jump to: navigation, search

    A chromatid is one of two identical strands making up a chromosome that are joined at their centromeres, for the process of nuclear division (mitosis or meiosis). The term is used so long as the centromeres remain in contact. When they separate (during anaphase of mitosis and anaphase 2 of meiosis), the strands are called daughter-chromosomes. [1]

    In other words, a chromatid is “one-half of a replicated chromosome” [2] It should not be confused with the ploidity of an organism, which is the number of homologous versions of a chromosome.

    The term chromatid was proposed by Hector from Glenbard South for each of the four threads making up a chromosome-pair during meiosis. It was later used also for mitosis. The term derives from the Greek chroma (colour); for the derivation of -id, see diploid.

  18. DaveScot:
    If someone can point me point me to a defintion of diploid that says identical pairs of chromosomes only count as one chromosome then I’ll concede I made a mistake in semantics (but still no mistake in principle). Good luck.

    Ibid page 129:

    “We say the chromosome number is diploid, or 2n, if a cell has two of each type of chromosome characteristic of the species.”

    It goes on to say it is NOT just the number of chromosomes that count.

    After Meiosis I our germ cells have 23 + 23 homologous chromosomes, which then get split down to just 23 in each of the 4 final gametes (end of Meiosis II).

    However I don’t think DS was “egregiously wrong”. And if we were in Allen’s class and he flunked Dave for that minor “error”, there would be he[[ to pay.

    I also found the following:

    diploid:

    Definition: A cell that contains two sets of chromosomes (one set donated from each parent).

    Biology on-line concurs.

  19. I guess my last comment got caught in the filter-

    Definition: A cell that contains two sets of chromosomes (one set donated from each parent).

    http://biology.about.com/libra.....iploid.htm

  20. DaveScot wrote:

    “I can’t find anywhere in the literature where the diploid number is defined as 2n unique chromosomes.”

    I don’t know what literature you’re reading, Dave. I have over twenty introductory biology textbooks in my library (the publishers keep sending them to me for free, hoping I will adopt them), and every single one of them defines “diploid” as consisting of two complete sets of chromosomes deriving from two genetically different parents. “Haploid” is defined as one complete set of chromosomes, which is what is in each daughter cell at the end of the first division of meiosis. Each of these first division chromosomes is double stranded, but that doesn’t make them homologous, it makes them identical. They are identical because, during the S phase of interphase, the single stranded chromosomes become double stranded, as a prelude to meiosis (and mitosis).

    Admittedly, a small number of my students get confused on this same topic every year, and so the fact that you misunderstood the definitions of “diploid”, “haploid”, and “homologous” isn’t unique. I would almost certainly be prone to the same kind of errors if I were to try to make statements concerning computer programming, as subject about which I am almost entirely ignorant. That’s what happens when people try to make definitive statements on subjects of which they have only an amateur’s understanding.

    Furthermore, I never meant to imply that development from a non-fertilized egg is impossible in any animal, only that it is virtually impossible in mammals. Indeed, in the order Hymenoptera (ants, bees, and wasps) all males (i.e. drones) are produced from unfertilized eggs, while all females (queens and workers) are diploid, a condition called haplodiploidy.

    And the link to Wikipedia that I included in my original post has a pretty good explanation of what parthenogenesis is, and in which groups of organisms it has been observed. Among vertebrates it is exceedingly rare, being common only among a few peculiar groups of lizards (the whiptails that I mentioned). In those organisms, the parthenogenetic individuals (which are all female, by the way) are able to develop from unfertilized eggs to adults because their genomes are a chimera produced by the hybridization of several closely related species. Apparently the complement of genes from such hybridization is sufficient to compensate for the lack of a homologous set of chromosomes from gametes from males in those species, thereby making haploid-to-diploid fertilization unnecessary.

    Come on, Dave, this is extremely basic introductory biology. Why can’t you simply admit that you were wrong on this one and move on? I’ve done it on many occasions (including several at this website). Remember, pride is the first and deadliest of the deadly sins (and humility the first and highest of the cardinal virtues)…

    P.S. As several other commentators have already pointed out, although parthenogenesis is common in plants, some protists, and the aforementioned whiptail lizards, it is virtually unknown in mammals. Speculation about how something “might” have happened isn’t science at all, it’s wishfull thinking.

  21. Joseph

    I’ll see your definition of diploid from “about.com” and raise you these:

    http://ghr.nlm.nih.gov/ghr/glossary/diploid

    http://www.genome.gov/glossary.cfm?key=diploid

    http://anthro.palomar.edu/biobasis/glossary.htm

    http://filaman.ifm-geomar.de/G.....sh=diploid

    http://www.emc.maricopa.edu/fa.....lossD.html

    http://www.stanford.edu/group/.....oss/d.html

    http://worms.zoology.wisc.edu/.....ary.html#D

    http://www.ggc.org/glossary.htm

    http://webpages.charter.net/te.....ssary.html

    http://naturalsciences.sdsu.ed.....ssary.html

    This is just a small sampling of definitions of “diploid” which exclude the requirement that paired chromosomes are one copy from each parent.

    I arranged two googlefights to resolve this situation.

    http://googlefight.com/index.p.....d+glossary

    http://googlefight.com/index.p.....d+glossary

    Add up the two searches with parent and parents and subtract from the search without either. The result is about an even match with a marginal lead in your favor. However, since it’s likely that many glossaries will contain the word parent or parents not contained within the definition of diploid I think that swings it back in my favor but that’s just conjecture.

    Furthermore, how do we describe asexual diploids if all all diploids must have genes from two parents?

  22. Allen

    I don’t know what literature you’re reading, Dave. I have over twenty introductory biology textbooks in my library (the publishers keep sending them to me for free, hoping I will adopt them), and every single one of them defines “diploid” as consisting of two complete sets of chromosomes deriving from two genetically different parents.

    See my previous comment for definitions of diploid that don’t specify two parents.

  23. Allen

    it is virtually impossible in mammals

    Do I detect a bit of backpeddling here? :-)

    Surely you didn’t think I’d miss that “virtually” qualification did you?

    What do you figure are the odds that a parthenogenetic mammal might slip through that crack you left open. Please support your estimate of the odds.

    And you’re darn right this is basic biology. 46 is the diploid number in humans and 46 is the exact number of chromosomes in the first two daughter cells produced during meiosis. About half the glossary definitions of “diploid” from reliable sources say it’s one set of 23 from each parent and the other half don’t make that qualification. If you marked me wrong on a test question and the class text used the latter definition I’d hound you until the cows came home to mark it correct and change the question on future tests.

  24. The Mexican males that you refer to in comment #16 are both diploid; they are phenotypically male simply because of an alteration in the expression of the SRY gene. This is totally unlike the situation that would have necessarily been the case for Jesus to have been born to Mary as the result of parthenogenesis. This would require that Jesus develop from an unfertilized, and therefore haploid egg cell, which even Tipler admits is a biological impossibility in mammals. Yes, parthenogenesis is possible in mammals, but the resulting individuals would be diploid and would necessarily be female, as they would have developed from egg cells in a female that does not include either a Y chromosome or a functional copy of the SRY gene.

    The mice described in the experiment in comment #12 were diploid (i.e. had two sets of chromosomes), but were parthenogenetic because the two sets were converted from a single set by chromosome duplication without cell division. However, this process can only result in an XX individual in mammals, since mammalian egg cells from females only contain X chromosomes. The author of the quote you supplied states this quite clearly: “In mammals parthenogenesis can begin if an egg is accidentally or experimentally activated as if it had been fertilised – but this parthenote never grows past a few days.”

    Tipler’s speculations are founded on a biological impossibility: that a phenotypically female mammal could somehow produce (by any mechanism at all) a diploid cell that could develop into a male without an SRY gene hidden somewhere in her genome. The reason? If a copy of the SRY gene were somehow inserted into Mary’s genome, she would have developed into a phenotypic male, because that’s what the SRY gene does: it throws a switch that produces (mainly via hormonal processes) a phenotypically male individual.

    Furthermore, if somehow a haploid egg cell of Mary could have undergone the same kind of chromosome duplication event described in the case of Kayuga’s mice, the resulting diploid cell would be female, as it would lack a copy of the SRY gene, which is normally only found in the Y chromosome.

    In other words, Tipler’s suggestion is quite literally impossible, given any known mechanism of mammalian development. However, a competing hypothesis has a lot going for it: Mary got pregnant the way nearly all other female humans do – by copulating with a human male. This requires absolutely no magic, nor stretching of the known principles of developmental genetics at all.

    Given the relative probabilities of the two hypotheses (i.e. birth of a male as the result of parthenogenesis from an unfertilized haploid female egg versus birth of a male as the result of normal fertilization by a male sperm), I (and virtually any scientist worthy of that name) would judge the latter hypothesis as the more likely. To accept the former would absolutely require a detailed genetic analysis of the subject in question, which (barring the Second Coming) would seem to be impossible for the foreseeable future.

    In other words, keep reminding yourself “magic isn’t science” and “science isn’t magic”…

  25. Come on, Dave, since when are links on the web considered superior to biology textbooks? Having written one, I can tell you that if I had stated in it that the cells that result from the first division of meiosis are diploid, I would have lost the contract for that (and any other) textbook.

    Yes, it is a “semantic” distinction, but it’s one that every biologist agrees with: the first division of meiosis produces haploid cells, in which the chromosomes are double-stranded. Once again, double-stranded chromosomes are NOT homologous, they are identical as the result of chromosome replication during the S phase of interphase.

    Once again, why is it apparently impossible for you to admit you are wrong on this?

  26. DaveScot wrote:

    “Please support your estimate of the odds.”

    Tipler has obligingly done this for me: they are 1 in 120 billion. Now, you supply the odds that Mary got pregnant the old fashioned way…

  27. Tipler also calculates:

    “Adding all these numbers gives about 60 billion people as the total number of people who have ever lived.”

    By his own admission, all of those people were conceived the old fashioned way. That is, given all of the human beings that have ever existed on the planet (i.e. somewhere in the ballpark of 60 billion), by Tipler’s own calculation not one of them would have been expected to have arisen as the result of the extremely convoluted (and virtually biologically impossible) mechanism that he himself proposes.

    In other words, the odds are:

    60 billion/60 billion = 1/1 = 1 = 100% in favor of non-virgin birth of a male (minus 0.5/120 billion, to compensate for the probability that Tipler’s “magical” parthenogenesis actually occurred)

    versus

    1/120 billion in favor of virgin birth of a male

    Honestly, I’ve never encountered a more skewed comparison of probabilities, and don’t expect to again (outside of this website, that is)

  28. “…46 is the exact number of chromosomes in the first two daughter cells produced during meiosis”

    Here is precisely the problem: a double stranded chromosomes are always counted as one chromosome, and so are single-stranded chromosomes. That’s the way chromosomes are defined in biology. The daughter cells that are produced by the first division of meiosis in humans therefore contain 23 (not 46) chromosomes. True, those chromosomes are double-stranded, but that doesn’t matter; they still only comprise 23 chromosomes.

  29. And yes, I’ve read Davison’s semi-meiotic hypothesis, and that’s all that it is: a hypothesis. As far as I’m aware, neither he nor anyone else has any empirical evidence to directly support it (i.e. actual organisms that have genomes that are unambiguously the result of semi-meiosis). Interesting, but without empirical verification, it’s just airy speculation…

  30. Allen

    The Mexican males articles was only to point out that XX males absent any SRY aren’t necessarily different in outward appearance. It was totally to address Robin’s contention that if Christ was an XX male he’d necessarily be all weird looking.

    Haploid eggs in humans can be easily stimulated to double their chromosome count and begin dividing as diploid cells. I should think their subsequent diploid form would be 100% homozygous to so would that make them still arguably haploid among pedants? They just don’t live very long after becoming diploid. At this point in time I don’t think anyone can say what mechanism might be disabled that would prevent them from dying young. Observed parthenogenetic reproduction in other species speaks to there being some simple mechanism in mammals and gymnosperms that is preventing them from maturing.

    Secondary sexual characteristics aren’t always dependent on SRY. That’s speculation on your part and doesn’t hold up in the literature as the SRY gene is definitively NOT expressed in some XX males and the Mexican sibs demonstrate that SRY negative males can be quite indistinguishable from normal males. Granted this makes the probability even smaller that Christ was a parthenogenetic XX SRY negative male but by your own admission this isn’t quite impossible.

    I’m still waiting for those odds… nobody said virgin birth in humans was common. In fact there’s only one claim of it in history. Our purpose here is only to determine if it is possible or not. You’ve already hedged in saying it’s virtually impossible which is really an admission that it is indeed possible but improbable.

  31. Precisely: “possibility” and “probability” are two entirely different things. Sure, it’s “possible,” but so “improbable” as to be virtually impossible.

    In science, that’s all we have: comparative probabilities. As I pointed out, the comparative probabilities are so overwhelmingly in favor of Jesus having been conceived as the result of normal copulation/fertilization as to render the “possibility” of “virgin birth” moot.

