Mimicry and neodarwinism

No it isn't. You will be hard pressed to find anyone in the 'neo-darwinian' camp here who argues much from Darwin's own writings, unless it is the content of those writings itself that are under discussion.This is not to say that an older reference may not be perfectly good. The main objection to many of JAD's references were that they had been superceded by subsequent research in genetics and evolutionary biology and that JAD refused to address any more recent developments which disagreed with his hypothesis. You are conflating a large mutation with a mutation with a large effect. The actual genetic differences betwen the various alleles is not, sadly, something that the paper you reference addresses.How can the variation of one phenotypic trait in a species be classed as macroevolutionary in any way, except as a possible substrate for speciation through mating choice? Because it makes them look superficially like another species? Without knowing the actual genetic bases of the differing patterns of expression it is hard to say whether the similarities between species are merely superficial or share a common genetic basis.The likeness is also 'superficial' to the extent that it is far from exact. Comparing the four species of Danaidae with the dardanus mimics from your first link, not a single one replicates the target species pattern exactly and the middle two are pretty wide of mark altogether except for the shading of the largest blocks of colour. The most similar is the first example which also happens to very closely resemble the male form of Papilio dardanus. I'm not sure where you find any lack of a neo-darwinian explanation, beyond the fact that there is no exact account of which specific mutations account for the differing alleles.A paper dealing with mullerian mimicry in Heliconius briefly reviews research on the genes repsonsible for the mimicry of the same target by two different Heliconius species and finds them to be genetically distinct although with some overlap in loci responsible for the pattern (Naisbit et al, 2003), this does not deal with the specific genetic mutations responsible for the different allelic loci so even those instances where the same locus is involved may be due to a distinct mutation. Clearly much of this resemblance is therefore superficial yet the mimics look similar.TTFN,WKEdited by Wounded King, : *ABE* Edited to redact a sentence due to my misreading of the figure legend.

You only suppose that because of your prejudice. Why in the absence of specific data about the exact nature of the genetic bases, and in the case of the two Heliconius species the differing bases producing the same phenotype, would you assume that the origin of the allelic difference was some never before seen phenomenon rather than the frequently observed and well characterised forms of mutation which we know to exist?Is there in fact anything in terms of actual evidence to support your view? It seems merely to be your own personal incredulity here in terms of argument.The Naisbit paper I referenced earlier was in fact discussing H. Melpomene and H. erato and the genetic evidence seems pretty conclusive that Brower is correct and the same phenotype has evolved twice between the Andean and Guianan populations and not in the same way, distinctly not the result one would expect in line with the PEH.TTFN,WK

It was considered a valid notion in the absence of contradictory evidence, once that evidence was produced it was incorrect that theory was discarded. In what way is this anything other than an example of the normal operation of science? Way to cast aspersions on a gigantic proportion of practicing biologists. Perhaps what you mean is that they will arrange experiments to test their hypotheses, as opposed to the ID or creationist scientist who will neglect to do any experiments but write smug little theoretical papers in obscure journals instead. If you want to show us the massive prevalence of scientific fraud however then I suggest you provide some evidence beyond a AIG link about Kettlewell.TTFN,WK

Except you didn't so much cite facts as make a few vague claims and offer as substantiation a link to Answers in Genesis.I don't even know what you think you are arguing now? You seem to have gone from saying that mimicry can't be explained by neo-darwinism to saying that in fact the phenomenon of mimicry doesn't exist and certain species just seem to resemble each other for no apparent reason.You seem to be moaning because biologists are doing exactly what they should do and formulating new hypotheses when the old ones are contradicted by evidence.The fact that there is no published experimental study of every case of mimicry seems like a ridiculous complaint. And when was this? The only Heikertinger I can find is Franz Heikertinger and he was already publishing in 1911. Is there any reason to suspect that he was familiar with modern molecular developmental genetics when he made this pronouncement? This is exactly why the sort of references JAD gives are so often scoffed at, not because their originators were cranks or bad scientists but because their ideas are clearly contradicted by subsequent evidence which they couldn't possibly have been familiar with. Those who do have the choice of familiarising themselves with more recent research must accept ridicule if they instead decide to hide behind the authority of the deceased.TTFN,WK

