The End of Evolution By Means of Natural Selection

The reason is because that reference is the original one for the Lac frameshift experiment, the other papers are the ones discussing subsequent studies of possible mechanisms. A mechanism which is unknown in 1991 may have been discovered since then.TTFN,WK

What you have described here fits the explanations for the Cairns experiment but not the Zhang and Saier paper that Bolder-dash was asking about.TTFN,WK

I think the Zhang and Saier paper is an interesting basis for such a discussion. Although I see no need for it to support Darwinian evolution, surely it merely has to not contradict it? As has already been noted umpteen times Evolutionary Theory does not exclude everything other than random mutation and natural selection, that is a creationist/idist charicature.The particular 'mutation' in question is the insertion of a IS5 transposable element. These elements can insert but they can also excise Zhang et al., (2010) show that the IS5 element can precisely excise fully reconstituting the original insertion site. This means that this adaptive mutation is readily reversible compared to most mutations.It is also worth noting that what happens when the adaptive mechanism is activated is not in fact the targetted upregulation of insertion but rather a de-repression. The GlpR protein normally represses the insertion of IS5 elements upstream of the glycerol metabolising gene, in other words the insertion frequency is below the base rate for target sequences of IS5 insertion.Given the reversible nature of the change It is not implausible for such a system to evolve and be a target for selection, if it were irreversible I agree that it would seem problematic.As it stands the repressive activity of GlpR on inserion is only effective when it is binding a particular site, this site is a sequence duplicated 4 times upstream only one instance confers repression. It is not hard to see how a duplication of this sequence which led to the repression of a recurrent but unstable insertion which caused constitutive activation of the glycerol metabolising gene would be beneficial. In the absence of glycerol such constitutive activation would be wasteful.In terms of the glycerol dependent regulation of the system, this should have already been in place since GlpR also acts to directly repress the expression of the glycerol metabolising genes. In other words there is already a reponse upregulating glycerol metabolising genes when glycerol is in the environment. This system seems to allow the occasional occurrence of a transient turbo-charged glycerol metabolising strain when the IS5 element inserts in the correct position.I have to say I don't see how any such system could arise in larger multicellular organisms, but that doesn't mean that it couldn't.I also don't see why this should be any sort of problem for Evolutionary Theory. It certainly runs contrary to the canonical picture of random mutation, but then it is a different type of mechanism and one that seems fairly unstable. It seems more like the sort of heritable epigenetic effects that have been observed than a traditional mutation, but it is a direct change in the primary sequence of the DNA so it can hardly be characterised as epigenetic.TTFN,WK

This is overstating things a bit, in order for it to stay extant in the bacterial population you wouldn't need constant exposure. I agree you would need exposure regularly enough for it to be maintained but I couldn't give you any reasonable estimate offhand of what that means in terms of such a trait in a bacterial population but I think your extended period of time would have to be quite substantial.What I think would be interesting would be finding out at what sort of frequency this insertion occurs at normally when glycerol is in the environment and there is an active Crp gene. All of the experiments from Zhang and Saier are done in a Crp^- genetic background where virtually all glycerol metabolism will have been abolished. Clearly this creates a massive selective pressure in favour of bacteria which are able to metabolise glycerol.But if we consider what we are seeing to be a form of regulation for further increasing glycerol metabolism when glycerol is in the environment, rather than the rather outlandish idea of an emergency backup system in the unlikely event that the Crp gene is deleted, then we would expect to see a sporadic amount of insertions in a wild type genetic background allowing increased glycerol metabolism. Zhang and Saier showed in a further paper that the level of glycerol phosphorylation, an indicator of Glycerol kinase activity ( a proxy for the glycerol metabolising activity of the proteins regulated by glpFK), is higher in bacteria carrying the insertion in a Crp^- background than in the Wild Type without the insertion (Zhang and Saier, 2009). I'd suggest that this would also mean that the insertion occuring in a Wild Type background would also have a higher level of glycerol metabolism.TTFN,WK

No, it has a specific type of mutation that is beneficial ocurring which is otherwise repressed. No, but if you are in a 'bad' environment then selective pressures aare going to be much higher and even a slight advantage can be greatly magnified in terms of reproductive success. That is a very big 'if', the idea that evolution should give rise to perfectly adapted alleles is a specious one. It is also worth noting that while living fossils are morphologically conserved we have no idea how genetically conserved they are. This is probably the most accurate characterisation. The more optimally adapted an organism is to its environment the less beneficial any given mutation is likely to be. This very much depends on the particular challenges that make it a 'bad' environment. Some challenges may have multiple possible mutations that could ameliorate them while others may simply be too restrictive, or perhaps only have a very small number of possible beneficial mutations available from the current bacterial genome.TTFN,WKEdited by Wounded King, : No reason given.