    By the way, my wife (a magna cum laud from Cornell in classics, with a specialization in Mediterranean religions around 0 A.D. and fluent in six classical languages, including Aramaic and Biblical Hebrew) just pointed out that the Aramaic word that is usually translated as “virgin” in English bibles can just as easily be translated as “young woman”…which also makes all of the foregoing debate moot as well.

  32. Allen

    When the definitions of diploid are in online biology glossaries from many major institutes of higher learning and so very many of them (about half) don’t define diploidy as requiring chromosomes from two parents you bet I’m going to argue the point. It’s inconceivable that so many of them would have erroneous definitions and I’d bet dollars against donuts most of those glossary definitions online were pulled straight out of text printed on dead trees.

    I have no dispute that the vast majority of texts call the first daughter cells of meiosis “haploid” but it appears that’s just by tradition. It’s a damn confusing tradition too. There should be a qualifier saying it’s a diploid number but we still consider them haploid cells because they are 23 identical pairs.

    Perhaps you can answer my question to Joseph: what do we call asexual diploids that don’t have a contribution from both parents in their 2n number? The literature still calls them diploid but their genetic compliment is derived from a single parent. That seems to dash the definition requiring two parents does it not?

  33. And, once again, where is the empirical evidence in favor of the “virgin birth” hypothesis? Airy speculation isn’t evidence, either direct or indirect. Simply showing that something is “possible” says absolutely nothing at all about whether it actually happened.

  34. If you’re asking me personally if I believe Christ was born to a virgin the answer is no. I’m an agnostic and that puts me pretty darn far from a biblical literalist. As an agnostic however I don’t deny the possibility that stories in the bible are literal truth. Science has demonstrated that Christ’s virgin birth IS possible. That’s all that matters. The door is left open a crack for it to be true.

  35. Allen

    Simply showing that something is “possible” says absolutely nothing at all about whether it actually happened.

    You got that right. How much of evolutionary theory regarding events in the distant past are possible but say nothing at all about whether it actually happened?

    I’ll be quoting you on that one. This possibility stuff cuts both ways.

  36. Re comment 32:

    Indeed, asexual diploids are still just that: diploids. And yes, it is sometimes confusing (as I stated, some of my students are confused by this every year). The point here is that the definitions of “diploid” and “haploid” are ultimately based on what objects are moved around by the microtubules of the spindle apparatus in meiosis. Anything that is moved as a single unit by a spindle fiber is, by definition, one chromosome, regardless of whether it is single or double stranded.

    This definition has several implications. As I point out to my students every year, since we count chromosomes by counting independently segregating units, the chromosome number of a cell dividing by mitosis temporarily doubles during anaphase, since the two chromatids of each double-stranded chromosome are separated by the cleavage of the centromeres that hold them together. Then, following cytokinesis (which usually happens during telophase) the original chromosome number is restored in the two daughter cells.

    In meiosis, however, something quite different happens. During the first division of meiosis, the chromatids of the double stranded chromosomes are not segregated from each other. Instead, the homologous chromosomes from each parent (which paired up during prophase I of meiosis) are segregated from each other.

    In humans, this means that each of the 23 chromosomes pairs up with its homolog during prophase I, and is then segregated from its homolog during anaphase I. These chromosomes are all double stranded, but they still only count as one chromosome each. Hence, once the two daugher cells separate from each other during interkinesis, each daughter cell contains one complete set of double stranded chromsomes: i.e. 23, the haploid or 1N number.

    Yes, it’s semantically tricky, but the trickiness is necessitated by the complexity of the process. We have to have some way of distinguishing between the genetically identical sister chromatids of a double stranded chromosome and the homologous (but not necessarily identical) chromosomes that line up during prophase I of meiosis.

    And in most animals (but not plants) the haploid and diploid numbers are essential; if they don’t match up, the organisms don’t develop normally. This is the basis of Down syndrome, in which there are three homologous chromosome 21s, a condition that results in mild to severe cognitive and developomental abnormalities. And chromosome 21 is the only chromosome that can be triploid (except for the X and y, for reasons peculiar to their developmental genetics), probably because it contains so few genes. None of the other homologous pairs can be anything except diploid; the result of any departure from diploidy in all other pairs (except the Xy pair) is spontaneous termination of development, usually in a very early developmental stage.

    I know; my wife and I lost a baby that way last Christmas…

  37. “I’ll be quoting you on that one. This possibility stuff cuts both ways.”

    Indeed, and I hope you do. As I hammer away with my students, scientific hypotheses are worthless if they (a) cannot be used to generate empirically testable predictions, and (b) are not supported by the results of empirical tests.

    By those criteria, evolutionary biology passes in most cases. For example, one can predict on the basis of the hypothesis of descent from common ancestors that species that appear to be related by descent (such as chimpanzees and humans) will have nucleotide sequences that are consistent with the hypothesis that they are indeed descended from a common ancestor. The observation that this is, indeed, the case is why Michael Behe accepts descent with modification from common ancestors, as do virtually all biologists.

    Furthermore, I would be the first to agree that if a scientist makes a statement that cannot be either empirically tested and either validated or falsified, that scientist is not talking about science. For this reason, I find Richard Dawkins’s pronouncements on the non-existance of God to be utterly outside the realm of the empirical sciences. But nobody who does actual field or lab work would rate Dawkins as “their kind of scientist” anyway; he does no field or lab work, but rather lots of semi-mathematical speculation and public relations. A lot like one of the founders of this website…

  38. And as to the “problem” of making scientific statements about events that happened in the past (and therefore cannot be directly observed), all forms of “historical” science have the same problem. As I tell my students, none of us can be certain that the people who claim to be our parents are, in actual fact, our parents. After all, we quite literally weren’t there until after we were conceived, and so can’t possibly know beyond a shadow of a doubt.

    However, there are empirical means of inferring events we cannot observe directly, either because they happened in the past or because our senses cannot detect them (as in the case of atomic structure). In those cases, we devise empirically testable hypotheses that can be validated/falsified that can allow us to infer whether those unobservable phenomena have, in fact, happened. That’s how we infer the existance of sub-atomic particles and the former existence of Homer’s city of Troy at what is now the “hill of Hysarlik” in Anatolia.

    Much of evolutionary biology is tested and validated in the same way. However, it is quite literally impossible to “prove” (i.e. beyond any shadow of a doubt) that descent with modification has occurred, or to “prove” that the principle mechanism for it has been natural selection. That just happens to be what most of the observable evidence points to so far. If someone eventually comes up with new evidence that points unambiguously to the contrary, then we’ll all have to change our minds on that score. Hasn’t happened yet, and won’t until the other side starts doing some empirical research (and publishing it).

  39. And I’m an agnostic too (and most emphatically NOT an atheist). I agree with T. H. Huxley (who coined the term) and Bertrand Russell (who most ably defended it): it’s the only philosophically justifiable position vis-a-vis assertions that are beyond any possibility of empirical verification/falsification…

  40. Allen

    How do you think meiosis evolved? Note I’m trying to conform to convention in calling 2n cells haploid if they don’t have two parents and making the distinction with 1n,2c to indicate there are really twice the number of chromosomes to work with. I’m still confused by the convention and probably got it wrong.

    My theory:

    Step 1: A 1n,1c haploid organism doubled its chromosome count through duplication.

    Step 2: Mitotic crossover was invented in the 1n,2c haploid above.

    Step 3: Segregation of the duplicate chromosomes evolved but still produced viable 1n,2c daughters.

    Step 4: The next mitotic division from the above failed to duplicate the DNA producing 4 1n,1c haploid daughters.

    Step 5: Automictic parthenogenesis where one of the 1n,1c cells from above merged with another to make a viable 1n,2c haploid.

    Step 6: Close proximity of single celled organisms from step 5 resulted in 1n,1c cells from two parents to merge into the 2n,2c diploid.

    Step 7: Automitic parthenogenesis was largely abandoned in favor of the two parent model.

    I just made that up on the fly. Anything in particular wrong with it that can’t be fixed?

  41. Actually, it probably got started by the fusion of two haploid cells to form a diploid “chimera.” This is very common among protists, and my friend Lynn Margulis has strongly defended the idea that the ancestors of all diploid organisms did this. Meiosis would simply be the mechanism by which the “temporary” diploids could get back to being “normal” haploids. After all, haploid organisms have a complete set of chromosomes.

    And then, once the haploid-haploid fusion to form diploid, followed by meiosis to form new haploid pattern became established, multicellularity followed, along with sex (with all its joys and sorrows).

    Lynn and her son Dorion have also proposed that the original fusion event was favored because it:

    (a) produced an organism that had a “backup copy” of its genome, thereby minimizing the damage caused by random mutations, and

    (b) allowed such organisms to use one genome to “proof-read/edit” the other.

    Sex, in other words, started out as editing.

    BTW, I just checked that old thread and read your comments about Scotland. Damn, son, are you a scot in addition to being a Scot? Is that where the Scot of DaveScot comes from? If so, we have a LOT more in common besides agnosticism…

    BTW, the clan Neil was on the side of Bonny Prince Charlie during the rising of ’45 (and has historically had little or no respect for the Campbells of Glencoe infamy). Where might you fall on these *ahem* rather touchy issues?

  42. gotta get some shut-eye; will check tomorrow…

  43. Allen

    Hmmm… skipping straight up to step 6 leaves a lot of meiosis to evolve in one fell swoop does it not?

    re Scotland – No, Scot is my middle name and contrary to the way everyone wants to spell it, it has only 1 t in it. My ancestors centuries ago were English (been in the new world since colonial times). We built the English Empire. The Scottish Empire (if you can call it an empire) was tiny in comparison. You hitched a ride with us in 1707, moved your parliament to London, and we called the combined empire the British Empire. I’ll grant that Scotsmen are fierce as individuals but we English are the ones that figured out how to be a fierce nation. Hence your family coat of arms puts family above nation and mine puts nation above family. It all makes perfect sense.

    I personally wouldn’t dream of flying any flag above the stars and stripes but I’d respect your right to do so and any local statutes to the contrary are probably a violation of your first amendment rights. The constitution doesn’t speak of how to fly the national flag so it’s a right reserved to the states and they could make the statutes on those grounds but the 1st amendment freedom of expression still seems to stand in the way and the 14th amendment means the 1st applies to all the states. I tend heavily towards libertarianism (with a few exceptions to the party plank) but since my vote is thrown away if I check the L candidate (if there IS an L candidate) I vote the lesser of two evils (R). My libertarian tendency stems from thinking adults should be treated like adults and if they want to do any damn foolish thing that harms no one other than themselves then let ‘em. Darwin will weed out the damn fools and we’ll be better off as a herd for it in a generation or three. I grew up in upstate New York and really love it there for a lot of reasons but it’s about as far from a libertarian’s dream as one can get. Texas is a great improvement in that regard but it just isn’t home for me and never will be no matter how long I live here.

    In closing, in the immortal words of Clint Eastwood playing Marine Gunnery Sergeant Highway in the movie Heartbreak Ridge, just because we agree on a few things “This doesn’t mean we’ll be swapping spit in the shower.” :-)

  44. DaveScot said:

    I deleted a previous response to Robin as it was unnecessarily offensive. I found a non-offensive rebuttal.

    I’d prefer it if I saw the offensive responses, as well as the non-offensive ones. If you’d prefer the blog not to be polluted, then send it by email.

    Allen has taken on the discussion on the remainder of your post…

  45. Dave,

    Did you read the definition in the first link you provided?

    The normal number of chromosomes in a somatic cell; in humans, 46 chromosomes (22 pairs of autosomes and two sex chromosomes)

    Somatic cells Dave.

    Link 2:

    The number of chromosomes in most cells except the gametes. In humans, the diploid number is 46.

    link 3:

    the full component of chromosomes normally found in somatic cells. In humans, the number is 46.

    I rest my case with my comment #18

  46. Allen:
    The observation that this is, indeed, the case is why Michael Behe accepts descent with modification from common ancestors, as do virtually all biologists.

    Then they accept it despite the data to the contrary. And there still isn’t any data (biological/ genetic) that demonstrates what caused the differences observed between chimps and humans. Or that any mutation/ selection can account for those differences.

  47. Does this discussion miss the point of such an “attesting sign” as the virgin birth? The Human-level objective of the miracle in question likely was to establish a germ of a small, immovable base of faith(in the old sense of the word: believing what one knows is true, in spite of limited circumstantial perspective) which would correllate with a prophetic reference in the Hebrew scriptures. This is not to mention whatever other divine objectives would be in play.

    Philosophically, an attesting miracle demonstrates God’s power over (‘interference with’, to offend the materialists) nature. therefore it is quite beside the point to demonstrate that it is “impossible.”

    Well, it would be, wouldn’t it?

