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gluadys -> RE: Documented evolution of new functions and behaviors in bacteria (5/1/2008 11:18:31 PM)
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quote:
ORIGINAL: Jhud Well you are generally ignoring the “separate yet interdependent” aspect of my requirement. I explained this pretty well in the thread ‘Designing a bat’ , if one looks at the genetic basis for the morphology of the bat and compares it to other mammalian genomes, one finds that bat morphology (longer forelimbs, greatly extended phalanges, a thin skin membrane, etc) is the product of a number of very specific modifications (generally through gene regulation) of a number of different genes that work together in concert to produce the overall morphology of the bat. Do we need "separate but independent" mutations to explain something like this? I got to thinking about a different morphological change: polydactyly. I was pretty sure the genetic basis is not necessarily terribly complex, yet here we have an additional digit that requires the cooperative formation of bone, skin, muscle, nerve, and blood vessels. Turns out that there are different types of polydactyly and different genetic bases are possible. But in some cases, at least, the genetic basis is a mutation in a single base nucleotide. A long-range Shh enhancer regulates expression in the developing limb and fin and is associated with preaxial polydactyly. [My paper] Laura A Lettice, Simon J H Heaney, Lorna A Purdie, Li Li, Philippe de Beer, Ben A Oostra, Debbie Goode, Greg Elgar, Robert E Hill, Esther de Graaff MRC-Human Genetics Unit, Western General Hospital, Crewe Rd, Edinburgh EH4 2XU, Scotland, UK. Unequivocal identification of the full composition of a gene is made difficult by the cryptic nature of regulatory elements. Regulatory elements are notoriously difficult to locate and may reside at considerable distances from the transcription units on which they operate and, moreover, may be incorporated into the structure of neighbouring genes. The importance of regulatory mutations as the basis of human abnormalities remains obscure. Here, we show that the chromosome 7q36 associated preaxial polydactyly, a frequently observed congenital limb malformation, results from point mutations in a Shh regulatory element. Shh, normally expressed in the ZPA posteriorly in the limb bud, is expressed in an additional ectopic site at the anterior margin in mouse models of PPD. Our investigations into the basis of the ectopic Shh expression identified the enhancer element that drives normal Shh expression in the ZPA. The regulator, designated ZRS, lies within intron 5 of the Lmbr1 gene 1 Mb from the target gene Shh. The ZRS drives the early spatio-temporal expression pattern in the limb of tetrapods. Despite the morphological differences between limbs and fins, an equivalent regulatory element is found in fish. The ZRS contains point mutations that segregate with polydactyly in four unrelated families with PPD and in the Hx mouse mutant. Thus point mutations residing in long-range regulatory elements are capable of causing congenital abnormalities, and possess the capacity to modify gene activity such that a novel gamut of abnormalities is detected. http://lib.bioinfo.pl/meid:216505 The key point here is that the mutation occurred in an enhancer---one of those regulators that govern gene expression. But because it occurred here, a multitude of separate yet independent mutations were not required (one for extra bone, one for realigning blood vessels, one for more nerve tissue, etc.) I am not clear on why a similar genetic basis could not underlie the appearance of a bat's wing. It can't be that extending the phalanges meant they poked through the skin, for example, or that the extra length of the digit was not served by appropriate nerve, muscle and blood vessel formation. Due to the way genes and their regulators program embryonic development, a mutation that lengthened the phalanges would be naturally accompanied by several necessary accompanying changes without separate mutations. quote:
Well, my main problem with common descent is that in reality, a number of major phylogenies have not been able to be resolved within the expected trees that Darwin predicted. But that would be a separate issue. Good Lord, why should that be a problem? Scientists don't always make correct predictions after all. We should not expect Darwin to be completely prescient. Surely the actual issue is whether the phylogenies as they presently stand pose a problem for common descent. And if they do, what are the specifics of the problem?
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