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Author | Topic: The Nature of Mutations | |||||||||||||
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maverick,
quote: Not sure what your getting at. I'm making two points, the first is that a chromosome pair can recombine & produce a chromosome that is different to the original two, given that this is heritable, it meets most definitions of mutation I've seen. Given that you accept that chiasma can occur within genes (I think), then potentially, at least, new genotypes can arise via recombination, as well as new phenotypes. Consider a gene pair that has a chiasma in the middle of it (where x is the chiasma.....) ATGCATGC X CGTACGTA AGGCATGC X CGGACGTA gives.... ATGCATGC X CGGACGTA AGGCATGC X CGTACGTA These genes may very well be unique, therefore change the genotype, & possibly the phenotype too. Now, I'm whistling in the wind a bit, & accept I can't support this, except theoretically. I can't find anywhere that says crossover doesn't occur in the middle of genes, but then I know that crossover favours high concentrations of G or C (if my memory serves me), so it seems plausible that genes may selectively avoid having these high levels of the specific nucleotides (which I can't support either), resulting in chiasma avoiding the genes themselves & "targetting" some rubbish sequence. I doubt the chiasma are that exact in getting exactly the right nucleotides in both chromosomes, but the principle stands. One chromosome could have a large gene, the other a small one (almost certainly deleterious), but it still would introduce a new genotype & phenotype, even if its only property is to be lethal.
quote: Agreed, but I never said it could. If mutation is, & I'll use Percies definition, "a heritable change of genetic material", then recombination is a mutation. It doesn't matter if recombination produces new geno/phenotypes, or not, it is a mutation. Secondly, I am proposing the possibility that recombination does produce new coding sequences when the chiasma occurs slap bang in the middle of a gene. Anyone? Mark ------------------Occam's razor is not for shaving with. |
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Here you go mark
Ann Hum Genet 2002 Jan;66(Pt 1):1-27 Related Articles, Links Sequence variation at the human ABO locus. Yip SP. Department of Nursing and Health Sciences, The Hong Kong Polytechnic University, Kowloon, SAR, China. The ABO blood group is the most important blood group system in transfusion medicine. Since the ABO gene was cloned and the molecular basis of the three major alleles delineated about 10 years ago, the gene has increasingly been examined by a variety of DNA-based genotyping methods and analysed in detail by DNA sequencing. A few coherent observations emerge from these studies. First, there is extensive sequence heterogeneity underlying the major ABO alleles that produce normal blood groups A, B, AB and O when in correct combination with other alleles. Second, there is also extensive heterogeneity underlying the molecular basis of various alleles producing ABO subgroups such as A2, Ax and B3. There are over 70 ABO alleles reported to date and these alleles highlight the extensive sequence variation in the coding region of the gene. A unifying system of nomenclature is proposed to name these alleles. Third, extensive sequence variation is also found in the non-coding region of the gene, including variation in minisatellite repeats in the 5' untranslated region (UTR), 21 single nucleotide polymorphisms (SNPs) in intron 6 and one SNP in the 3' UTR. The haplotypes of these variations reveal a specific relationship with the major ABO alleles. Fourth, excluding the common alleles, about half of the remaining alleles are due to new mutations and the other half can better be explained by intragenic recombination (both crossover and gene conversion) between common alleles. In particular, the recombination sites in hybrid alleles can be quite precisely defined through haplotype analysis of the SNPs in intron 6. This indicates that recombination is equally as important as point mutations in generating the genetic diversity of the ABO locus. Finally, a large number of ABO genotyping methods are available and are based on restriction analysis, allele specific amplification, mutation screening techniques or their combinations. I also take issue with the concept that recombination cannot result in a point mutation..you can generate chimeric sequences via recombination (PCR does this some time "pcr jumping"). If the sequences are not very different, you will have an apparent point mutation..anyway..more on chimeras and their effects below J Clin Endocrinol Metab 2001 Sep;86(9):4445-52 Related Articles, Links Unequal crossing-over between aldosterone synthase and 11beta-hydroxylase genes causes congenital adrenal hyperplasia. Hampf M, Dao NT, Hoan NT, Bernhardt R. Max Delbruck Centrum fur Molekulare Medizin, 13125 Berlin, Germany. Congenital adrenal hyperplasia is one of the most frequently inherited diseases. It is characterized by a severe decline in cortisol secretion, which results in a compensatory increase in ACTH and consequent adrenal growth (hyperplasia). Here we describe the first case of 11beta-hydroxylase deficiency that is caused by an unequal cross-over of the genes encoding aldosterone synthase (CYP11B2) and 11beta-hydroxylase (CYP11B1). CYP11B1 and CYP11B2 are located on chromosome 8q24 approximately 45 kb apart from each other. The investigated genetic recombination deleted the normal alleles of the two genes and created a chimeric fusion gene, which consists of the promotor and exons 1 through 4 of the aldosterone synthase gene plus intron 4 through exon 9 of the 11beta-hydroxylase gene. This recombination event subordinates any remaining 11beta-hydroxylase activity of the chimeric enzyme to the control mechanisms of CYP11B2, the expression of which is mainly regulated by angiotensin II and K(+). Normally the 11beta-hydroxylase activity is controlled by ACTH. The existence of the CYP11B2/CYP11B1 chimera was discovered by means of a PCR method and was confirmed with a Southern blot. Furthermore, by applying a minigene expression method we demonstrated a point mutation in intron 3 (IVS3+16G-->T) of the patient's second 11beta-hydroxylase allele that radically diminishes proper splicing of the pre-mRNA by giving rise to a new, highly preferred donor splice site.