  48. Actually, as you pointed out earlier, meiosis probably evolved as a modification of mitosis, which evolved as a modification of binary fission. This is the kind of step-wise evolution that Darwin originally proposed, and that virtually all of the observational evidence supports (notice, please, that I don’t use the word “prove” – science never “proves” anything, unlike abstract mathematics).

    And I agree with you on the conundrum of voting the Libertarian line. I generally vote on the basis of the candidate, rather than their party affiliation. This sometimes means I don’t vote. So it goes…

    As to the Scots in my family, they’ve only been in the new world a few generations, and then only in Nova Scotia. My Dad’s father came here from Weymouth right after WW I, where he served in the 48th highland regiment (the “ladies from Hell” – so named because they wore kilts rather than “trews” as part of their dress uniform). The motto of the clan Neil is vincere vel mori (buaidh na bas in Scots Gaelic), “conquer or die”. And my reading of history is that the Scots have never been interested in having an “empire,” particularly if that meant invading and subjugating other people. Nearly all of their “disagreements” with the Sassenach stemmed from the latter’s distressing tendency to invade them, rather than the other way around. True, Bonnie Prince Charlie marched on London (and didn’t get there), but that was to reassert the line of James I/VI to the throne, not to subjugate the English people. If history (especially recent history) has shown us anything, it has shown us that “empire-building” is utterly incompatible with personal liberty, political stability, and peace. The United States was the best and brightest hope of the world when it was first founded, but squandered its moral legitimacy and dishonored the legacy of those who fought and died to defend it by attempting (so far unsuccessfully) to transform itself from a republic to an empire. And so, I’m even more proud of my Scottish ancestors who sat tight on their little island in the outer Hebrides (Barra, to be exact), didn’t invade or subjugate anyone else, and were never, ever (since Kisimul castle was built around the year 1000) defeated or subjugated themselves.

  49. And no, I’m not interested in “swapping spit in the shower”, I’m simply pointing out that it is possible to treat each other like gentlemen and scholars without necessarily agreeing. If we disagree with each others ideas, we attack the ideas with all the means at our disposal, but we treat each other with civility and respect (so long as that civility and respect are reciprocated).

  50. Re comment #47:

    To me, it seems that an “attesting sign” is simply a form of induction, and a pretty poor one at that. Miracles are unique events by definition. As such, they cannot be used as part of an inductive argument, since such arguments are quite literally probabilistic: the more evidence one has in favor of a proposition, the higher one’s confidence in the logical inference to that proposition. As such, therefore, miracles are indistinguishable from what is referred to in the natural sciences as “anecdotal evidence”: interesting perhaps, but logically worthless.

    These are among the “rules” of “doing science”, and if you want to be accepted in the community of scholars that plays by those rules, you have to play by them yourself. In other words, miracles don’t count…

  51. Re comment #46:

    “Then they accept it despite the data to the contrary. And there still isn’t any data (biological/ genetic) that demonstrates what caused the differences observed between chimps and humans. Or that any mutation/ selection can account for those differences.”

    All three of these statements are demonstrably false.

    If there are “data to the contrary,” please provide a reference (and remember that “data” means empirical evidence, derived from observations and experiments and preferably published in scientific journals, not theoretical speculation or unsupported assertions).

    And yes, there is abundant evidence supporting the inference that chimpanzees and humans descend from a common ancestor. To list just three, humans share a homeotic gene designated as FOX2P with chimpanzees. However, the human version of that gene is significantly different, and the direction of that difference is correlated with the human capacity for spoken language.

    Humans differ from chimpanzees and other great apes in chromosome number as well. Humans have 46; all the other great apes have 48. Human chromosome #2 contains the “missing” chromosome, however, so it didn’t disappear, it’s simply translocated to that chromosome (a translocation that is also correlated with some of the differences between humans and the other apes).

    I can provide journal references for the foregoing if requested, but it will take a while, as I am currently preparing a final exam for my biology students. If you dispute these examples, please be so kind as to provide references to the scientific literature that support your assertion.

  52. Did a quick Google search; here are some published references supporting the FOX2P inference:

    Wolfgang, E.; Prezeworski, M.; et al. Molecular Evolution of FOXP2, a gene involved in speech and language. Nature. Vol. 418. 22 August 2002. 869-872.

    Balter, Michael. “First ‘Speech Gene’ identified”. Academic Press: Daily Insight. Science. 3 October 2001. http://www.academicpress.com/i.....grapha.htm

    Balter, Michal. “‘Spech Gene’ A Debut Timed to Modern Humans”. Academic Press: Daily Insight. Science. 14 August 2002. http://www.academicpress.com/i.....grapha.htm

    Lai, C. S.; Fisher S. E.; et al. A forkhead-domain gene in a severe speech and language disorder. Nature. Vol. 413. No. 6855: 465-466.

    Bruce, H. A.; Margolis, R. L. FOXP2: novel exons, splice variants, and CAG repeat length stability. Human Genetics. Vol 111. No. 2: 136-144.

  53. Sorry; the links in post #52 seem to have expired. I would recommend doing a search for the bibliographic reference using Google Scholar, or going through an academic library gateway.

  54. **The following post seems to have been eaten by the spam filter; I will try to post it again**

    And here’s some for the chromosome 2 translocation/fusion inference (the first is the landmark paper reporting the discovery, including an abstract; the rest provide more recent supporting evidence and applications):

    JW Ijdo, A Baldini, DC Ward, ST Reeders and RA Wells
    Origin of Human Chromosome 2: An Ancestral Telomere-Telomere Fusion.
    Proc. Nadl. Acad. Sci. USA Vol. 88, pp. 9051-9055, October 1991 Genetics

    ABSTRACT:
    We have identified two allelic genomic cosmids from human chromosome 2, c8.1 and c29B, each containing two inverted arrays of the vertebrate telomeric repeat in a head-to-head arrangement, 5′(TTAGGG)n-(CCCTAA)m3′. Sequences flanking this telomeric repeat are characteristic of present-day human pretelomeres. BAL-31 nuclease experiments with yeast artificial chromosome clones of human telomeres and fluorescence in situ hybridization reveal that sequences flanking these inverted repeats hybridize both to band 2q13 and to different, but overlapping, subsets of human chromosome ends. We conclude that the locus cloned in cosmids c8.1 and c29B is the relic of an ancient telomere-telomere fusion and marks the point at which two ancestral ape chromosomes fused to give rise to human chromosome 2.

    J. E. Horvath, C. L. Gulden, R. U. Vallente, M. Y. Eichler, M. Ventura, J. D. McPherson, T. A. Graves, R. K. Wilson, S. Schwartz, M. Rocchi, and E. E. Eichler
    Punctuated duplication seeding events during the evolution of human chromosome 2p11
    Genome Res., July 1, 2005; 15(7): 914 – 927.

    S. Zhao, J. Shetty, L. Hou, A. Delcher, B. Zhu, K. Osoegawa, P. de Jong, W. C. Nierman, R. L. Strausberg, and C. M. Fraser
    Human, Mouse, and Rat Genome Large-Scale Rearrangements: Stability Versus Speciation
    Genome Res., October 1, 2004; 14(10a): 1851 – 1860.

    S. G. Nergadze, M. Rocchi, C. M. Azzalin, C. Mondello, and E. Giulotto
    Insertion of Telomeric Repeats at Intrachromosomal Break Sites During Primate Evolution
    Genome Res., September 1, 2004; 14(9): 1704 – 1710.

    M. Ventura, S. Weigl, L. Carbone, M. F. Cardone, D. Misceo, M. Teti, P. D’Addabbo, A. Wandall, E. Bjorck, P. J. de Jong, X. She, E. E. Eichler, N. Archidiacono, and M. Rocchi
    Recurrent Sites for New Centromere Seeding
    Genome Res., September 1, 2004; 14(9): 1696 – 1703.

    M. Ventura, J. M. Mudge, V. Palumbo, S. Burn, E. Blennow, M. Pierluigi, R. Giorda, O. Zuffardi, N. Archidiacono, M. S. Jackson, and M. Rocchi
    Neocentromeres in 15q24-26 Map to Duplicons Which Flanked an Ancestral Centromere in 15q25
    Genome Res., September 1, 2003; 13(9): 2059 – 2068.

    T. K. Bera, D. B. Zimonjic, N. C. Popescu, B. K. Sathyanarayana, V. Kumar, B. Lee, and I. Pastan
    POTE, a highly homologous gene family located on numerous chromosomes and expressed in prostate, ovary, testis, placenta, and prostate cancer
    PNAS, December 24, 2002; 99(26): 16975 – 16980.

    Y. Fan, T. Newman, E. Linardopoulou, and B. J. Trask
    Gene Content and Function of the Ancestral Chromosome Fusion Site in Human Chromosome 2q13-2q14.1 and Paralogous Regions
    Genome Res., November 1, 2002; 12(11): 1663 – 1672.

    Y. Fan, E. Linardopoulou, C. Friedman, E. Williams, and B. J. Trask
    Genomic Structure and Evolution of the Ancestral Chromosome Fusion Site in 2q13-2q14.1 and Paralogous Regions on Other Human Chromosomes
    Genome Res., November 1, 2002; 12(11): 1651 – 1662.

    J. E. Horvath, J. A. Bailey, D. P. Locke, and E. E. Eichler
    Lessons from the human genome: transitions between euchromatin and heterochromatin
    Hum. Mol. Genet., October 1, 2001; 10(20): 2215 – 2223.

    M. Ventura, N. Archidiacono, and M. Rocchi
    Centromere Emergence in Evolution
    Genome Res., April 1, 2001; 11(4): 595 – 599.

    G. Montefalcone, S. Tempesta, M. Rocchi, and N. Archidiacono
    Centromere Repositioning
    Genome Res., December 1, 1999; 9(12): 1184 – 1188.

    D. B. Zimonjic, M. J. Kelley, J. S. Rubin, S. A. Aaronson, and N. C. Popescu
    Fluorescence in situ hybridization analysis of keratinocyte growth factor gene amplification and dispersion in evolution of great apes and humans
    PNAS, October 14, 1997; 94(21): 11461 – 11465.

  55. I’ve now twice tried to post a list of published references concerning the human chromosome 2 translocation/fusion event, without success. Again, I recommend a Google Scholar search.

  56. Here’s a better link to FOX2P references:

    http://scholar.google.com/scho.....tnG=Search

  57. [off topic]
    Allen and everyone else,

    I’ll be away starting this afternoon. I wanted to make sure I wished you a Happy Thanksgiving.

    regards,
    Salvador

  58. Allen MacNeill,
    Please accept my sincere sympathies on the loss of your baby.

    Was the cause trisomy 18?
    If so, why do you say that only chromosome 21 can be triploid?
    What is the difference in the trisomy of chromosome 18 and that of 21 (Downe’s Syndrome) that allows you to make this distinction?

    Again, my condolences on your very sad loss.

  59. Dave Scot, I think you’re my own personal “Uncommon Descent” spam filter or “censor”, so how are you?

    We two at least are engaged in dialog; I don’t know if applying “science” to the [Christian] Bible is of value, i.e., a scientific explanation for “virgin birth”.

    As to dark energy, Wal Thornhill shall be presenting a paper to IEEE in the summer. My own preference, of which you are aware, is that The Electric Force explains what gravity, the weakest force, cannot do, and so forces reliance of dark energy, dark matter, black holes, et al.

    However, electrical theorists cannot explain, since it is not observable, the “generator”; I believe there is an underlying Intellect behind our interconnected “Hologram”. Yet I realize I cannot prove it, and that does not trouble me.

    I suppose the “big bang” is attractive to some because of creation ex nihilo ; yet given its proponents, e.g., Weinberg, Hawking, Dawkins (see alpha and omega thread), it is to me suspect.

  60. Dave Scot, I think you’re my own personal “Uncommon Descent” spam filter or “censor”, so how are you?

    Actually, I doubt Dave has anything to do with it. Most of your comments have been getting caught in the filter automatically and I’ve been letting them all through myself.

  61. Patrick, Dave a while back said he’d be “monitoring” my posts, so I thought that was it — “by design”.

    Anyway, I forgot a link, and here it is, and I did make a mistake typing “principal” instead of “principles”; I have a long reply on the “Delta and Omega” thread.

    Happy Thanksgiving to you all, in any event! ;)

    http://www.holoscience.com/new.....e=9kpgc4td

  62. Joseph

    They’re not gametes until the *end* of meiosis.

    Nice try.

    Those cells have 46 individual chromosomes arranged as 23 duplicate pairs. There’s really not much more to say about it. I understand the structure now and did when I wrote the article.

    My mistake, if any, was not knowing that biologists call the intermediates a haploid cell as a matter of convention. I think that’s wrong. They aren’t haploid until the end of the process but in any case it’s entirely semantics. Pedantry at its finest. If that’s the best argument that can be made about what I wrote then it’s not much of an argument.

