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Politics : Evolution -- Ignore unavailable to you. Want to Upgrade?

To: Giordano Bruno who wrote (28997)	7/29/2012 12:12:52 PM
From: Solon	Read Replies (2) \| Respond to of 69300

This essay is the second of a series authored by Dave Wisker, Graduate Student in Molecular Ecology at the University of Central Missouri. As I wrote in the previous essay in this series, Intelligent Design advocate Casey Luskin doesn’t think the fusion which produced human chromosome 2 could have become fixed in the human population: Miller may have found good empirical evidence for a chromosomal fusion event. But our experience with mammalian genetics tells us that such a chromosomal aberration could have created a non-viable mutant, or a normal individual who could not produce viable offspring. Thus, Neo-Darwinism has a hard time explaining why such a random fusion event was somehow advantageous. Luskin (and other ID/creationist apologists I’ve seen on internet discussion fora) maintain that the fusion which resulted in human chromosome 2 must have had drastic negative effects on the fertility of heterozygotes for the fusion. This reduction in fitness, they argue, would effectively prevent the propagation of the fusion throughout the population. On the surface, this sounds like an effective argument, since it is known that translocations and fusions can have such a negative effect by producing non-balanced gametes (see PZ Myers’s article on his blog Pharyngula for a detailed explanation). However, anyone familiar with the cytogenetic literature of mammals knows that one cannot claim that these rearrangements greatly decrease fertility with any certainty, since there are numerous examples where such an expected reduction does not occur. For example, daMota and da Silva (1998) observed centric fusions in goats that had no discernable effect on fertility: The results suggest the involvement of chromosomes 6 and 15 in the fusion demonstrated by G-banding in prometaphase cells. The Brazilian sample of animals carrying structural rearrangements did not present any reduction in fertility, suggesting the existence of prezygotic selection against unbalanced gametes They also cite several other goat studies which found the same thing. In rodents, Nachman and Myers (1989) found a similar situation in a population of marsh rats: The observation of karyotypic uniformity in most species has led to the widespread belief that selection limits chromosomal change. We report an unprecedented amount of chromosomal variation in a natural population of the South American marsh rat Holochlus brasiliensis. This variation consists of four distinct classes of chromosomal rearrangements: whole-arm translocations, pericentric inversions, variation in the amount of euchromatin, and variation in number and kind of supernumerary (B) chromosomes. Twenty-six karyotypes are present among 42 animals. Observations of the natural population over a 7-year period and breeding experiments with captive animas indicate that heterozygous individuals suffer no detectable reduction in fitness. This is at odds with a central assumption in current models of chromosomal speciation and provides a firm rejection of the view that selection necessarily restricts chromosomal change. In another study, Bardhan and Sharma (2000) studied heterozygote fertility for numerous translocations and fusions in mice, and concluded: The three chromosomal species exhibit a high incidence of polymorphisms for Robertsonian fusions and pericentric inversions. Breeding experiments and histological analysis of testis show that heterozygosity for pericentric inversions and Robertsonian fusions had no effect on fertility. Nachman and Myers (1989) reported similar results in marsh rats: The observation of karyotypic uniformity in most species has led to the widespread belief that selection limits chromosomal change. We report an unprecedented amount of chromosomal variation in a natural population of the South American marsh rat Holochlus brasiliensis. This variation consists of four distinct classes of chromosomal rearrangements: whole-arm translocations, pericentric inversions,variation in the amount of euchromatin, and variation in number and kind of supernumerary (B) chromosomes. Twenty-six karyotypes are present among 42 animals. Observations of the natural population over a 7-year period and breeding experiments with captive animals indicate that heterozygous individuals suffer no detectable reduction in fitness. This is at odds with a central assumption in current models of chromosomal speciation and provides a firm rejection of the view that selection necessarily restricts chromosomal change. Researchers in speciation are interested in the fertility effects of chromosomal rearrangements because reduced fertility in heterozygotes can be an effective barrier to gene flow between populations differing by such rearrangements. But they have come to the conclusion that this reduced fertility is not as common as cytogenetic theory predicts. Coyne and Orr (1998) summed up the situation this way: A further problem with chromosomal speciation is that it depends critically on the semisterility of hybrids who are heterozygous for chromosome rearrangements. It is not widely appreciated, however, that heterozygous rearrangements theoretically expected to be deleterious (e.g. fusions and pericentric inversions) in reality often enjoy normal fitness, probably because segregation is regular or recombination is prevented (see discussion in Coyne et al. (1997)). Spirito (1998) pointed out that the type of rearrangement was not a reliable indicator of its effect on fertility: [quote] In conclusion, the reduction in fitness due to the presence of a chromosomal rearrangement (especially in the case of inversions and Robertsonian rearrangements) is not foreseeable a priori solely on the basis of the nature of the structural rearrangement. The absence of definite rules means that it is necessary to experimentally analyze the level of selection against the heterozygote for each particular rearrangement of evolutionary interest. (p.321). So, it should be clear that Casey Luskin’s remarks are simply not reflective of the current thinking in mammalian cytogenetics. In the next essay, I will take Spirito’s advice and examine the situation in mammals and specifically in humans more closely, so that we can get a better picture of the factors affecting the fixation of Human Chromosome 2. pandasthumb.org