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I apologize, but I do not have a lot of time the last week...a lot of work, but I wanted to at least answer a couple of things...
quote: Evolutionary theory is not a fear of mine, nor do I think the big bad scientific community is after me. What Mayr has stated is very appropriate and even though I think that he is off his rocker on some issues he does seem to be a thinker. He has stated that there is hardly ever an argument over the facts, but the interpretations of those facts. He has hit the nail right on the head. This is how it works...TOEists (grin) see genetic change, ANY genetic change, and call it mutation because they need that interpretation for TOE to seem real. A definition problem. Evolution is not variation, and variation is not evolution. Period. Variation does not lead, in "evolutionary time" to legs or wings where before there were none. This is an assumption on the TOEist part and it is not supported by the data. Evolution is based upon the assumption that nature is the best explanation for the beginning and maintenance of biological entities...and this reasoning only stands because the naturalistic paradigm denies the supernatural. It is a fact that the supernatural does exist. It is also a fact that because TOEists refuse to investigate the supernatural, but instead choose to make fun of it, invalidates all scientific claims regarding TOE. What better way to promote your own theory than by refusing to investigate and choosing to ignore the only alternative explanation? TOE is not supported by a plethora of scientific disciplines. It is supported by by illusions. TOEists take the facts of nature that seem to explain some things that they need for their theory, redeifne some others, use some of the most cockamamie reasonings and illogic that I have ever read...Dawkins is the perfect example. But, if it seems to give some kind of credence to TOE, it is accepted with little intolerance, no matter how ridiculous it may be. Paleontology...how does this support evolution? Without the doctored interpretations of TOE, all the fossil record supports (on either side) is the fact that certain organisms have lived, died, and were somehow preserved as a fossil record. Nothing more. Everything else is extrapolated from the assumption of the grand paradigm. Biology? Does it really give evidence for TOE? In TOEist interpretations, sure, what else could POSSIBLY be reasponsible for anything biological, beause of the grand paradigm? As Mayr has also pointed out in truthfulness, there are two biologies: Functional Biology (which IS biology) and evolutionary biology...an exercise in story telling. TOEist theorists making up and comparing stories with each other on their opinions on how a dog came to be in its present form today. The only difference is, TOEists try to spruce this story-telling up by calling them narratives. Telling me that a lobsters claws are modified forelegs from ancestors gone by is not scientific, it is not even a supported assumption. With all of the wonderful scientific advancements that we have existance today, when we can manipulate the DNA of, say a horse, and add the genetic information to its genome for expression of wings (just an example), then you will have my full attention. It can't be done. Futuma even admits this, in the same textbook that you have quoted to me, only I can't remember which page. And here is the crux of the matter, a horse will never sprout wings because, as admitted by Futuma, the genetic information for wings is not present in the horses genome. This we both agree upon. The problem is that Futuma says, as I am sure you will agree, that mutations + time could eventually give horses wings. THIS IS UNFOUNDED ASSUMPTION. This is my argument. It doesn't have to be wings, it could be anything in an organism that is not a part of its genetic make-up today. It could be an ant with a trunk like an elephants. It could be a cat with gills. Heck...it could be a fish with legs, and that should be easy enough since TOEists claim that it has already happened. This is proof of speciation, not adaptational changes. Variation does not lead to diversification of fish, cats, elephants and human beings. There is no evidence for this except in interpretational foul play and brain washing concepts and definitions. Cheers! Also, I do not know how things will go with me from this point on, I am moving and have evrything packed but my computer for the move so that I can continue as often as possible. If I suddenly "disappear" it will only be for a short while. If this happens, it is not because I got "scared" and ran off. I also would not blame you all if this thread dies off if this happens. Blessings to you all....
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Hi Phopho,
No problem with the time constrainst...I was at a meeting myself last week..and I will be popping out again the rest of this week. So I can fully sympathize with the difficulties of maintaining this dialogue. Ok..to your post.
quote: Mayr is not the scientific community. He is not even the voice of the evolutionary biological community. He is one of the few that communicates with the general public through more easily accessible books like Gould and Dawkins do. I note you never mention Darwin. In any case, could you more specifically detail where Mayr is "off his rocker"? He writes copiously so determining what you specifically disagree with would be rather difficult to pinpoint.
