What exactly is ID?

I do not contend that all functional sites have only ever evolved once, my point was that given other scientists have already performed experiments showing that, and we have substantial comparative genetic data suggesting it is wide spread, such functional domains are swapped between genes creating chimeric proteins (see Hallast et all, 2005) there is no need for each binding site to always evolve de novo. So the fact that this occurs is already well established, I don't need to do the research myself because I look at the published research where it has already been done.If you extend the 'argument from authority' to cover all previous published academic research then no progress could ever be made in any field as everyone would have to repeat every previous foundational experiment from scratch.TTFN,WKEdited by Wounded King, : No reason given.

It isn't the nerve itself that is the problem, no one has said that the RLN is a functionless vestigial feature. The issue is why it goes miles out of its way to loop around the aortic arch, even in Giraffes.You are trying to counter an argument no one was making.TTFN,WK

In humans every offspring has on average ~130 de novo mutations which were not in either parent's genome (Kondrashov, 2003;Xue et al., 2009), except arguably in that small set of it in certain germ cells.Some studies estimate that the detrimental mutation rate is slightly over 1 mutation/zygote (specifically around 1.3) (Gianelli et al., 1999). There is no equivalent estimate that I am aware of for rates of beneficial mutations in humans as they are much harder to detect. Most would only be post hoc measures based on comparative genetics identifying mutations which seem to have been subject to positive selection.Maybe we should start a new thread on pesticide resistance.TTFN,WK

The most commonly cited instance, the putative frame shift mutation from the Ohno (1984) paper, certainly doesn't seem to involve any loss of specificity. For me ranting at length about frequent problems I have with discussions of this paper see 'Is the evidence concerning the Nylon bug being exaggerated'.TTFN,WK

If I were to see Ohno (1984)PDF , where exactly would I find anything supporting this claim? I've searched for poison, toxin, temperature, transposase, transposon, mobile elements, starvation, starve and activate; none of those words are to be found anywhere in the paper.So where precisely is this claim supported by Ohno (1984)?I'm quite prepared to agree that a number of bacteria change their mutation rates dependent on elements of their environment, but that isn't something that the Ohno paper talks about. Nor does it mean they adapt based on selective pressures.TTFN,WK

The idea that genes are not rearranged by genetic recombination is simply wrong. What do you even think genetic recombination means if not that the genes are recombined? The closer genes are to each other the less likely they are to be seperated by crossing over, but that is just a question of probability, it doesn't mean that they can't be seperated, even different regions of the same gene can be recombined. And that is without even beginning to look at other mechanisms which can lead to changes between complementary gene regions. All this shows is that you A) don't understand what ENCODE was looking at, and B) dont understand genetics at all.The main problem is that 'unit of selection' is not a very useful term. A single nucleotide change can certainly produce the neccessary phenotypic difference to form a basis for selection to act on.The whole point is that the mixing of different complements of genes within a population's gene pool does allow a degree of seperation between genes allowing us to look at the increase in specific alleles rather than looking at whole genomes. It is impossible to make any sort of case in sexual organisms that whole genomes are inherited.In terms of the ENCODE data what you are talking about is presumably the identified ransripts, the thing is that the ENCODE data showed that the majotrity of the genome is transcribed, but only 5% of it seems to have any sort of selective constraint suggestive of function. This makes it a pretty substantial leap to go from the existence of transcripts to their having a functional role which would be destroyed by any single nucleotide changes.Rememeber we aren't talking about the order of genes being rearranged wholesale on a chromosome, just the mixing of different allelic combination amongst multiple genes. So the other gene that your fusion transcript hops onto will still be in the same place, you'lll just have one nucleotide difference in the transcript, which may or may not translate to any functional difference in the resulting fusion transcript, assuming that it had any activity in the first place.It is important to understand that when the ENCODE project talks about functional areas of the genome they are talking about biochemical function in the context of transcription or identifiable binding sites, this doesn't mean that these regions actually perform any functional purpose in the life of the organism. Indeed one of their conclusions is that there is a large amount of functionally active but selectionally neutral genetic material.ENCODE certainly showed that the transcriptome is much more complex than we would have expeected, but it doesn't show in any way that single nucleotides cannot form a suitable substarte for selection, or that genetic recombination cannot resegrate nearby beneficial and deleterious mutations.Clearly there are deleterious mutations which hitchhike to fixation, but it would be very hard to make a coherent case for any way in which this could happen unless the beneficial mutation they are accompanying outwieghs them.Anyone interested in ENCODe should go to their site they also have their nature paper available as a PDF there which describes their inital findings, including the sort of transcriptional odditites that SO was talking about.TTFN,WK