To: Giordano Bruno who wrote (28997)	7/29/2012 5:40:35 PM
From: 2MAR$	1 Recommendation Read Replies (1) \| Respond to of 69300

To answer your questions why go to a creationist site that specializes in ignorance of modern genetics ? Why not go to one that does if you really seek answers? What we do know is that the mystery of the ape family chromosomes 2a & 2b has been shown by the clearest evidence to be a fusion of the two resulting in human chromsome 2 explaining this with the highest degree of certainty . Leaving what we all know of as of the ape/chimp similarity to humans intact & most elegantly solved once gain usuing Evolutionary predictions . Finding this fusion that exactly matches those above offers again even more of the strongest evidence for the theory . So one just keeps adding to the list of findings that are growing as large as the DNA moelcule is long comparatively only validating Common Descent once again definitvely . "Zoom-Pan video of human and chimpanzee chromosome 1 to 9" http://www.youtube.com/watch?v=KEk6ESOZOdU (You can even turn off the sound & let the images talk )

To: Giordano Bruno who wrote (28997)	7/29/2012 5:53:38 PM
From: 2MAR$	Read Replies (1) \| Respond to of 69300

How did the fusion of Chromosome 2 get passed on to future generations? http://richarddawkins.net/discussions/642203-how-did-the-fusion-of-chromosome-2-get-passed-on-to-future-generations Comment #3 covers some territory the a little primer : The base-pairing rules of DNA due to hydrogen bonds cause the two strands of DNA to be complementary (A against T, C against G). This allows DNA to reproduce by splitting into two separate strands (an enzyme breaks the hydrogen bonds), each of which is a template on which a complementary strand is grown. But this specific AT/CG pairing also allows genes on one chromosome to attract to similar genes on another chromosome. When chromosomes pair up in mitosis and meiosis, this mechanism works despite the fact that the chromosomes differ slightly because the mother's and father's inherited DNA are not identical. The allelomorphic forms of a gene differ at a very small fraction of their places if they differ at all, as does happen in a significant percentage of genes (a condition for that locus called heterozygosity). When 2A & 2B fuse together, it creates a super-chromosome which attracts a 2A and 2B to the right places. This means that chromosome fusion doesn't affect either mitosis or meiosis. It is effectively a neutral mutation, which means it has a chance of becoming the norm in the population. The probability of this happening for any one such mutation and the number of generations it will take for that mutation if it does happen are respectively inversely and directly proportional to the population size. Theoretically, if you know how often chromosomes fuse you can calculate how often in 100 million years a chromosome fusion should become "fixed" in a species Comment #23 follows on with chances of a fused mutation increasing when talking smaller numbers of individuals as in a bottle neck situation we know happened several times , very probable situation The small number of trisomy 21 individuals due to a fusion of chromosome 21 with another chromosome in one of the parents is relevant here. The fused chromosome will never go to 100% in the current population of almost 7 billion, but if there was a global catastrophe that reduced the human population to just a few thousand, as happened 70,000 years ago with the eruption of Toba, and if the fused chromosome or a new one arose in a few of the individuals, then neutral drift allows it to go to dominance by just chance .You don't need two individuals with the chromosome fusion mating. Just one is enough, as happens with any genetic variation occurring in small populations evol meme