  63. Allen

    The United States was the best and brightest hope of the world when it was first founded, but squandered its moral legitimacy and dishonored the legacy of those who fought and died to defend it by attempting (so far unsuccessfully) to transform itself from a republic to an empire. And so, I’m even more proud of my Scottish ancestors who sat tight on their little island in the outer Hebrides (Barra, to be exact), didn’t invade or subjugate anyone else, and were never, ever (since Kisimul castle was built around the year 1000) defeated or subjugated themselves.

    I thinks it’s really melodramatic to say all that about the U.S. squandering its legacy and empire building. What empire would that be? Peacekeeping in Afghanistan and Iraq hardly seems like empire building to an Englishman. I can see how might to a Scotsman. And like it not since 1707 your homeland has willingly been part and parcel of Great Britain and shares credit and blame for everything done in the name of the British Empire. No one held a gun to Scotland’s head to remain part of Britain.

    The former soviet bloc countries worship us for winning the cold war and setting them free to determine their own destiny. Is that empire building? Some increased percentage of the population of Europe might not care for us but nothing else has changed with our relation with Europe. They’re still NATO members, still rely on us for defense, still host our military bases, still buy our products… in short nothing substantial has changed. Dislike of America in Europe is all bluster and no action. When they make some real gestures that go beyond empty rhetoric I’ll take them seriously. Otherwise it’s nothing more than a fashion trend.

    Nothing has really changed anywhere else in the world except we’ve gone from Arabs viewing us as paper tigers to real tigers. No doubt with Democrats in charge for a while we’ll go back to being paper tigers and the terror attacks on US shores and our embassies and ships at sea will resume. Militant Arabs are like dogs. They sense fear and it emboldens them to attack. George Bush understands that. Weak kneed liberals don’t. Show weakness to Arabs and they go for the throat. You can hide in your corner of upstate New York or on your isolated British Isle but keep in mind your redoubt is still safe because someone like me (former US Marine) was out in the big bad world keeping the bad guys away from you.

  64. P.Phillips you’re still being moderated and I’m still not approving your comments when they’re overly long and/or too far removed from connection with the thread. I killed one of them earlier today for both those reasons but mostly the former.

  65. Allen

    As I hammer away with my students, scientific hypotheses are worthless if they (a) cannot be used to generate empirically testable predictions

    Quite so. I was thinking about writing an article on the predictive value of NDE.

    I think what we need focus on there are two words: “worth” and “predict”.

    Worth is a specific value. Predict is a foretelling of the future.

    ToE is great at making assertions like humans and chimps share an ancestor. But does that have specific value and does it foretell the future? I’d argue little if any of the former and definitely none of the latter.

    I’m waiting for some ToE apologist to predict a future event in evolution where the prediction has some specific value. I say this is impossible for ToE as random mutations are by definition unpredictable. All ToE is able to do is connect dots in the history of evolution which has little if any practical value and foretells nothing about the future. I challenge anyone to predict some future dots in evolution. Those would be a foretelling of the future and have specific value. And I’m not talking about things that are based on statistical analysis of empirical observation. For instance we all know bacteria acquire resistance to new antibiotics. We need only our direct observations of bacteria to know that. In fact ToE, which has been around longer than antibiotics, didn’t predict anything about bacterial response to antibiotics. ToE explained bacterial resistance only after it was observed. No value or prediction there.

    So tell me not how humans and chimps were linked in the past. Tell me how evolution will change humans and chimps in the future. Good luck. :razz:

  66. And when ToE apologists say things like ToE is as well established as the theory of gravity it’s just laughable. The theory of gravity can predict the precise position of the planets a million years in the future. What can the theory of evolution predict a million years into the future?

  67. bebbo:
    As for peacekeeping, Saddam Hussein did a better job of that in Iraq, though many citizens of his own country had to pay in blood for it.

    An oxymoron if I ever heard one. Truly incredible.
    ——————————————————–

    Dave,

    They are NOT somatic cells if meiosis is involved.

  68. DaveScot: “What can the theory of evolution predict a million years into the future?”

    Good point, but I’d like to see the NDE proponets make a firm prediction about something as mundate as “Junk DNA.” It’s here now. What’s the final word on this? They don’t know. Their ideology is no help here. One prediction is as good as another.

  69. Allen sez:
    And yes, there is abundant evidence supporting the inference that chimpanzees and humans descend from a common ancestor.

    And the SAME evidence demonstrates they share a Common Design.

    FOXP2- one amino acid difference between mice and chimps-> 2 amino acid differences between chimps and humans. I read all about this when it was aired. Common Design if I ever saw it.

    HOX genes/ clusters are switches- master switches to be sure, but switches nontheless.

    Just like the PAX6 – where a mouse PAX6 was used to restore eyes to a fly- FLY eyes- HOX genes do not determine the structure although they do influence its development. Someone in your position should know that.

    Ya see Allen IF you were correct there shouldn’t be ANY biologists or geneticists who are Creationists. Yet we have Giuseppe Sermonti telling us that sex was the end of evolution. And everythinmg we have observed in the lab AND in nature supports him:

    Sexuality has brought joy to the world, to the world of the wild beasts, and to the world of flowers, but it has brought an end to evolution. In the lineages of living beings, whenever absent-minded Venus has taken the upper hand, forms have forgotten to make progress. It is only the husbandman that has improved strains, and he has done so by bullying, enslaving, and segregating. All these methods, of course, have made for sad, alienated animals, but they have not resulted in new species. Left to themselves, domesticated breeds would either die out or revert to the wild state—scarcely a commendable model for nature’s progress.

    (snip a few paragraphs on peppered moths)

    Natural Selection, which indeed occurs in nature (as Bishop Wilberforce, too, was perfectly aware), mainly has the effect of maintaining equilibrium and stability. It eliminates all those that dare depart from the type—the eccentrics and the adventurers and the marginal sort. It is ever adjusting populations, but it does so in each case by bringing them back to the norm. We read in the textbooks that, when environmental conditions change, the selection process may produce a shift in a population’s mean values, by a process known as adaptation. If the climate turns very cold, the cold-adapted beings are favored relative to others.; if it becomes windy, the wind blows away those that are most exposed; if an illness breaks out, those in questionable health will be lost. But all these artful guiles serve their purpose only until the clouds blow away. The species, in fact, is an organic entity, a typical form, which may deviate only to return to the furrow of its destiny; it may wander from the band only to find its proper place by returning to the gang.

    Everything that disassembles, upsets proportions or becomes distorted in any way is sooner or later brought back to the type. There has been a tendency to confuse fleeting adjustments with grand destinies, minor shrewdness with signs of the times.

    It is true that species may lose something on the way—the mole its eyes, say, and the succulent plant its leaves, never to recover them again. But here we are dealing with unhappy, mutilated species, at the margins of their area of distribution—the extreme and the specialized. These are species with no future; they are not pioneers, but prisoners in nature’s penitentiary.

    And guess what? There isn’t anything in peer-review that demonstrates otherwise. All you can offer is an inference based on the assumption. And all of that is based on similarities! Nothing you presented explains the differences!

    Chimps and Humans- the differences

    The (alleged) chromosome fusion is a great example- what change did it convey that it would be so conserved as to serve as some sort of divergence marker? Have we tried to induce this fusion to see what would occur?

  70. The fusion event that produced human chromosome 2 didn’t change any of the genetic information in the fused chromosome at all as far as we know. That’s the general situation in translocations: the same information is still there, it’s just located somewhere else.

    However, chromosome fusions, fissions, and inversions all have one very important effect: they render meiosis difficult or impossible in a hybrid. Many of the animals know to produce infertile hybrids (e.g. horses and donkeys, lions and tigers, etc.) differ in either chromosome number or gene sequence (but not genetic information) along the chromosome, and it is these chromosomal differences that generally account for the infertility of the hybrids.

    In other words, the chromosomal fusion/fission/translocation/inversion event genetically isolates two subpopulations of a formerly panmictic population, which then “drift” apart, either randomly or via directional selection.

    This process has been observed in real time in numerous species of plants, as most plants (especially those adapted to disturbed ecosystems, such as burned over grasslands) are relatively tolerant of aneuploidy. However, it has not been directly observed in many animal species because nearly all aneuploidies in animals are developmentally fatal (that was one of the main points of this thread, BTW). In general, we can only observe the outcome of such events, as in the case of the fusion of human chromosome 2.

    Which leads me immediately to a question: do you think that the evidence indicates that such a fusion event has, in fact, taken place, and if not, of what possible function could the massive amount of sequence evidence detailed in the journal reports I linked to above have, if any? In other words, why is there so much evidence supporting an event that did not happen?

    Personally, I think there is a surprisingly simple explanation for how chromosomal fusion/fission/translocation/inversion events can successfully proliferate in a hybrid population, even in animals. I am preparing a publication detailing my hypothesis and presenting supporting evidence, which I hope will be available in the next year or two. I will announce the actual completion and pulication date(s) on my blog:

    http://evolutionlist.blogspot.com/

  71. Allen MacNeill stated,

    “By the way, my wife (a magna cum laud from Cornell in classics, with a specialization in Mediterranean religions around 0 A.D. and fluent in six classical languages, including Aramaic and Biblical Hebrew) just pointed out that the Aramaic word that is usually translated as “virgin” in English bibles can just as easily be translated as “young woman”…which also makes all of the foregoing debate moot as well.”

    A rebuttal to and engagement of the scholarly kind from a lay person.

    First, congratulations on your wife’s academic accomplishments.

    The Isaiah reference does not make the debate moot by your way of definition, although I agree from a different angle. That of direct intervention. But to your argument, by referencing one single word, you omit larger well known facts, which can mislead people from the truth. The Aramaic word for “virgin” has been debated nearly 2000 years and is not a new revelation, nor does it prove your point. The first argument is to point out the word “virgin” in Hebrew is translated from the Massoretic text, not the Septuagent which is older than any known copy, including the Isaiah scroll of Qumran. The Massoretic text appeared nine centuries after the original translation by Jews of Hebrew into Greek around 250BC. Keep this in mind.

    Your wife I think is referencing Isaiah 7:14 speaking of EmmanuEl(meaning “God with us”) as in a specific reference to a special intervention of future born King, not a simple human, but “God with us.” Skeptics disbelief center on Isaiah’s own child. But this is easily dismissed.

    Instead of arguing this one verse, the Bible for those who accept Yeshua is not limited to one word interpretations of the Tenach. Instead, the words and stories are interwoven threads of revelation between both Old and New Testaments. The Old foreshadowing the events of the New.

    In the Greek New Testament, Miryam herself ask a question about her own virginity directly to God’s messenger Gabriel.

    Beginning with the Greek word; “parthenos”, which you will immediately recognize as the base for the “parthenogenesis” term you referenced wiki above. Parthenos is written in the New Testament to describe Miryam as a virgin(Mat 1:23). Now, critically in the Septuagent, the translation from Hebrew to Greek is the same word, “parthenos.” As you see the disciples, authors of the Greek New Testament were true to text of the time period. The Septuagent in 2nd Century BC completed before the time of Yeshua.

    Seeing how the conversation has referenced some form of the word; “parthenos,” understanding how it was utilized two thousand years ago to describe a “young maiden” as a “virgin” is important for clarification.

    But, lets not leave it open for speculation on one word. What did Miryam herself think about her condition and the revelation brought to her by the messenger Gabriel?

    In the New Covenant, Miryam ask the messenger Gabriel how will she conceive? Stating “How shall this be, seeing I know not a man?”(Luke 1:34) This is a clear and unambigious statement claiming her virginity.

    Word usage in the Old Testament is “superceeded” by the direct claim of Miryam and the Disciples in the New Testament who in fact reference Isaiah 7:14. The same Isaiah 7:14 translated into Greek by 70 Jewish scholars prior to Yeshua’s birth, utilizing the same greek word, “parthenos.”

    “Know not man” is a Hebrew idiom prior to the days of Yeshua, used in the Old Testament for being a virgin. Check with your wife, she should attest to this fact in Genesis and Leviticus among other Books of the Bible of this easily recognizable saying.

    Therefore, it is left to the reader to either believe Miryam’s version of the story, or to denounce her as a liar. The choice is left to each individual reader.

    Your quoting Aramaic words opens the topic for a wider view not previously mentioned in this discussion. Science ignores Miryam’s response and the Gospel author’s statements. Gabriel specifically tells Miryam that she will be visited by God and “overshawdowed.” The Greek language and the context do not give the specific physical aspects of the process. Whatever happened it was not an act of nature, but a boldly claimed intervention to introduce God as man fully into the equation of life on earth, to walk, talk, eat, bathe, sweat, suffer, and die with “humility.” To deliver a message of Salvation.

    Miryam’s conceiving of Yeshua is never put forward in the Gospels as a natural act of copulation. For such messages delivered by God, see the story of Abraham and Sarai prior to her giving birth, upon which her name changes to Sarah. The message delivered to them foreshadowed Christ, the story of a womb opened and a ram sacrificed in place of Isaac. This foreshadows the Messiah’s birth and personal sacrifice for all mankind.

