A Prescribed Evolutionary Hypothesis

It is good to have you back Salty. Congratulations on getting the PEH published.I was wondering if we might discuss in some more detail your ideas on the role of 'position effects' in the derepression of 'latent' genes.This seems to require a couple of other accessory systems beyond merely the rearrangement of chromosomal segments. I'm not sure whether you are maintaining that there is no species specific information in the genome, I doubt that this is your contention, or merely that such information is not the source of the differences between the species.Small, species specific, genetic changes have been shown to affect the interfertility of Drosophila species (Orr, 2005). So if there is a role for small species specific differences in DNA in establishing or maintaining reproductive isolation between species is the origin of these differences one driven by the sort of position effects you hypothesise?Are the position effects merely at the level of gene expression or might they actually mediate genetic changes within coding regions?TTFN,WKp.s. sorry if my pesudonymity upsets you.

Sadly those luminaries aren't actually here to conduct a debate, nor are they aware of more recent research.If you have anything that actually contradicts the cases reviewed in Orr's paper then that would be very interesting, as it is I am not talking about chance at all, I am hoping to discuss possible mechanisms by which the genetic factors which have been experimentally shown to be involved in the reproductive isolation of certain species may have been generated as a result of the position effects you posit.If you believe that the differences in 1ary genetic sequence are not responsible then what alternative do you propose?If the deprepression of latent information doesn't involve the addition of novel, or modification of previously existing, genetic sequence then how is it operating? Was all of the genetic sequence information already fully formed in ancestral species and the current patterns of genetic sequences and expresion are merely the result of a combination of derepression leading to novel expression patterns and loss of genetic sequence in some lineages?TTFN,WK

Could you provide some specific references for these failed enterprises? I'm not familiar with any extensive experimental efforts to transform species in the sort of 'macro' sense that you and Goldschmidt seem to be describing. I believe for the scansion to work the final line should be "Or else a little conservative."None of this seems to have anything to do with possible mechanisms by which latent information could be derepressed. Do you not wish to discuss this specific topic?TTFN,AW

Don't you have any interest in considering how it might be derepressed? The example of repression of genes localised near the telomeres is certainly a starting point, but either you require a very large number of loci under the repressive effect of telomeres or we should be looking for an aternative form of chromatin structure which has a localised repressive effect.Perhaps epigenetic factors such as histone methylation/acetylation or DNA methylation would be suitable mediators of repression.TTFN,WK

Surely you are still quite capable of keeping up with current literature. Why should you need to be 'an authority' on a specific field, epigenetics is still a part of developmental biology and you have been doing that for long enough surely? Unless you think that you are losing the faculties you have applied to your research previously why not familiarise yourself with other relevant molecular mechanisms which might mediate the processes you hypothesise?I'm not sure how discussing my views on neo-darwinian theories would in any way be a discussion of your Prescribed evolutionary hypothesis, surely that would be a topic for a different thread?TTFN,WK

Where in this thread have I criticised it? What I am trying to do is understand what if any mechanisms there are by which your hypothesis might reconcile with a number of observations documented in the literature, such as genetic differences associated with reproductive isolation.Simply saying 'position effects' does not actually provide a mechanism. Perhaps a better example of the sort of posiiton effects that might be relevant would be those seen in position effect variegation as has been widely studied in Drosophila (Wakimoto, 1998). Alternativley there may be a case to be made for psudogenes being part of an RNA based repressive system which might then be subsequently altered by chromosomal reorganisation to allow expression of a complementary gene.TTFN,WK

I've been trying to discuss possible mechanisms with John but he seems to feel that that would be outside of his field of expertise and doesn't want to speculate. I think there is a problem with this, if there has been a loss of genetic material then reversing the chromosomal changes might fail to recapture the state of the ancestral species genome. It seems to me that there are some similarities between John's theory and that put forward by Maresca and Schwartz (2006) which we discussed previously. Maresca and Schwartz's theory suggests a mechanism which might account for periodic occurrences of major chromosomal rearrangement but still leave the context as that of a chance occurrence contrary to what John's theory would posit.They do however suggest that a heterozygote with a non-lethal chromosomal rearrangement, and presumably not one producing sterility, which had a recessive phenotype could spread through the population being sporadically expressed in homozygotes as the rearrangement spreads, this may allow a number of homozygotes to appear suddenly. The same could be the case in a scenario based on John's theory of PEH.John himself obviates this problem with his semi-meiotic theory and gynogenetic production of homozygotes, but I don't see why Maresca and Schwartz's theory wouldn't be an equally plausible explanation although they don't avoid the crossing-over problems as John's does.TTFN,WK

Hi Herepton,In response to your question at Message 38...I don't understand what you mean by replacement. Are we merely talking about numbers of species or new organisms filling in niches vacated by an extinct species or new organisms evolving which effectively mimic the extinct species functionally and morphologically?In terms of the first the fossil record shows a number of cycles of large scale extinction followed by rediversification. Similarly there are a number of examples of different species apparently fulfilling the same sort of ecological niche.Without knowing what you, or John, mean by replacement I can't really answer.TTFN,WK

Perhaps you could give some details of these 200 years of experimentation. I am unaware of any persistent experimental efforts to introduce the sort of macroevolutionary changes you claim are impossible, although I am aware of attempts with varying degrees of success to produce new reproductively isolated species.Genetic homeostasis still isn't the sort of barrier you are talking about, just as it wasn't the previous time we discussed it.TTFN,WK

I don't think you could ever unequivocally show the descent of all species from a single source experimentally. The best you could hav eis converging lines of genetic and morphological fossil evidence, it isn't really something amenable to experimental investigation beyond that of comparative genetics.I'm not sure what sort of 'successful results' you are thinking of.TTFN,WK

It isn't as if they evolved twice completely independently, this isn't some extreme case of convergent evolution but rather an example of parallel evolution.There may well be other designs that would work, but both placentals and eutherians would have started with the same structure from which the inner ear would have evolved. The inner ear as we know it might just be the simplest solution from that starting position, it almost certainly isn't the only solution though.TTFN,WK

Certainly there are going to be some mutations which are more likely than others for a given sequence, but being predisposed is not the same as being prescribed. Is this anything other than mere assertion? What exactly are you basing your analysis on? The purported evolutionary history of the ossicles? A cladistic analysis of mammals? The developmental genetics of ear development? Some numbers you made up off the top of your head? And you complain about 'magical thinking' from evolutionists?TTFN,WK

As I understood the PEH it was a case of the pathway leading to changes at specific sites.There certainly isn't any reason why the changes produced could not then act to modify the subsequent behaviour of the pathway, but given the prescribed nature of the hypothesis all of the neccessary alterations to the pathway would still be present if repressed, from the original creation of the most ancestral organism.TTFN,WK

I'll try and address the rest of your post later but first off, do you have any examples of this from the scientifc literature, or pretty much anywhere in fact. To me this sounds like a pretty blatant strawman or at least an equivocation. suggesting that natural selection would favour a more efficent extant allele over a less efficient extant one is not equivalent to saying that it will consequently lead to the most efficient possible design being the end result.TTFN,WK

First things first Ray, you claimed there were 200 years of failed experiments, presumably with this end in mind or else why mention them, are you now conceding that that was just made up for rhetorical effect?TTFN,WK