And that is what is wrong. There is no such thing as a genetic block which is immune from recombination. It sounds like you don't know what genetic linkage really is, it is no universal law producing indivisible genetic blocks, it is a statistical reflection of the distance between discrete genetic loci.These discrete loci could even occur within one gene. To state baldly that genes cannot undergo recombination Intragenically is simply to ignore the molecular biology in favour of your own fantasy.The fact that you wilfully ignore the reality of crossing-over naturally lead you to continue being wrong when you talk about natural selection. Yes, of course it is organisms that survive and pass on their genetic material, but they don't pass it all on and the allelic complements get rearranged by meiosis. It is this rearrangement which allows the breaking of linkage between alleles not genes and can allow us to consider the gene an appropriate level of selection. Obviously the genome isn't since the whole genome is never passed on, your contention that a beneficial mutation must carry with it every deleterious mutation in its originating genome just flies in the face of so many basic principles of genetics it is hard to know where to begin. Um, for someone who likes to whine about being misrepresentied you seem to be doing a bang up job here yourself. The point is that selection is a statistical phenomenon, by breaking linkages between discrete allele loci mechanisms such as recombination allow for the alleles to be selected more independently.No one other than you is positing any mechanism in the cell picking out the best genes. What I am describing is that within a population the various rounds of recombination will lead to a dissociation of particular genetic allelic combinations, which will be proportional to their linkage but still provides the possibility of even the most closely linked loci being seperated. Over time this means that selection will tend to lead a favourable allele to increase in proportion.No one is denying the existence of deleterious hitchiking residues, there is plenty of genetic evidence for them although since you don't seem to accept gentic evidence, questioning as you do the idea of sequence conservation between mammalian genomes, I guess you must just be assuming this based on common sense since you deny the actual scientific basis which has allowed those determinations to be made.Sorry about the mixup on the 5% thing, I was talking about the ENCODE data, which is what you claimed you were talking about. It turns out that in fact you were talking about a part of the review you cite which in fact had nothing to do with ENCODE. I think this rather supports my contention that you don't know what ENCODE did. What you are ascribing to ENCODE is research that has been ongoing for decades, the review itself discusses how Jaques Monod in the 60's was disrupting the naive 'one gene == one trait' conception. That doesn't make the idea of a gene being the unit of selection erroneous, although myself I think the nucleotide might be a better choice since it is a truly discrete genetic unit, it just shows that the historical conception of what constitutes a gene was erroneous.You say you don't care about the distinction the ENCODE project highlight between biochemical function, a region of DNA being transcribed, and biological function/effect. But by this standard it is trivially easy to show the generation of novel biochemical function in the genome, many trx factor binding sites and transcription start sites are comparatively simple to create by chance and certainly may be moved around very easily.All you are doing by talking about pervasive neutral evolution is agreeing that in fact most of the genome serves no biological function even if it is biochemically functional. I though the more common ID position was the exact opposite of that, that the majority of the genome does perform a neccessary function but that we just don't understand it yet.You complain about being misunderstood, but as far as I can see that is because you are talking about things you yourslef don't understand which makes your argument very unclear.Recombination within genes happens, recombination between closely linked loci happens. The fact that you think a new mechanism is needed to explain this just shows how unfamiliar you are with the already well characterised mechanisms. Here you have confused weight for number, if I have 1 block of granite wieghing a tonne and you have 800 feathers weighing only a few kilogrammes then clearly my block outweighs your feathers for all that they outnumber it. It isn't the number but the effect that is important. Of course deleterious mutations are hitchhiking, and some are just being fixed by drift, it is the size of the effect of these mutations that is important.TTFN,WK

I'd quibble with this, specifically based on SO's point 3, 'Genes and functional parts will be re-used in different unrelated organisms', after all in a framework incorporating common descent, even just for the animalia, there are no 'unrelated' organism examples for this to apply to.I'd also point out that it is far from established that most of the genome serves any function other than just being there. So far the proportion with any actual identified biological functionality is still in single figure percents, although if we allow the ENCODE project's very loose concept of biochemical function then I agree that this increases the proportion massively, but it doesn't actaully have any clear relevance to the actual biological functioning of the organism. There clearly is a large amount of genetic baggage in terms of repetitive elements and processed pseudogenes. That isn't to say that some such elements are not functional, but to leap from that to saying that almost all of them are is to go way beyond anything the evidence actually supports.TTFN,WK

This is ridiculous, the wolves are clearly all lying down on a snowfield and the photo was taken from a helicopter, I admit it does look like it was photo-shopped afterwards.TTFN,WK