    Again, the individual is left with a decision.

    Believe Miryam, the Disciples and authors of the New Covenant that God did in fact intervene, or not.
    It is that simple within certain context, but obviously more complex once one searches for the truth and finds a deeper meaning within the whole Biblical story woven beautifully across roughly 4004 years with concealed truths.

    Certainly, if there is an opportunity to see greater than what is in this world, I’d investigate it fully. Twelve disciples for at least 70 years traveled the earth by foot proclaiming this good news, giving up their lives, some by brutal methods.

    The scientific discussion is interesting. But I dispute its validity from the start as I personally believe God intervened as a specific moment and time. And as the Creator, His knowledge far advanced, did not need to worry about some natural mechanism, but utilized his knowledge to circumvent the situation. Think of it as an advanced in vitro process.

    That is my two cents…

    There is much to be thankful for tomorrow. I hope you all have a good thanksgiving and blessings.

    Also, whether we agree or not, there are others today who voluntarily have gone afar and sacrifice being with family and friends while we are safe at home. Sometimes giving their lives. We can all send a simple message of thanks and put politics aside on days like these.

    Link here: http://www.mnf-iraq.com/index.html – see right and click on leave message. It takes all of one minute to let them know we care.

  72. “Which leads me immediately to a question: do you think that the evidence indicates that such a fusion event has, in fact, taken place, and if not, of what possible function could the massive amount of sequence evidence detailed in the journal reports I linked to above have, if any? In other words, why is there so much evidence supporting an event that did not happen?”

    It possible the fusion did happen but it pure speculation what kind of results were produces. One thing I’ve learn from reading about genetics is there’s a lot of mixed results so the predictions doesn’t always come true. Again it’s also just aspossible this fusion was designed this way on purpose. (maybe Gods didn’t want a butch of apeman hanging around. :)

  73. If a supernatural God can cause this universe to exist, he/she/it/they can certainly cause a woman’s egg to develop into a full human baby. What’s the deal here?

  74. To continue, at the bottom (or at the origin) of this spacetime there is a non-rational conceptual brickwall. The Darwinistas complain that the skeptics’ imaginations are not open enough, and true or not, for some reason they themselves suffer from the malady when it comes to what might be the cause and nature of the spacetime system we find ourselves in. But that’s just their nature “religion” talkin’. They ain’t fooling me.

  75. Allen,

    In reading your assessement of chromosome fussion (eg chromosome 2 in humans):

    However, chromosome fusions, fissions, and inversions all have one very important effect: they render meiosis difficult or impossible in a hybrid. Many of the animals know to produce infertile hybrids (e.g. horses and donkeys, lions and tigers, etc.) differ in either chromosome number or gene sequence (but not genetic information) along the chromosome, and it is these chromosomal differences that generally account for the infertility of the hybrids.

    In other words, the chromosomal fusion/fission/translocation/inversion event genetically isolates two subpopulations of a formerly panmictic population, which then “drift” apart, either randomly or via directional selection.

    I have a question, which may be answered in your forth-coming hypothesis:

    Would this fussion event have to occur within at least two members- one male, one female- of the same population in order for it to have any chance of getting passed on?

  76. Allen

    I was just about to ask the exact same thing Joseph did.

    If the fusion caused infertility in hybrids then how on earth did the first individual with the fused chromosome pass it along?

    Maybe you’d care to take this opportunity to rethink your argument against virgin birth in mammals. You might want to read Davison again too as he gets around this problem. Oh but hold on, you dismissed Davison as “all hypothetical” as I recall. Are you planning on doing some experiments to transform your “all hypothetical” into something different than Davison’s “all hypothetical”?

    I love the smell of hypocrisy in the morning.

    :razz:

  77. #66 & 67 DaveScot,

    I think you are mistaken here. You underestimate ToE. It is so plastic it can “predict” just about anything. So called, “Junk DNA” is the point in case. And I bet you, as Mike Gene pointed out, if paleontologists find rabbit fossil in Pre-Cambrian, it would be no problem for ToE. Didn’t you know that ToE is really a FoE?

  78. Joseph, Dave,
    you should be aware that patients with translocations can be viable and that such translocations are inherited. From OMIM (http://www.ncbi.nlm.nih.gov/en.....?id=190685)

    Most individuals (95%) with trisomy 21 have 3 free copies of chromosome 21; in about 5% of patients, 1 copy is translocated to another acrocentric chromosome, most often chromosome 14 or 21

    To get further insight into this issue you may also look for ‘uniparental disomy’.
    In addition, through MICER clones such mechanisms can be investigated in vivo today. (http://www.ncbi.nlm.nih.gov/en.....med_docsum)

  79. In comment #76, Joseph asked:

    “Would this fusion event have to occur within at least two members- one male, one female- of the same population in order for it to have any chance of getting passed on?”

    In a word, no. All that would need to happen to make this possible would be for two first-degree relatives carrying the translocation to mate and have offspring. First degree relatives (i.e. parents and offspring or full siblings) can easily have the same chromosomal mutation (i.e. a fusion/fission/translocation/inversion), as they would inherit it from a single parent. If they were to mate with each other (a not uncommon event among non-humans…and even among some humans), they would be able to produce fertile offspring carrying the same chromosomal mutation.

    Yes, it is true that first degree mating carries with it the possibility of reinforcement of recessive lethal alleles. However, as many geneticists and evolutionary biologists have repeatedly pointed out, this is actually beneficial to the population within which such reinforcement happens, as the alleles are removed from the population as a result.

    In other words, mating between first degree genetic relatives within a small, isolated population would have the effect of both removing deleterious alleles from the population and allowing chromosomal mutations to spread throughout the population, especially if such mutations were at all beneficial (although they would diffuse almost as well if they were selectively neutral, as would probably be the case given that no change in overall genetic information would have occurred).

    Furthermore, the hypothesis that I have presented above squares very well with the currently prevailing theory of speciation: that of peripatric speciation, as first proposed by Ernst Mayr. According to Mayr’s theory, speciation occurs most often in small, isolated populations on the periphery of large, panmictic populations. There is abundant natual history evidence that this is the case, especially in animals.

    However, no one has yet explained how peripatric speciation would come to be associated with the kinds of chromosomal changes that we have been discussing. My hypothesis – that first-degree inbreeding facilitates chromosomal speciation – is an attempt to reconcile those two observations.

    In a large, panmictic population, selection would tend to eliminate individuals who mate with first-degree relatives as a result of decreased viability due to inbreeding depression and the increased frequency of expression of homozygous lethal alleles.

    However, in very small, isolated populations individuals who occasionally mate with first degree relatives (i.e. “facultative first degree inbreeders”) could easily have a selective advantage of individuals who avoid mating with first degree relatives (i.e. “obligate outbreeders”).

    Males in particular would tend to loose less as the result of mating with first degree relatives, as their parental investment in offspring is lower (i.e. they can waste gametes and even zygotes by mating with their first degree relatives, without significantly decreasing their reproductive success).

    However, even females can cut their losses by mating with first degree relatives if the likely alternative is failure to mate at all due to unavailability of non-relatives. This would especially be the case in small, isolated populations, which are exactly the kind of populations in which speciation is most likely to occur.

    The effects described above would be facilitated by increased genomic homogeneity, such as would result from genetic bottlenecks and founder effects. This is because close inbreeding intensifies genomic homogeneity and decreases genetic variation, especially in isolated populations with decreased gene flow from other populations.

    This hypothesis – that first degree inbreeding facilitates chromosomal speciation – immediately suggests a series of predictions, all of which are empirically testable:

    • The frequency of mating between first degree relatives should be inversely correlated with effective breeding population size. That is, the smaller the effective breeding population, the greater the frequency of mating between first degree relatives (i.e. “first degree inbreeding”).

    • The increased frequency of “first degree inbreeding” in such populations should be more pronounced in males. That is, males should be more likely to attempt mating with first degree relatives, especially in small, isolated populations.

    • The frequency of “chromolocal mutations” (that is, chromosomal fission/fusion/inversion/translocation mutations) should also be inversely correlated with effective breeding population size. That is, the smaller the effective breeding population, the greater the frequency of viable “chromolocal mutations.”

    • Peripatric speciation events should be correlated with small population size, chromolocal mutations, and first degree inbreeding.

    • Speciation resulting from chromolocal mutations should be much less common in large, panmictic populations.

    • First degree inbreeding should also be much less common in large, panmictic populations.

    • The success rate of artificial (i.e. facilitated/forced) first degree mating should be directly correlated with the degree of inbreeding. That is, the more inbred a population, the more successful artificial first degree inbreeding should be.

    • Paleogenomic analysis should find close correlations between genetic bottlenecks, founder events, and peripatric speciation events and the frequency of chromolocal mutations and genetic homogeneity (resulting from first degree inbreeding).

    • Relatively large changes in phenotype resulting from chromolocal effects should be more common in small, isolated populations.

    • Speciation should be easier (and therefore more frequent) among asexually reproducing eukaryotes, such as plants and parthenogenic animals (among whom aneuploidy is largely irrelevant).

    Let me stress two things about the foregoing:

    • What I am suggesting is, at this stage, merely a hypothesis, but one that generates a series of immediately testable predictions.

    • The hypothesis is, of course, based on the idea that incest (i.e. first degree inbreeding) is the most likely explanation for the diffusion of chromolocal mutations throughout small, isolated populations of animals. Let me stress as strongly as possible that I am NOT advocating incest, I am simply pointing out that first degree inbreeding would facilitate the kind of chromolocal mutations that are often correlated with species differences in animals. The same is also true for plants, of course, but in plants we don’t call it “incest,” we call it “self-pollination.”

    I would like to also add at the end of this presentation that my reading of John Davison’s papers in which he details his “semi-meiotic hypothesis” for the origin of species were an indirect inspiration for my own efforts. While his hypothesis would work, its most significant drawback is that it requires an almost unlimited number of independent “reinventions” of the same mechanism (i.e. semi-meiosis) for speciation that results from chromolocal effects to be the basis for speciation throughout the animal kingdom. Not impossible, but extremely unlikely.

    By contrast, my “first degree inbreeding hypothesis” does not require independent “reinventions” of semi-meiosis at all. The only thing it requires is that first-degree inbreeding occur in small, isolated populations of animals, an easily testable prediction that does not require elaborate genetic mechanisms to produce the predicted outcome: that is, genetic isolation and subsequent speciation.

    I am a little perplexed at why no one has yet proposed this mechanism, given the fact that it is already used as the explanation for speciation in plants via polyploidy. The only explanation that seems reasonable to me is that most evolutionary biologists assume that animals will always avoid mating with first-degree relatives as a result of the increased frequency of inbreeding depression and expression of homozygous lethal alleles that result from it.

    Anyway, that’s my hypothesis in brief. At my place (at Lyonesse, in Utopia, far above Cayuga’s waters), the only thing I’m smelling right now is the turkey in the oven and the hard cider in the jar…

    Have a good one, folks!

  80. Allen

    I’m afraid you completely missed the nature of the objection.

    A chromosomal fusion happens instantaneously in a single individual. You indicated that this individual would not be able to reproduce with those of its parent species because meiosis would be mucked up from incompatibile chromosome count. Therefore, the only way for the fusion to become a new species is there must be another individual of the opposite sex born with the same fusion and the two individuals with the fused chromosome must find each other and mate.

    Are you suggesting any other way for this to happen?

    In order for that to happen there would have to some predisposition for that particular chromosomal aberration such that there are enough of them in the population at any given instant to make it reasonable two of them would find each other. In other words, two hopeful monsters fall in love.

    For the children of the monsters to find more compatible children of monsters somewhere in order to avoid the complications of inbreeding adds improbability on top of improbability.

    Possible, I suppose, but there really has to be a strong predisposition for that particular fusion mutation to get enough of the hopeful monsters around at the same time for mating purposes.

    Also, I think you’ve misinterpreted Davison’s work. I don’t recall him saying that a semi-meiotic mechanism is something needing to be invented over and over. It’s something that was always there but seldom used. I mean, c’mon Allen, if a haploid egg cell can be coaxed into becoming a replicating diploid by pricking it with a needle or giving it a little electric shock, it doesn’t seem much of a stretch that a little something out of the ordinary can happen during meoisis as Davison describes.

    Davison also claims his hypothesis is testable and he would have done it had he not had his lab privileges taken away by UVM in retaliation for being an outspoken anti-Darwinian. I don’t know if that that’s true and the testability of his hypothesis is beyond me. It’s stretching what I know of reproductive biology just to get the gist of it. He says what’s required for testing are amphibians that are heterozygous for chromosome translocations. How one would locate in the wild or engineer in the lab such amphibians is also beyond my ken.