To: Giordano Bruno who wrote (28997)	7/29/2012 6:05:47 PM
From: 2MAR$	Respond to of 69300

Comment #38 speaks to evolutionary history , considering & looking beyond population bottleneck events & phenotypic and environmental, genetic/karyotypic changes : A further point, Ken, is that there would have been other population bottlenecks in the hominid line leading to humans, because speciations are often associated with such events. The 71KYa event was not a speciation event, so was probably not the worst bottle neck we've ever had. Further, the understanding of evolutionary history requires a broader approach than just looking at population bottlenecks - phenotypic and environmental, and genetic/karyotypic changes are all important, and conclusions are only safe when we have enough information about all three, IMO. We do not have all three for any of the bottlenecks at present. Also, there were reports (which, unfortunately, I can no longer find) of an attempt to date the fusion on the basis of the DNA clock, which came up with the figure of about 6.5MYa, which corresponds to the split with the chimps. I am not sure how safe that concluson was, but I do not know of a falsification of it either

To: Giordano Bruno who wrote (28997)	7/29/2012 6:15:39 PM
From: 2MAR$	Read Replies (1) \| Respond to of 69300

And lastly this rather brilliant input in comment #45 from an anthropological paper by Evelyn J Bowers: New Perspectives and Problems in Anthropology pointing to the possibility of the fusion of chromosome #2 may have been associated with the development of bipedalism . (You can also attribute all this to Aliens or that God just introduced a fused chromosome #2 with Noah & his wife on the Ark , therebye creating a new race of hominids , your choice and go on quoting Creationist websites ) What is of interest here is the Hox gene found in Chromosome 2 Chromosome #2 may have been associated with the development of bipedalism (walking upright), because the fusion of chromosomes could have altered the function of the Hox B genes which are now found on our chromosome two. The Hox B genes are one of several groups of genes which control morphology, and the Hox B genes (on chromosome 2) specifically control the way the pelvis and lower spine and genitalia develop. Humans have five lumbar vertebrae, chimps have three, so it's very plausible that that's one of the changes that led to walking upright.

To: Giordano Bruno who wrote (28997)	7/29/2012 6:18:27 PM
From: 2MAR$	Respond to of 69300

From Richard Dawkins' discussion site (great stuff !) "They also pointed out that the family structure of chimpanzee-like creatures may well have led to quick speciation. With a dominant male impregnating multiple females, the family clan would quickly have multiple children and grandchildren with at least one fused chromosome, and inbreeding would have led to a number of individuals with two fused chromosomes - and if those individuals with 23 chromosome pairs were better able to walk upright, and this offered a significant survival or reproductive advantage, it might take no time at all before you had a new species, living with their cousins, but perhaps preferring to mate with their like, and eventually competing with and/or separating from the original species. http://richarddawkins.net/discussions/642203-how-did-the-fusion-of-chromosome-2-get-passed-on-to-future-generations#page2 * They also suggested that the considerable brain area devoted to grasping by the panids' feet would probably have then be devoted to other skills." really interesting thinking Evelyn J Bowers: New Perspectives and Problems in Anthropology