Yes, and Darwin's lack of knowledge on genetics lead to him making several erroneous speculations. Did you have a point? The difference is that if the recurrence of these similar phenotypes in at best distantly related species is due to some form of genetic front loading being derepressed in response to certain cues, or for whatever reason, then we would expect the genetic basis of the phenotypes to be the same in both cases.The fact that the same patterns, and indeed the same patterns of mimicry, can have distinct genetic bases strongly suggests that rather than some prescribed genetic program the origins of these phenotypes has a random component although these mutations may cluster around specific signalling pathways important in the pattern specification for the wing pigmentation. I don't think that whether the mimicry is Batesian or Mullerian has any relevance to the genetics or vice versa. I also don't think which type it is is an important evolutionary factor either. Batesian and Mullerian are simply artificial classifications we give to the relationships between animals that have similar colourings/phenotypes. In evolutionary terms the only issue is whether a specific pattern of markings confers some fitness advantage. We may be able to distinguish between these classification, but in and of themselves wht label we ascribe to them make very little difference and certainly a mis-classification is not some outstanding flaw in evolutionary theory. There has rather been extensive stufy of the general concept of discrimination of unpalatable prey with common patterns and the avoidance of the same. Indeed current theories seem to suggest that without some discriminatory ability on the parts of predators mimicry may be an unsustainable strategy (Gamberale-Stille and Guildford, 2004) and that a variety of cost benefit factors acting on the predator as well as other contingent factors are required for mimicry of an unpalatable aposematic signal to be beneficial. Similarly others have performed controlled empirical studies of palatable prey discrimination, several such are reviewed in an article by Mallet (2001). A number of these studies focus on automimicry rather than strict interspecies mullerian mimicry, but I see no reaon why the same factors would not apply. Wow, you have three hands!! Or maybe you chanegd what was in one of your hands halfway through.TTFN,WKEdited by Wounded King, : No reason given.

In the absence of any reference to get the details on this from the best I can do is speculate. If the patterns of mimicry on females do confer a fitness benefit while male patterning is less important then the selecitve pressures on females to maintain certain patterns of mimicry would be stronger than constraint on males to maintain their patterning. Consequently the regulation of pattern development on the male could be allowed to change, it really depends what forces of selection are acting on male patterning, i.e. predation, sexual selection, etc....TTFN,WK

You are correct, in Heliconius both males and females show mimetic patterning. An interesting paper has studied whether the mimetic patterns affect mate choice and it seems that by and large males prefer mates with the same mimietic patterning (Jiggins et al., 2004).There almost certainly are different selective pressures on the males in those different locations, even from within the population itself alone in terms of mating choice.TTFN,WK

Even if a species is itself unpalatable it may still gain a benefit from mimicry of a more unpalatable species. I don't think these two are neccessarily contradictory. An environment which is monotonous in terms of colour may still be visually complex in terms of form with multiple layers of overlapping foliage. You are assuming that visually complex means multi-coloured but I'm not sure that that neccessarily follows. Also lets not forget that the point of the mimicry in these cases is to look conspicuous rather than inconspicuous, this is not leaf mimicry after all but mimicry of an aposematic signal.TTFN,WK

Can you provide a reference for bees being specifically cryptic? Bees are a pretty heterogenous group and I'm pretty sure there are species which use aposematic signals, escpecially in Bombus.TTFN,WKEdited by Wounded King, : Changed subtitle

I agree that that particular bee doesn't seem to be aposematic, but cryptic? It may shock you that I found the cunnungly hidden brown bee on that green leaf. As crypsis goes this fellow is not in the leaf insect category. I can see however that perhaps in a pollen rich region of the flower he might blend in rather better.And as others have shown a lot of bees, especially bumble bees, do have highly conspicuous aposematic colouring, rather reminicent in fact of the aposematic colouring of wasps and hornets. This figure shows 3 species 2 of Bombus, B. soroeensis and B. terrestris, as well as Apis mellifera.TTFN,WK