  81. Dave,
    pleas have a look at balanced trisomy here
    http://www.tokyo-med.ac.jp/genet/trc-e.htm

  82. Great stuff, guys! Now let’s eat!

  83. Hi, Dave:

    You make good points (all of which I agree with, and which also demonstrate that you understand the problem), but you miss mine. In particular, you state:

    “…the only way for the fusion to become a new species is there must be another individual of the opposite sex born with the same fusion and the two individuals with the fused chromosome must find each other and mate.”

    If a single individual (say a male) has a chromolocal mutation (i.e. a fission, fusion, inversion, or translocation in/of one of his chromosomes) it will generally not affect him phenotypically at all, since the same genetic information is still there, it’s just located in a different place. If he mates with someone else, he will pass his chromolocal mutation to half of his offspring on the average, as some will get the normal version of the chromosome and some will get the altered one (as the result of the segregation of the homologous chromosomes during the first division of meiosis). Again, since there is no change in genetic information, his offspring should have approximately the same fitness as himself, and so at least some of them may survive (after all, he did at least long enough to mate and reproduce). The offspring that share the chromolocal mutation can then successfully mate with either each other (or with him), as they will share the same mutation. This means that it would be unnecessary for the mutation to happen more than once, so long as the individual in which the mutation occurred can pass it on to his/her offspring.

    As I pointed out, this would be more likely to happen in the case of males (who loose little or nothing from mating with someone with whom they share potentially lethal alleles), and would be more likely to happen in very small populations anyway (since alternative mates would be few and far between, or missing altogether). This squares nicely with the prevailing theory of speciation (Mayr’s peripatric theory), which states that the probability of speciation events is inversely correlated with effective breeding population size.

    And so you are absolutely right in one sense: if it were necessary for two individuals who independently had the very same chromolocal mutation happen to them to find each other, it would be extremely unlikely that they would, rendering the probability of speciation as the result of chromolocal mutation almost impossible.

    However, we know from simple observation that many of the differences we see in closely related species are indeed the result of chromolocal mutations. Therefore, quite apart from the question of how such mutations participate in speciation, it is necessary to explain how they can possibly get established in a population at all (barring magical intervention, of course).

    My hypothesis explains how this can happen, using an extremely simple mechanism (first-degree inbreeding) and without requiring the simultaneous mutation of multiple individuals in a breeding population. It also avoids a similar problem with Davison’s hypothesis, which requires a switch from one form of gamete production to another (i.e. a fairly radical alteration of an otherwise stable genetic process) at just the right time to allow for speciation.

    Davison is correct in stating that his hypothesis could be tested using amphibians, primarily because amphibian eggs can be coaxed into dividing without being fertilized. However, my hypothesis has no such limitation, and can easily be tested in virtually all animals via relatively simple observations (i.e. not requiring complex artificial manipulations under controlled laboratory conditions).

    That is, my hypothesis does not require any new genetic mechanisms at all beyond chromosome fission/fusion/inversion/translocations, which we know from empirical observation are surprisingly common. All it requires is that first degree genetic relatives occasionally mate with each other, an observable and easily testable requirement (and one that artificial breeders use quite often, although for other reasons).

    Furthermore, such mutations are not rare. Indeed, it is likely that every one of us acquires several of these mutations as we age, occuring in various cells throughout our bodies. Such mutations have been shown to occur regularly at a steady “background rate” in all cells. For example, at least one form of leukemia is known to be caused by a translocation of a small part of one chromosome to another, producing what is known as a “Philadelphia chromosome” (see http://en.wikipedia.org/wiki/P.....chromosome ). This is also one reason for the decline in fertility with age in most animals; they accumulate chromolocal mutations that eventually make meiosis less likely to produce viable gametes.

    Also, an individual in which a chromolocal mutation has occurred will probably not be a “monster” at all. None of the genetic information carried by the chromosomes has necessarily been altered, it has simply been located somewhere else in the genome. This means that such individuals would generally be phenotypically indistinguishable from individuals who do not have such mutations.

    But you are right in one sense: my hypothesis strongly implies that speciation that results from a chromolocal mutation is an event that happens in single individual, and happens essentially instantaneously. This directly contradicts mainstream evolutionary theory (i.e. the so-called “modern evolutionary synthesis”), as it strongly implies that macroevolution (i.e. speciation and the origin of higher taxa) is virtually instantaneous, rather than the long-drawn-out result of millions of years of gradual change, as implied by the “modern synthesis.”

    However, this (IMNSHO) is yet another factor in favor of my hypothesis, as it squares nicely with Eldredge and Gould’s theory of “punctuated equilibrium,” which strongly suggests that macroevolution happens in relatively rapid “bursts,” followed by long periods of evolutionary “stasis.” As E&G’s theory has been steadily gaining ground, this is just great for my own hypothesis, which provides an easily testable genetic mechanism for such macroevolutionary “revolutions.”

    To sum up:

    As you correctly point out, the problem is having sufficient numbers of individuals sharing the same chromolocal mutation to mate and produce fertile offspring (since such individuals generally can’t successfully mate with individuals who do not share such mutations).

    The solution as I see it is surprisingly simple: having individuals who share the same mutation because of common descent/parentage (i.e. full siblings or parents and offspring) mate with each other. That this would be most likely to happen in small, isolated populations squares nicely with what we know about species differences and the circumstances in which they are observed.

  84. Allen,
    What am I missing?

    The solution as I see it is surprisingly simple: having individuals who share the same mutation because of common descent/parentage (i.e. full siblings or parents and offspring) mate with each other.

    You are saying the male with the mutation can mate with his like-wise afflicted offspring, or that they can interbreed amongst themselves.
    With whom did the male mate in the first place to create these offspring?

    Are you not offering initially that the mutant can breed with a normal female?
    If so, can’t his mutant offspring as well?

    You seem to suggest not:
    The offspring that share the chromolocal mutation can then successfully mate with either each other (or with him), as they will share the same mutation.

    To my reading your theory has either one of two holes:
    1) the mutant can breed with normal members of the population, and therefore, your mechanism of first-degree inbreeding is superfluous;
    or
    2) the male couldn’t have bred with a female in the first place to create the mutated offspring with whom he would then incestuously mate, and therefore the line dies before your proposed mechanism can kick in.

    What’s the first step that I am missing?

    ps.
    What was your response to trisomy 18 v. trisomy 21?

  85. Allen

    I’m still missing something here. Let’s stick with the chromosomal fusion which reduces the chromosome count by one but doesn’t alter anything else. I believe this came up in talking about the differences between chimps and humans.

    The first fused chromosome starts out in a single egg or sperm as a mutation. When that mutated egg or sperm joins with a normal gamete a hybrid animal is produced. The hybrid will be sterile because meiosis is mucked up due to having an unequal number of chromosomes from each parent. You began this subtopic by saying that hybrid sterility in the case of unequal chromosome counts is due to meiosis being mucked up.

    Therefore, the only way to produce a fertile animal with the new fused chromosome is by the combination of a sperm and egg which both contain the fusion. Then meiosis will proceed normally as both parents had the same number of chromosomes.

    Am I missing anything so far?

    Given a predisposition for certain types of fusions (say a fusion of chromosome X and Y occurs in 1/1000) then 1/10^6 matings would be between egg and sperm both containing the fusion and a fertile animal with the fusion would be born. It would be a single individual of a new species as it would not be able to produce a fertile hybrid with the parent species but could produce fertile offspring with another individual like itself. However, for this individual of the new species to continue the species it would have to mate with another individual like itself. Since it is already a one in a million individual, mating with another one in a million individual is a one in a trillion chance. If the XY fusion was a random mutation in one of ten gametes the one in a trillion mating is reduced to a one in ten thousand mating and it becomes plausible. However, is it plausible for the exact same fusion to hit one of every ten gametes? That doesn’t seem reasonable but I suppose it might be possible and that would be the key to making the whole gimmick a plausible method of saltation via chromosome reorganization.

    This is what makes Davison’s hyothesis so attractive. The semi-meoisis mechanism he describes is capable of producing both male and female of the new species from a single parent and have them in close proximity for mating purposes.

    That’s what earned Davison the nickname “salty” (from saltation). I certainly understand why you’re searching for a saltation mechanism, and instantaneous chromosomal reorganizations sure look like a way for it to happen, but I don’t think you have yet proposed a credible way for both male and female of the new species to be produced in close enough proximity so they’d meet and mate to continue the new species.

  86. Allen

    Doctor Davison requests your presence at Brainstorms to discuss meiosis, semi and otherwise.

    http://www.iscid.org/boards/ub.....-p-20.html

  87. Allen

    Let me know if I have this diploid business right now.

    If two chromosomes are connected by a centromere they become two chromatids but one chromosome. Burn the bridge and the chromatids are transformed back into two chromosomes.

    This is like if two ships at sea come together and extend a gangplank between them they are no longer two ships but rather one ship composed of two shiplets. Once the gangplank is retracted they’re two ships again.

    LOL

    You really expect me to take you seriously when you say distinctions like that are important?

  88. OK wait:

    I asked:
    “Would this fusion event have to occur within at least two members- one male, one female- of the same population in order for it to have any chance of getting passed on?”

    Allen responded with:
    In a word, no. All that would need to happen to make this possible would be for two first-degree relatives carrying the translocation to mate and have offspring.

    But that is what I aksed and you said, “In a word, no.” What gives?

    So we do need two with the same fusion.

    Also Mayr tells us that in populations under 1000 (2 being well under), the chances of survival are slim.

    I guess what we nedd is some way off testing Allen’s “way out”. Because without that it appears we have a contradiction- either the alleged fussion event causes genetic isolation or it does not.

    Normal mom 48 (2n where n = 24)
    Normal dad 48
    Fused son 46 (?) – 2 fusion events would have had to happen one event in each parent!- so perhaps it would be son 47- getting one normal set and one set with a fused chromosome.

    OK son 47
    his mate 48
    their offspring- either 47 or 48, unless another fusion event occurred in his mate!

    Getting one offspring (to start with) with said fusion does not defy the odds. Getting two, having BOTH survive and successfully reproduce is pushing it.

  89. I woud like to thank both Allen and Dave for this discussion. Even though I am basically in the background this discussion, I believe, is leading to some nice critical thinking and hashing out an idea- which is a good thing.

    Thanks again- may we work this out one way or another. Or at least provide some fertile ground to start a foundation from which to carry-on.

  90. “You really expect me to take you seriously when you say distinctions like that are important?”

    They are very important, especially when describing the processes that occur during meiosis (and thereby avoiding the kind of misunderstanding to which you and some of my students have fallen prey). Chromosome number is absolutely crucial in meiosis and gamete formation, and being semantic precision in describing these processes makes intelligent discussion about them possible (as is true in all of science, BTW). Clearly, geneticists in particular and scientists in general have found it not only convient but necessary to make these distinctions, and will undoubtedly continue to do so. Whether you find them necessary or not is completely irrelevant.

  91. In comment #85 Charlie asked:

    “Are you not offering initially that the mutant can breed with a normal female?
    If so, can’t his mutant offspring as well?”

    Indeed, that is exactly what I am suggesting. As long as there is no serious developmental problems, an individual with a chromolocal mutation can easily interbreed with an individual lacking such a mutation. They just can’t produce fertile offspring, as the mutation would interfere with meiotic gamete formation. However, the offspring of such a cross would not face such a difficulty, as they would all share the same mutation (this would also be true for such offspring and their parent who had the original mutation). That’s the whole point behind my hypothesis: that first-degree inbreeding makes speciation via chromolocal mutation possible…indeed, likely.

  92. DaveScot wrote:

    “Since it is already a one in a million individual, mating with another one in a million individual is a one in a trillion chance.”

    Nope; among the offspring of a mating between a normal individual and an individual with a chromolocal mutation, the frequency of that mutation would be 1 in 2, not one in a trillion. That is, half of the offspring would share the same mutation. If two of them interbred with each other (a one-in-four chance: 1/2 X 1/2 = 1/4), then their offspring would be homozygous for the mutation.

    Piece of cake, IOW.

  93. Thank you, Joseph: respect given and reciprocated, as it should be in debates between intelligent adults. You are a gentleman and a scholar, who realizes that the way to clarity is reasoned debate, supported by evidence, without resort to ridicule and personal attacks. Thank you, and have a great weekend!

  94. As to the trisomy 18 versus trisomy 21 question, the former is always fatal, whereas the latter is often survivable, and even genetically transmissable. If a person with Down syndrome has a child with someone who does not, the chances that they will have a child with Down syndrome are one in two. This is especially the case when the extra chromosome 21 is translocated to the tip of another chromosome (a so-called “Robertsonian” translocation).

    As to which specific trisomy was the cause of death of what would have been my sixth child, we don’t actually know (and haven’t had the heart to investigate). She is gone; that’s all we need to know.

  95. The word “prediction” is used somewhat differently in science than in everyday speech. When we speak of “prediction” in the context of the scientific method, what we are referring to is specific, testable predictions that flow via deductive reasoning from a hypothesis.