quote: M: This paragraphs suffers from being 1) a re-assertion of points you were asked to support with evidence in prior posts 2) that it is so wrong I hardly know where to begin dissecting it. 1) Do you have specific evidence that biologists re-define mutations to fit the theory of evolution? Specific evidence since evolutionary biology uses the same mutations as geneticists including those who work at the drug companies producing medicine for people like you.2) I provided you with a largely agreed upon definition of evolution yet you claim to be the absolute authority to say that it is wrong..why should we believe YOU when you say that evolution does not involve variation? Even Darwin was obsessed with variation yet you claim the thoery has nothing to do with it...how about an analogy for you? Christianity has nothing to do with Jesus Christ. period quote: If it is a fact please provide 1) the hypothesis of the supernatural 2) how is it falsifiable 3) supporting evidence that supports the hypothesis. If you cannot then it is simply not science. that is the reason nobody in science studies the supernatural not because they refuse. The supernatural is by definition not amenable to scientific inquiry.
quote: Agian, you seem very paranoid. Please provide specific evidence that it is suppoted by illusions (I assume you mean all the genetic and paleontological evidence that has been accumulated) and specifically which "cockamamie reasonings"...you are making assertions without support which does not further your case and is not at all persuasive.
quote: LOL! Hmmm you sure nothing more? And an extinct horse species is similar to modern horses because.....fossil primates?...mammoth fossils are similar to elephants because?...their DNA is similar to modern elephants because....
quote: It is pretty clear you did not even attempt to read any of the references I provided to you and yet persist in your false accusations...but in any case, show me then the profound difference in the "narratives" of any paper on Hox genes in Drosophila, segregation of muscular dystrophy (Becker's form please since I am interested) in families, and the original paper on the genetics of the neandertal type specimen...while you are at it, you can point out the vast difference in story telling of any paper in this weeks issue of Science on physics. I will be interested to hear your results.
quote: Dev Biol 1997 Jun 1;186(1):1-15 Related Articles, Links A conserved cluster of homeodomain binding sites in the mouse Hoxa-4 intron functions in Drosophila embryos as an enhancer that is directly regulated by Ultrabithorax. Haerry TE, Gehring WJ. Biozentrum, University of Basel, Switzerland. The evolutionary conservation of the homeodomains suggests that their in vivo DNA binding sites may also be conserved between vertebrates and invertebrates. The regulatory function of the mouse Hoxa-4 and Hoxb-4 introns were analyzed in Drosophila since they both contain a cluster of three homeodomain binding sites, the HB1 element, which was also found in the introns of other Hox genes ranging from fish to humans as well as in the Ultrabithorax (Ubx) and decapentaplegic (dpp) genes of Drosophila. The enhancer of the Hoxa-4 intron was found to respond to several homeobox genes activating a lacZ reporter gene in particular cells of the epidermis in Drosophila embryos. The enhancer activity was found to be similar to previously described autoregulatory elements of Deformed (Dfd), the Drosophila homolog of Hoxa-4, but additional expression was observed in more posterior segments activated by Ubx and repressed by abdominal-A (abd-A). Point mutations in the homeodomain binding sites in HB1 abolished the enhancer activity. A second site suppression experiment showed that UBX interacts directly with the HB1 element. When the HB1 element in the Hoxa-4 intron was replaced by that of the mesodermal enhancer of dpp, which was previously shown to be directly controlled by Ubx, Ubx-dependent activation was retained, but repression by abd-A was lost. The same result was obtained when the third binding site of HB1 was altered, suggesting that this site is responsible for abd-A-dependent repression. Finally, deletion of potential cofactor binding sites flanking the HB1 element that are also conserved in the medaka, chicken, and mouse genes revealed that they are important for enhancer function in Drosophila and that the Dfd-dependent and the Ubx-dependent expression requires different sites. The evolutionary and functional conservation of the HB1 elements indicates that not only the homeodomains but also some of their in vivo binding sites are conserved between vertebrates and invertebrates. Monitoring expression of conserved genes and expressing foreign genes in organisms has been going on for decades...rather than getting your attention you should have been paying attention rather than a priori assuming all biology is false. Another example is the Pax6 gene of mice which can be switched with that of Drosophila and still regulate eye development.
quote: Why is it a unfounded assumption? He is not even saying that you would get anything that looks like a horse with wings. Only that a horses could with selective pressure and time give be the common ancestor of a mammal capable of flight...much like the non-flying ancestors of bats. If you are arguing from incedulity then you will not get very far...the IDists are stuck in this position as well.
quote: It actually sounds more like you have been brainwashed by either an ignorant thought controlling individual or religious organization which says beleive your assertions without actually gathering any evidence for them. I and others have been providing you with references which are the tip of the iceberg in terms of volumes of studies that support our assertions. Yet you persist to claim to be the sole authority that says that variation does not produce anything nor does it play a part in evolution. You will never be taken seriously unless you can actually argue against what evolution actually is rather than the strawman you wish to be. You will also never be taken seriously when you make pronouncements about what experiments have or have never been tried when all of them have been done...you are arguing from ignorance. And that is the hallmark of brainwashing. I hope you make it out of that hole. Take your time in answering. I would much rather you delayed your posts and gathered actual evidence for your assertions which we could discuss rather than having you ignore what I am saying and then re-posting the same assertion...believe me, you don't want to end up like salty. Good luck with your move and I hope you continue to post. It has been enjoyable. Best wishes,M |
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