MartinV,You don't seem to have any coherent argument against neo-darwinism. All you have produced here is a string of one after another arguments from incredulity.As soon as one example is addressed you skip onto a new one, anything from leaves to mushrooms.Do you have any argument that isn't on eof simple incredulity? Anthing that might actually argue for a prescribed evolution as Davison subscribes to?TTFN,WK

They do, in terms of yellow/black aposematic signalling, and they do. They do, why not read some more of the replies you get.I'not sure why you assume that all of the selective pressures should be the same. Many bees and wasps fillquite distinct ecological niches, why should the selective pressures operating on them be identical? You really just say whatever comes into your head don't you? Do you have any evidence to back up this claim? All of your arguments from incredulity have had the ssame whiny complaint that neo-Darwinist's ignore this absolute nail in their coffin, and this seems to invariably turn out to be untrue, suggesting that you might be better employed looking into more recent literature to see what neo-Darwinist's actually do say.TTFN,WK

Since Darwin wasn't a proponent of neo-darwinism this seems pretty much completely irrelevant.TTFN,WK

This all seems to be pretty tenuously based on Clarke and Sheppards hypothesis. Nijhout himself suggests that a polymorphic regulatory gene may be the source of the variation and in his discussion states that whether the origin is a supergene or a regulatory gene is still unclear. The very concept of what constitutes a gene has undergone some drastc re-evaluation since Clarke and Sheppard's paper came out.Taking into account that regulatory regions controlling pattern expression can be located megabases away from the gene they control so recombinatorial events could break up alleles based on differences in such regulatory elements.Not all 11 loci need be located on seperate genes, even if we accept a 'supergene' scenario, so taking 11 as the number of seperate genes is maximising the improbability. It is also not a reliable assumption that a) all of the genes arrived in this fashion and b) that all recombinations are equiprobable.If you look at the paper we mentioned previously about Heliconius ( Joron et al., 2006) they suggest that 'supergene' regions regulating mimetic patterns in heliconius may be the result of either mutations in numerous cis-regulatory elements of a single gene, duplicate versions of a gene which have acquired divergent functions or 'a cluster of nonparalogous but functionally related genes' which seems to be what Clarke and Sheppard were proposing for Papilio.Is there any reason why you feel the papilio locus of 11 alleles needs to be due to 11 distinct paralogous genes clustered together due to function rather than one or a mixture of these other factors? Other than as a basis for a specious probability calculation that is. Does that number even actually make sense as a basis for allelic variation. Surely the 11 genes would need their own variation in order to account for the patterns seen, which would mean that 11 genes would produce more than 11 alleles. What you might be looking for would be at most 6 genes one of which had 3 rather than 2 alleles.TTFN,WK

Eh? 2 of those extra morphs are from different 'races' which resemble the male form and the hybrids suggest that there is no clear dominance pattern in these interracial crosses. Another 2, hipocoon and hipocoonides, represent one allele 'h'.Also note that the planemoides allele 'appears to have a mix of dominance effects on different portions of the pattern', which sounds like the sort of intermediate forms you did not expect, and that the dionysos allele is not even examined for dominance.So where are the 14 neccessary origins of dominance? From 1000 what? 11 alleles do not require 11 discrete genes. Given that you don't know the basis of the dominance relationships between these alleles how can you estimate the likelihood of such relationships occurring? Sure, such as a constraint as to what mutations affect pigment patterning at all, such as natural selection. Assuming only a limited number of genes control the patterning then mutations which would be selected for mimicry would need to occur at sites within or controlling those genes.The constraints of the system bind may these alleles together. Imagine there is only 1 regulatory key gene controlling the distribution of dark pigmentation by its action on a number of downstream targets, polymorphisms in multiple cis regulatory regions could account for different patterns of expression in discrete areas and distant enhancers would still allow for the breakup of the locus by recombination. I'm not suggesting that this is the case but it is as good an explanation as a high number of genes in a clustered supergene.Naturally to affect the key gene all the mutations would need to be in the locus which defines the regulatory elements controlling the genes expression.Until the actual locus is properly sequenced and mapped this is all pretty much idle speculation. You don't have any better basis for your improbability calculations than if you had just made the numbers up off the top of your head.TTFN,WK