    For example, my “first-degree inbreeding” hypothesis for the origin of species by means of chromolocal mutation immediately suggests a series of testable predictions, as listed above. One of those would be that such mutations would be more common in small, isolated populations, a prediction that is easily testable and that, if verified, supports the hypothesis from which it was derived.

    Amazingly, I have already received an email from an Evolution List reader that provides confirming evidence for this very prediction. You can read all about it at:

    http://evolutionlist.blogspot......m-one.html

  96. Allen,

    As I just stated on my blog, if I am wrong I want to know about it.

    So let me see if I have this straight-

    Would your original mutant have 47 or 46 chromosomes?

    If 47 we would have a 47 mating with a 48 to get some combination of 47s and 48s.

    The surviving 47s (group A) could mate with each other or the 47 parent. The resulting ofspring would then give some possible combination of 46s, 47s and 48s.

    The same surviving 47s (group A) could also mate with the existing 48s to give new combinations of 47s and 48s.

    Somewhere along the line the 47s disappeared, except now we see 47 in some Down’s cases.

  97. Allen

    re chromatid

    What’s in a name? That which we call a chromosome by any other name would have as many genes.

    Spare me.

  98. Allen

    Nope; among the offspring of a mating between a normal individual and an individual with a chromolocal mutation, the frequency of that mutation would be 1 in 2, not one in a trillion.

    You misunderstood. I’m starting to wonder whether it’s on purpose.

    Take two populations with one million individuals in each. One individual in each population is unique. If you selected one individual from each population at random to make a pair, the chance of selecting both unique individuals in one pair is one in a trillion.

    If you don’t understand that then there’s not much hope of this discussion getting anywhere.

  99. Allen,
    Thanks for your responses.
    I’ll have to chalk up my problem with your hypothesis to my ignorance on the subject.
    I still see no distinction between the original male being able to mate with a normal female and the ability of his offspring to do so.
    There’s something basic in the problem I don’t understand, so I’ll leave it to those who do.

    As for this
    As to the trisomy 18 versus trisomy 21 question, the former is always fatal, whereas the latter is often survivable, and even genetically transmissable.

    I would have to pick at nits here with you.
    Trisomy 18 is always fatal, but then, ultimately, so is birth.
    Trisomy 18 individuals, although rarely, can live and develop into their teens. This seems to contradict your statement of fact that all departures from diploidy (other than trisomy 21) result in spontaneous termination of development.

  100. Just an observation but the mice in comment 97 are still mice.

    In the chimp/ human scenario the “population” of genetically isolated 46ers would also require some number of mutations that effect phenotypical and morphological changes.

    FOXP2 doesn’t appear to be of much help:

    FOXP2 and the Evolution of Language

  101. Re comment #97:

    The original chromolocal mutant would have 47 chromosomes, assuming it started out with the “normal” ape complement of 48. However, it might make it easier if one considers the two haploid sets of chromosomes in such an individual:

    Let us assume for the sake of illustration that the fusion event we are discussing fuses together chromosome #2 and #3; in that case,

    One set would consist of chromsomes #1, #2, #3, #4,…#23 + either an X or a y, for a total of 24 chromosomes (the “ape” haploid number)

    The other set would consist of chromsomes #1, #2 fused to #3, 4,…#23 + either an X or a y, for a total of 23 chromosomes (the “human” haploid number)

    During meiosis in this individual, the fused chromosome (#2+3) could pair up with the unattached #2 and #3 (such pairings are possible and have been observed in nature and in the lab), and then the two sets of chromosomes would be segregated into the first division daughter cells. which would then go through the second division, becoming haploid gametes. The result would be two daughter cells/gametes containing 24 chromosomes (i.e. the haploid number) and two daughter cells/gametes containing 23 chromosomes (i.e. the haploid number minus 1, because two of the chromosomes are fused together).

    When these gametes are combined with normal gametes from another individual following mating, the result would be that half of the offspring would have 48 chromosomes (the normal “ape” number) and half would have 47.

    If these individuals then went through meiosis and mated with each other (i.e. “first-degree inbreeding”), the result would be a population in which half of the offspring would have 48 chromosomes and half would have 46 (i.e. the normal “human” number). Et voila. the soon-to-become human genome would be off and running.

    Although meiosis can proceed with uneven numbers of chromosomes (as described above), it proceeds easier when every chromosome has a single homolog with which it can pair during prophase I of meiosis. For this reason, once a small group of individuals had been established that had 23 pairs of chromosomes instead of 24, these individuals would be more fertile mating with each other than mating with individuals that had 24 pairs. As a result, the two populations would tend to diverge over time, and if there were any differences in their phenotypes at all (not necessarily related to their chromosome number) and there were any correlated differences in reproductive success, then the two clades would continue to diverge, eventually becoming humans and chimpanzees (or perhaps bonobos…we don’t know yet).

    As to the comment that the mice on Madeira are still “mice,” this misses the point entirely. They are, in fact, six different species of mice, all descended from one original ancestral species brought ashore about 500 years ago.

    The same thing (i.e. rapid speciation) has been documented in other locations, most spectacularly in Lake Victoria, where over 600 species of cichlid fish speciated from three or four ancestral species in about 12,500 years (see Goldschmidt/Darwin’s Dreampond for a detailed discussion).

  102. First Thanks again for the response and I will digest the bulk a little later. I would like to take a few seconds to repond to this:

    As to the comment that the mice on Madeira are still “mice,” this misses the point entirely. They are, in fact, six different species of mice, all descended from one original ancestral species brought ashore about 500 years ago.

    I have no doubt that the points being made are entirely different. But six different species of mice in 500 years from one ancestral stock pales in comparison to what would have had to have occurred in the YEC scenario following The Flood.

    IOW in light of the evidence you presented post-Flood rapid speciation claims do not seem so far-fetched. However even that does not explain the differences that need to be explained between chimps & humans.

  103. Allen,
    If half the offspring have 48 chromosomes and half 47, and the offspring are inbreeding freely (but inbreeding exclusively) then isn’t the ratio in the next generation 3:2:1 for 48-chromosome individuals: 47-chromosome individuals:46 chromosome individuals?

    Are you presuming a breeding bias in the first daughter population?

  104. I can’t read my own scribbling.

    Where a 48-chromosome individual can breed with another 48 or a 47, and the 47 can breed with another 47 or the 48, isn’t the next generation ratio of 48:47:46 actually 7:4:1?

  105. Pitiful.

    I mean 9:6:1.

    I forgot to breed the 47 and 48 a second time.
    Should have quit while I was behind.

  106. In comment 71 Allen said:

    However, chromosome fusions, fissions, and inversions all have one very important effect: they render meiosis difficult or impossible in a hybrid.

    In comment 92 Allen said:

    Indeed, that is exactly what I am suggesting. As long as there is no serious developmental problems, an individual with a chromolocal mutation can easily interbreed with an individual lacking such a mutation. They just can’t produce fertile offspring, as the mutation would interfere with meiotic gamete formation.

    In comment 102 Allen finally admits:

    During meiosis in this individual, the fused chromosome (#2+3) could pair up with the unattached #2 and #3 (such pairings are possible and have been observed in nature and in the lab), and then the two sets of chromosomes would be segregated into the first division daughter cells.

    So the first animal with the fused chromosome (fused by random mutation instead of inherited) isn’t really infertile. I’ve been trying to tease this admission out of Allen for the longest time in this thread. His hypothesis made no sense at all if meiosis wasn’t possible with a mismatched chromosome count.

    My next question is just how possible is it and where in the literature may we find this documented?

  107. I was just reading that sequence myself, DaveScot.
    I was pondering bringing it up but the humiliation of my ratio saga left me gunshy.

    Your quote in 92 continues:

    They just can’t produce fertile offspring, as the mutation would interfere with meiotic gamete formation. However, the offspring of such a cross would not face such a difficulty, as they would all share the same mutation (this would also be true for such offspring and their parent who had the original mutation).

    Are the offspring in both sentences not the same creatures?
    Can the offspring form gametes via meiosis or not?

  108. Allen:
    When these gametes are combined with normal gametes from another individual following mating, the result would be that half of the offspring would have 48 chromosomes (the normal “ape” number) and half would have 47.

    That’s not true. Females- one egg, 3 polar bodies from one meiosis cycle. The polar bodies will never become an egg. If the female is a diploid 48 that isn’t an issue. If the female is a diploid 47 the prediction of 50% being this or that is nothing more than a guess. And that is just in the number of viable female eggs produced And there is more.

    If the male is diploid 47, female is diploid 48- Even when every female egg will be haploid 24, is there really a 50% chance a haploid 24 sperm will fertilize it? I am pretty sure it isn’t that nicely divided.

    Male is diploid 47, female is diploid 47- Female drops a haploid 24 egg, what prevents a haploid 23 sperm from fertilizing it first- that is before a haploid 24 sperm from the same donor (or other) does the trick? That should give us the possibility of more diploid 47s. Female drops a H23 and the male deposits mostly H24s. More possibilities of diploid 47s.

  109. DaveScot wrote:

    “So the first animal with the fused chromosome (fused by random mutation instead of inherited) isn’t really infertile. ”

    You are quite right, and I was being obtuse in not understanding your objection. Translocations do not render meiosis impossible, only somewhat more difficult in most cases. To be precise, an individual that has a normal set of chromosomes and a set with a translocation will have somewhat more difficulty producing haploid gametes via meiosis than an individual that has the same number of chromosomes in each set. This is why I proposed that, once there were offspring from an individual that had a chromolocal fusion mutation, the offspring that were homozygous for either the normal complement (48, in the case of apes) or the fusion complement (i.e. 46) would almost certainly be more fertile than individuals that had one of each set (i.e. had a total of 47 chromosomes). Therefore, selection on the basis of fertility alone would tend to cause these two groups to diverge (i.e. the individuals with 47 chromosomes would consistently have fewer offspring than those that were homozygous for either 48 or 46 chromosomes.

    Such selection would be enhanced if there were any phenotypic differences between the 48-chromosome and 46-chromosome subpopulations, as the individuals in those subpopulations could then use such differences as guides for choosing mates, on the basis of higher fertility. Such sexual selection is rampant among animals, especially vertebrates, in which females choose potential male mates on the basis of their phenotypic characteristics.

    For the sake of completeness, I here note that my explanation for the diffusion of chromolocal mutations works least well for explaining the diffusion of inversion mutations. The reason for this is that inversions, unlike fission, fusion, and translocation mutations, result in chromosomes that have a great deal of difficulty pairing up during prophase I of meiosis. There may be a way around this (having to do with regions of the chromosome that do not necessarily pair up, probably as the result of a high proportion of non-coding nucleotide sequences – that is, so-called “junk” or “spacer” DNA), but I don’t know enough chromosomal genetics to be able to speculate intelligently on this problem).

    Another interesting correlation with my hypothesis is with Lynn Margulis’s theory of the origin of species by means of acquiring genomes, primarily as the result of endosymbiosis. Lynn has focussed her proposed model for speciation on clear-cut examples of symbiosis that have resulted in speciation. However, her general principle – that of acquiring new genetic material – can just as easily be generalized to acquiring new genonmic arrangements as the result of chromolocal mutation. I intent to correspond with her on this subject in the near future, and will report her answers at my blog: http://evolutionlist.blogspot.com.

  110. Allen

    Therefore, selection on the basis of fertility alone would tend to cause these two groups to diverge

    Absolutely. That’s obvious. The new species, especially if the chromosome relocation has survival advantage, can take off like a banshee once two homozygous individuals come together.

    The question in my mind has always been how two individuals (male and female) homozygous for the chromosome reorganization are generated in sufficient number so there’s a reasonable chance of them finding each other in large populations where the vast majority of breeding partners will produce progeny with hybrid infertility.

    I would put forward the chances are vastly improved if there’s some very marked predisposition for the chromosomal reorganization to spontaneously appear during gametogenesis in the parent species. Suppose some random point mutation (let’s say it’s selectively neutral) in an individual causes meoisis in that individual to produce a chromosome fusion in 25% of its gametes. The fusion wouldn’t propagate because of hybrid infertility but the neutral mutation that causes the excessive number of fusions during gametogenesis would propagate. After a small number of generations you’d have a large number of individuals producing 25% of its gametes with the fusion. Then the chance of two of those gametes coming together to produce individuals homozygous for the fusion is quite good.

    Davison’s hypothesis gets around this by postulating that meiosis interruptus (so to speak) directly produces individuals (both male and female) homozygous for the chromosome reorganization. Now that I think about it, the method outlined above where a random point mutation causes a significant fraction of spontaneous reorganizations during gametogenesis is a more likely explanation. Experimental support would be obtained by finding or engineering an organism whose gametes carry a significant percentage of identical chromosomal reorganizations.

  111. Come to think of it, the animal described above sounds like the same animal Davison wants to work with – one that is hetereozygous for chromosome reorganizations. However, I think once you find or show how to create such an animal there’s no longer any need for semi-meiosis as normal meiosis will work to establish the new species as long as the percentage of gametes carrying the reorganization produced by the parent species is up around 10% or more.

