Population Genetics

Care to substantiate any of that? 'Typically' covers a multitude of sins. As was discussed in the recent threads about human/chimp divergence the mutation rate for length mutations is roughly 1/10 that of single nucleotide substitutions but length mutations account for almost four times as much of the divergence between chimps and humans. Well it can also prove beneficial or prove completely neutral and the same holds true for single nucleotide substitutions as well as length mutations. I certainly don't know that. Some sequence of DNA need to be in a specific order to function correctly but there are also large independent sections of chromosome that could quite easily be transferred wholesale somewhere else with no ill effects. Similarly while the particular order of exons in a gene might be important that gene could almost certainly still withstand a considerable change in its nucleotide composition and even in the amino acid sequence of its product. Care to show us your working? This looks like a calculation for 84 specific mutations to have occurred. Are you claiming this is the probability of any 84 beneficial nucleotide substitutions to have occurred? If so Haldane and ReMine seem to both think that it would only take 504,000 years for the impossible to happen at least once assuming it takes 300 generations for each beneficial allele to become fixed and a generation is ~20 years. Is the impossible really that easy or is your entire probability argument specious from the get-go.TTFN,WKEdited by Wounded King, : No reason given.

In what way are flies any 'simpler' on the molecular level than humans? They may have less genes but they still use the same basic molecular mechanisms, with the arguable exception of DNA methylation.If you object to bacteria and invertebrates as model organisms what would you accept?Mice? Monkeys? Only actual human experimentation? Don't you see the contradiction here? Given that beneficial mutations aren't obvious what rationale do you have for claiming that they are 'so rare as to be absurd to hang the theory upon them', how do you know how rare they are? Do you have a reliable way of measuring the rate of beneficial mutations in humans? Or are you just ignoring the fact that such mutations aren't obvious and basing your rate estimates on the fact that you don't see many egg headed super intellectual psychic mutants roaming the countryside?TTFN,WK

One of the virtues of recent trends in academic publishing is that to a large extent you no longer need to go to a university library to get access to even recently published research.There are open access publishers such as PLOS and Biomedcentral not to mention the centralised databases of abstracted reference material such as Entrez which often have links to the full texts of older papers, many journals release their papers after a year or so to open access, Entrez also hosts Pubmed central which is a searchable database of free access full-text journal articles.If there is any particular topic you want to find papers on I'm sure we could find some on these sources that everyone can get access to.TTFN,WK

Albert Einstein wasn't a Christian. Is this an example of one of your facts?TTFN,WK

So would the short answer then be, 'No, it is not a fact that Einstein was a Christian'?Why all these shifty circumlocutions instead of just admitting you were wrong?Some of Einsteins's views on religion have been extensively publicised and it seems clear that whatever exact term would best describe his religion he wasn't a christian.See Some of Einstein's Writings on Science and Religion .TTFN,WK

Yeah, that's our new motto 'Spare the rod and spoil the newbie'. The trick is to make sure you bash them twice as hard when the reason is good.TTFN,WK

I'm not convinced that your 'address' space needs to change in order for speciation to occur. As you posit it all you seem to be doing is inventing a new genetic rationale for the old creationist argument about who the first member of a new species would have to breed with. This assumes an extreme discontinuity exists between a directly ancestral species and its direct descendant which is similar in scale to those seen between two extant modern species, an assumption for which there is no evidence.One important thing with regards to gene duplication is that you don't change the 'address' so much as you just add a new one. Be that as it may there is not even any reason to assume that a single change in any particular 'address' space renders one no longer of the same species.We certainly know that some 'address' changes can lead to infertility, or reproductive isolation in species terms, but that deosn't mean that all such changes do. To assume it does is the equivalent of assuming that all mutations must be detrimental because the vast majority of mutations seen in humans in biomedical research are associated with syndromes and diseases or because mutagenesis screens cause severe developmental abnormalities in fruit flies.Similarly I would argue that there are cases where a change in the genetic content of a gene could be the causative factor in the development of reproductive isolation.TTFN,WK

To be more exact, there are probably many such qualitative differences but there are also many between differences within the set of gene duplications or the set of different point mutations. It may be that one tends to have a larger effect but I don't know that that is equivalent to 'adding a new dimension'. A single point mutation can create or destroy a transcription factor binding site, thereby changing at least part of a genes 'address', and indels or domain swaps in the protein coding region can lead to the gain of novel binding properties or functions to a protein.There is an interesting blog post which inks out to a number of research groups studying these sort of issues, evolgen archive: Why Study Speciation Genes? .TTFN,WK