Uncommon Descent Serving The Intelligent Design Community

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

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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. 😆

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.

Comments
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.DaveScot
November 24, 2006
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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.Joseph
November 24, 2006
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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.com/2006/11/island-mice-may-evolve-faster-from-one.htmlAllen_MacNeill
November 24, 2006
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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.Allen_MacNeill
November 24, 2006
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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!Allen_MacNeill
November 24, 2006
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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.Allen_MacNeill
November 24, 2006
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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.Allen_MacNeill
November 24, 2006
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"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.Allen_MacNeill
November 24, 2006
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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.Joseph
November 24, 2006
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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.Joseph
November 24, 2006
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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?DaveScot
November 24, 2006
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Allen Doctor Davison requests your presence at Brainstorms to discuss meiosis, semi and otherwise. http://www.iscid.org/boards/ubb-get_topic-f-6-t-000370-p-20.htmlDaveScot
November 24, 2006
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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. DaveScot
November 24, 2006
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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?Charlie
November 23, 2006
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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/Philadelphia_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.Allen_MacNeill
November 23, 2006
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Great stuff, guys! Now let's eat!Barrett1
November 23, 2006
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Dave, pleas have a look at balanced trisomy here http://www.tokyo-med.ac.jp/genet/trc-e.htmsparc
November 23, 2006
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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.DaveScot
November 23, 2006
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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!Allen_MacNeill
November 23, 2006
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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/entrez/dispomim.cgi?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/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15235602&query_hl=3&itool=pubmed_docsum)sparc
November 23, 2006
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#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?Srdjan
November 23, 2006
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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: DaveScot
November 23, 2006
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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?Joseph
November 23, 2006
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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.mike1962
November 22, 2006
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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?mike1962
November 22, 2006
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"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. :)Smidlee
November 22, 2006
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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.Michaels7
November 22, 2006
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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/Allen_MacNeill
November 22, 2006
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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?Joseph
November 22, 2006
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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.mike1962
November 22, 2006
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