    Probability examples of new species establishment by % gamete production carrying the identical reorganization:

    00.1% is a 1/10^12 chance
    01.0% is a 1/10^8 chance
    10.0% is a 1/10^4 chance
    20.0% is a 1/625 chance
    33.0% is a 1/81 chance
    50.0% is a 1/16 chance

    Those might not be quite correct since it’s not even a cocktail napkin calculation but it should be close enough to show the correct shape of the curve.

  112. This is interesting speculation. And it has a fascinating corrollary: if this was the mechanism of Jesus’ birth, such that he had XX chromosomes, he was not properly biologically male. So much for those who insist on the theological significance of Jesus’ maleness.

    But if anyone is looking for a naturalistic explanation of a virgin birth, the following seems more plausible to me. I don’t know what girls in Mary’s time used as sanitary towels. But if Mary accidentally (in God’s providence) used a towel which was contaminated with human semen, a stray sperm could have found its way into her womb and fertilised her egg.

    I guess this may have happened rather more often than the apparent uniqueness of the virgin birth suggests, but many of the girls it happened to would have been condemned as prostitutes. After all it took divine intervention (Matthew 1:20) for Joseph to accept Mary.

    Thus at the cell level Jesus’ conception would have been normal, but without normal sexual intercourse, and Jesus would have been a biologically normal male. And in terms which would have meant anything to the biblical authors, Mary would have been a virgin. So the miracle might have been only in the timing, this rare form of apparent virgin birth having coincided with Mary’s vision of the angel Gabriel (Luke 1:26-38).

    Well, I’m not sure if we need to look for a non-miraculous explanation, but my one seems to fit the bill rather better than Dave’s one.

  113. In comment #112 DaveScot wrote:

    “However, I think once you find or show how to create such an animal there’s no longer any need for semi-meiosis as normal meiosis will work to establish the new species as long as the percentage of gametes carrying the reorganization produced by the parent species is up around 10% or more.”

    Exactly right, and this is why I have proposed that the easiest (and most likely) way for this to happen is for the offspring of an indivual with a chromolocal mutation simply mate with each other.

    Since posting this hypothesis, a reader of my blog has posted a bibliographic reference to an alternative theory, based in this case on inversion mutations, rather than including all chromolocal mutations (i.e. fissions, fusion, inversions, and translocations). Here is a link to the reference:

    http://www.bioone.org/perlserv.....2.0.CO%3B2

    Unfortunately, I cannot locate an electronic version of this article that does not require paying for the priviledge. If I find one, I will let you know on this thread.

  114. Allen

    I think we might still not be quite on the same page. In my scenario the parents never have the reorganized genome in somatic cells. They carry a mutation that results in the reorganization occuring in some percentage of their gametes. The reorganization could occur in the second stage of meoisis. That way you don’t run into the problem of meiosis being exceeding difficult because of a mismatch in chromosome count. The chromosome count changes only in the haploid gametes at the last instant of gametogenesis. The mutation which causes the reorganization during meiosis can can propagate a long time until a significant percentage of the population is producing a small percentage of gametes with the fusion (or translocation or whatever). Since the majority of the gametes would be normal the species would continue as before as mating would usually produce offspring with the normal count. Some smaller percentage of offspring would be sterile hybrids and, here’s the key, a still smaller percentage of offspring would be homozygous for the fusion and quite fertile. Those individuals would be a new species. A few of those homozygous individuals could then meet up, all their offspring would be homozygous for the fusion, and it’s off to the races for the new species.

    This way there doesn’t have to ever be a single fertile hybrid.

    The question then becomes finding (or genetically engineering) an otherwise perfectly fertile animal that doesn’t have the fusion in somatic cells but dependably produces some percentage of gametes (10% or more would be good enough) with the fusion.

    I’m just using fusion for brevity. It could be any chromosomal reorganization, even something quite large scale, as long as it’s an identical reorganization. It doesn’t seem like much of stretch for there to be the possibility of some small mutation which causes the second stage of meiosis to produce a small percentage of gametes which exhibit an identical pattern of reorganization in the chromosomes. One tiny mutation that only effects the second stage of meiosis thus causes speciation in just a handful of generations. It would appear as saltation in the fossil record even though it might take ten generations or so for enough members of the new species to build up so they have a good chance of meeting up to form a breeding population. There also wouldn’t be any close inbreeding as the homozygous individuals would be produced by parents that aren’t any closer related than normal for the species.

    Follow?

  115. For Faid at ATBC

    chromatid

    One of the two side by side replicas produced by chromosome replication in mitosis or meiosis. Subunit of a chromosome after replication and prior to anaphase of meiosis II or mitosis. At anaphase of meiosis II or mitosis when the centromeres divide and the sister chromatids separate each chromatid becomes a chromosome.

    Any questions?

  116. Why would the fusion observed in human chromosome 2 be evidence for a chimp/ human common ancestry and not just that modern humans once had human ancestors with more chromosomes?

    In order for that to be used as evidence for a chimp/ human common ancestry one would have to demonstrate the differences observed can be accounted for by the culling of mutations.

  117. In comment #115, DaveScot asked:

    “Follow?”

    And I answer: Yes, indeed. The mechanism that you describe is essentially the mechanism that I have proposed. Perhaps I didn’t make it as clear as a I could, but I find it gratifying that we both have now come to the same conclusion as to the overall mechanism and its implications.

    And in comment #117, Joseph asked:

    “Why would the fusion observed in human chromosome 2 be evidence for a chimp/ human common ancestry and not just that modern humans once had human ancestors with more chromosomes?”

    By itself, it would not be. However, when combined with the well-established observation that humans and chimps share over 98% of the same genetic information, and that essentialy the same genes are located in the same positions along the chromosomes, except for those that are located in human chromosome #2 (and its ape homolog, in which the the same genes are located in the same order, but in a separate chromosome), plus all of the phenotypic similarities, plus the fossil evidence (i.e. Dryapithecus, Ramapithecus, etc.), there is overwhelming evidence from multiple independent sources all pointing to the same inference: that humans and chimps shared a common ancestor that lived somewhere around 6 million years ago (or less, if some of the more recent fossil and genomic evidence is factored in).

    Now, one might argue that each of these lines of evidence might somehow be either mistaken or the result of an intelligent designer with sufficient magical powers to shape reality to look as if it had the properties (age, etc.) that it appears to have, but if such a designer existed and had such powers, S/He would be using them to produce the appearance of common ancestry between apes and humans, without such ancestry being, in fact, the case.

    Personally, I don’t want to have to believe in a designer with such a penchant for deliberate deceit, and luckily (as an evolutionary biologist) I don’t have to.

  118. Dave:

    You also mention in your scenario that speciation by the kinds of mechanisms that we are discussing would appear to be saltatory when viewed in the fossil record. That’s interesting, because that is indeed what the fossil record of speciation looks like for quite a few phylogenetic lines. This was Eldredge and Gould’s point in their paper on punctuated equilibrium, published in 1972. Since then, quite a bit of evidence has accumulated to support their model, and with the new discoveries in evo-devo, genetic/developmental mechanisms have also been discovered that can explain the surprisingly rapid shifts in phenotype and function seen in nature (the Lake Victoria cichlids come to mind).

    And, as an evolutionary biologist, I would like to point out that all of the foregoing mechanisms for descent with modification are purely “natural;” that is, they do not require intervention by an “intelligent agent” that “tweaks” the laws of nature. Yes, it does go against some of the central tenets of the “modern evolutionary synthesis” of the 1930s-1950s, but what branch of the natural sciences hasn’t changed as much in the last half century?

  119. Joseph

    Great similarity in junk dna (non-coding, unconserved) between chimps and humans is the most compelling evidence of common ancestry.

  120. Allen

    If chromosomal reorganization can result in the expression of new species with significant taxonomic differences it overcomes a major objection to the front-loading hypothesis of ID. The objection is that unexpressed genomic information would be under no selection pressure and therefore would be obliterated by random mutation over geologic timespans. If position effect is the big kahuna in species diversity then the potential rearrangments of highly conserved regions is how the unexpressed forms are conserved. Not proof of a front-loaded genome certainly but another drop in the bucket of things that fit well with it.

  121. Allen

    By the way, I found a paper talking about successful meiosis with mismatched chromosomes. As a general rule fertility is at least reduced and often reduced to sterility from chomosome mismatches in meiosis.

    http://www.nature.com/nature/j.....01418.html

    Also I did a little checking on fertility in those with Down’s syndrome. Women with Downs are reported as 50% able to become pregnant but men with Downs are very near 100% sterile.

  122. DaveScot:
    Great similarity in junk dna (non-coding, unconserved) between chimps and humans is the most compelling evidence of common ancestry.

    That is ONLY IF DNA is the sole “entity” which makes an organism what it is. However we know that isn’t so.

    What hasn’t been explained is what caused the differences we see.

    For example we don’t even know if selected mutations can allow for upright walking.

  123. Allen MacNeil:
    By itself, it would not be. However, when combined with the well-established observation that humans and chimps share over 98% of the same genetic information, and that essentialy the same genes are located in the same positions along the chromosomes, except for those that are located in human chromosome #2 (and its ape homolog, in which the the same genes are located in the same order, but in a separate chromosome), plus all of the phenotypic similarities, plus the fossil evidence (i.e. Dryapithecus, Ramapithecus, etc.), there is overwhelming evidence from multiple independent sources all pointing to the same inference: that humans and chimps shared a common ancestor that lived somewhere around 6 million years ago (or less, if some of the more recent fossil and genomic evidence is factored in).

    Fossil evidence is in the eye of the beholder. And where are the fossils of the chimp or ape lineage?

    And I don’t think that 98% similarity is real. But even if it were I know I could create two long senetences with 98% similarity and yet those sentences will have different meanings. The same can be done with computer codes.

    And now that we know about alternate gene splicing, sequence may not mean as much as it once did.

    And why is it that organs from other animals- not chimps- are better suited to be used in humans? That should count against the alleged common ancestry.

    Also I doubt the designer has anything to do with deceit. I would again say that is in the eye of the beholder. IOW people who believe in Common Descent are fooling themselves by insisting they know what should be observed if Common Descent were indicative of reality. Yet in reality we don’t have a clue.

    People who focus on the similarities between alleged divergent populations miss the point. It is the differences that must be explained:

    Chimps & Humans- DNA does NOT explain the differences

    So to sum up if something looks like common ancestry it is scientific evidence for that. However if something looks designed we still have to provide the designer and the process before that can be accepted as scientific evidence for ID.

    I think we are making progress.

  124. Joseph

    What would it take to convince you that humans and chimps share a common ancestor?

    I suspect you’re beyond reasoning with when it comes to these things.

  125. DaveScot:
    What would it take to convince you that humans and chimps share a common ancestor?

    The same as it has always been- demonstrate that we know what makes an organism what it is beyond the following:

    The scientist enjoys a privilege denied the theologian. To any question, even one central to his theories, he may reply “I’m sorry but I do not know.” This is the only honest answer to the question posed by the title of this chapter. We are fully aware of what makes a flower red rather than white, what it is that prevents a dwarf from growing taller, or what goes wrong in a paraplegic or a thalassemic. But the mystery of species eludes us, and we have made no progress beyond what we already have long known, namely, that a kitty is born because its mother was a she-cat that mated with a tom, and that a fly emerges as a fly larva from a fly egg.– geneticist Giuseppe Sermonti

    Denton tells us that although genes may influence every aspect of development they do not determine it. So if genes do not determine what makes an organism what it is, and DNA is also not “it” (because we do observe organisms with the same DNA take on varying identities), how can we objectively test the premise (that humans and chimps shared a common ancestor)?

    It would be helpful if someone could start accounting for the differences. Similarities can be accounted for by any number of explanations.

    Then there is still that obstacle of observed wobbling stability.

    I also say that looking at a genome the way we do is like trying to understand a C++ program by looking at the ones and zeros on the data bus.

  126. Joseph,

    Keep fighting the good fight. Hope everyone had an excellent Thanksgiving. It appears this turned into a robust discussion.

    I thought the latest findings of Neandertal were interesting. It appears they were merely humans all along?

    The thing about history and picking apart bones is much is left to willful interpretation.

    Genetic isolation and myriad other issues, disease, and environment can lead to skeletal features that appear in a wide variety.

    I’m still waiting to find out about Frodo the Hobbit(Flores). The finding was supposed to be a slam dunk. Now, it appears nothing more than a diseased and isolated branch of humans. Go to North Korea today and see the result of lack of diet and disease on skeletal remains.

    There is a long way still to go to prove with absolute certainty a chimp to man jump. And the other issues is how the mechanisms work within the cell and in communication. Design does not go away on mere assumptions of the past.

  127. Ah, looky here! The London Zoo documents the first known virgin birth of a komodo dragon.

    http://www.usatoday.com/tech/s.....rgin_x.htm

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