This simply isn't true, there are many documented beneficial mutations. As to disease causing mutations being speculative, I can't see how anyone with even the faintest familiarity with actual research into such things could make such a claim. There are a wide range of genetic diseases for which the causative mutations are well known and the mechanisms by which they cause disease well understood. I doubt it though these sea slugs are a fascinating example of both endosymbiosis and horizontal gene transfer. I'm not sure what you mean by this, as far as I know these sea slugs haven't just suddenly switched to this strategy of harvesting plastids from algae. This seems to be hinged on you assumption that there is an ongoing process which will eventually transfer all the neccessary nuclear genes for plastid function to the sea slug, but there isn't really any basis for such an assumption. Any evidence for this? Incidentally it is the algal DNA not that of the chloroplasts that has been transferred since the chloroplast DNA does not in fact provide all the necessary genetic infromation for producing functioning chloroplasts.I know there is evidence for the transfer of algal genes into the sea slug genome but I don't know of anything to support your contention that this is an incremental process 'each generation'.I agree that were the correct genes all to be transferred then it is possible that a sea slug could eventually evolve which was independent of the algae as a source of chlorplasts, but I certainly don't see that outcome as inevitable.TTFN,WK

No ... ... and yes. As I have said several times evolutionary biology does not pretend that random mutation and natural selection are sufficient explanation for the entire observed diversity of life on Earth. I'm not trying to downplay anything just to portray a more realistic version of modern evolutionary biology than the straw man you put forward. The other mechanisms are not some vague incohate concept they are things like horizontal gene transfer, endosymbiosis, heritable epigenetic variation and probably others not as well understood. Well that wasn't really what I was talking about in terms of other mechanisms, but I would certainly not quibble that the transposon insertion is a mechanism which forms part of the glycerol metabolism regulation system. This fits so many wrong assertions and assumptions into one sentence it is hard to know where to begin. We haven't somehow lost RM and natural selection as explanations. Their not being able to explain the entire diversity of life on Earth doesn't mean they can't contribute substantially towards explaining that diversity. We don't lose anything by gaining understanding of other mechanisms which generate heritable variation. Well now you seem to be reaching to semantic cheeseparing in the absence of any substantial argument. Despite continual Idisat/Creationist bleatings evolutionary biology is not an atheist religion, if traditionally held 'dogma' is challenged by solid evidence it will be overturned, it happened with the central dogma of molecular biology when reverse transcription was discovered and arguably with Prions. Unless its offspring subsequently had 2 heads then it wouldn't be anything to do with evolution. I really don't see how this is the case. The point of evolutionary theory is not to dictate to reality how it must behave but to allow us to explain and model the reality of biological evolution as accurately as we can.TTFN,WKEdited by Wounded King, : corrected typo

Not quite sure why these highly related questions took the form of two separate posts.The answer for endosymbiosis and epigenetic inheritance is a mixture of yes and no in both cases.The initial engulfment part of endosymbiosis is not a random mutation as I would think of it, but the subsequent transfer of genetic material from the engulfed organism to the host which leads to it becoming a subsidiary organelle seems consistent with stochastic genetic processes we are familiar with.Similarly for epigenetic inheritance it is associated in large part with Modifying enzymes produced by the cell which are viable targets for RM/NS to operate on. The primary sequence of the DNA can also have significant effects on possible patterns of epigenetic modification in terms of providing binding/recognition sites for modifying enzymes. The one element which is clearly distinct from random mutation is the environmental factors which can alter the balance of epigenetic modification.As to transposon insertion, if anything this is the one which can most clearly be ascribed as the result of processes of RM/NS. The tranposon's transposing activity is a result of its genetic sequence, that sequence can be modified by random mutation causing functional changes in its behaviour. Similarly the insertion sites for a transposon are specific sequences of DNA, often very short motifs which can easily arise randomly.in the case of the IS5 transposon in the Zhang and Saier paper the recognition site is simply C-(A or T)-A-(A or G) which is not highly specific. The position of this sequence was such that binding of a protein which regulates glycerol metabolism was sufficient to block access of the transposon to the sequence and prevent it inserting under normal conditions.So many of these mechanisms do indeed involve significant roles for rm and certainly ns in both their origination and their maintenance.TTFN,WK

I'd say this was a pretty contentious claim. It might be true looking at a traditional readily identifiable Mendelian characteristic, such as your coat colour example, but for any complex trait it is almost certainly false.Comparative genomics within populations has revealed a large amount of heterogeneity at both the copy number and SNP level and whole genome association studies have identified small but still significant effects from such variations. So there could easily be multiple SNP variants of a gene or set of genes interacting with the environment to produce a spectrum of fitness.TTFN,WK

You seem to assume that natural selection is the normal driver for speciation, there is considerable reason to doubt this even from the same sort of bird song ring species studies you refer to. Indeed one of the main points arising from the study of the greenish warbler ring species is that the variations in song seem to be stochastic, resulting primarily from either cultural or genetic drift, rather than a product of selection (Irwin et al, 2008). A single gene can have many alleles, even the sickle cell anaemia allele HbS is only one of 2 known haemoglobin alleles which offer some protection from malaria (Verra et al, 2007). I can't see how this relates to what you say about speciation and ring species. I also don't see any evidence for this claim and, as I pointed out previously, there is a staggering weight of genetic evidence countering it. Perhaps you are using some idiosyncratic definition of what constitutes an allele, or discounting all neutral or nearly neutral allelic variants?And now you are conflating traits and alleles, which makes things even more confusing. To be clear, do you claim that most genes only have at most 2 alleles? So one example would be the Malaria resistant Haemoglobin variants (A,C and S)which currently forms a dynamic balance in the population. Heterozygotes of both AC and AS can be selected for in response to malarial pressures while for heterozygotes CC is very mild in terms of symptoms compared to SS. This also emphasises another another exception to your claim that natural selection will tend to favour one of two alleles, heterozygote advantage where heterozygotes have higher fitness than homozygotes of either allele.TTFN,WK