Does the Darwinian theory require modification or replacement?

No, claiming that "There is decidedly no homology of genes corresponding to homology of biological structures." means instead that she is talking nonsense.There is certainly no universal expectation of conservation of function, it is easily shown that developmental pathways can be modified to different endpoints and triggers. However there is a wealth of data showing substantially conserved homologies of function and genetic networks across species and indeed across phyla.TTFN,WK

Not only are you not a biologist but you seem to have little to no grasp of any of the terminology associated with evolution.Natural selection is not an active operating force, it is the name given to the observed patterns of differential success between different genetic variants. What determines those patterns is the environment in which the organism exists. Selection works, in the extreme sort of cases studied here, because organisms which are incapable of surviving in a given environment will have a drastically reduced chance of contributing their genes to subsequent generations. Over time, over multiple separate experiments as well in some of these cases, we can track the patterns of gene prevalence and see which ones are successful in a specific environment. Generally selection is categorised as natural or artificial, artificial selection is what is practised by human livestock breeders and agriculturalists to produce novel strains or to breed for specific characteristics in an animal or plant. So natural selection is selection without a human agency directing it.Humans choose traits for the benefit of humans so the sort of things that result from artificial selection and the strength of it, as seen by the associated genetic patterns, tend to be different from natural selection which essentially shows the effects of all the organisms traits interacting with the environment simultaneously.If you mean how can we know that selection isn't the result of capricious invisible fairies then the answer is that we can't but what we know is that the interaction between the environment and the genome appears sufficient to explain what we observe. So what purpose is served by positing intangible and unnecessary additional entities? No, even asking that question suggests you don't understand even the basics of evolutionary theory. The effect of random changes in the prevalence of particular alleles from one generation to the next is called genetic drift. Genetic drift results from a wide variety of phenomena from localised freak environmental factors up to extreme population crashes causing bottlenecking. It is essentially a result of random sampling of the genetic makeup of the population. This represents a fundamental misunderstanding of selection and beneficial mutations. The only way to determine what mutations are beneficial is as a result of studying their success. So the fact that a mutation has been positively selected is what tells us it is a beneficial mutation. We can estimate to some extent what mutations will be beneficial, but only in very limited controlled circumstances where we have a very good understanding of the organisms genetics and the specific environmental challenges involved. In many experiments there will also be neutral mutations occurring and it may require a considerable number of generations or experiments to be able to definitively discriminate between patterns due to selection and those due to drift.Just to emphasise, no one says that natural selection is random.TTFN,WK

That is what I meant, "a mutation conferring resistance to an antibiotic" is not any specific mutation but rather a wide class of different mutations whose molecular nature we don't know. Also your 'other things being equal' covers a multitude of possible antibiotic resistance conferring mutations that also negatively affect the organisms reproductive success enough to outweigh the benefits.Certainly the frequency of one of that particular class of mutations arising is interesting from a pop. gen. perspective, but knowing the actual molecular bases is much more informative and certainly much more relevant when one is discussing directed mutation.TTFN,WK

Yes, lets look at the abstract for that paper ... So misleading claims, check!No paradigm shift, check!Enxtension of current theory to acount for new findings, check!Yeah, it really sounds like they are tearing down the whole structure of modern evolutionary theory, oh no, wait! It doesn't sound like that at all, it sounds like what we have been telling you for this whole thread. The modern synthesis is roughly a century old and unsurprisingly we have learned a hell of a lot of new things in that century.Pigliucci's extended synthesis already exists, it is called modern evolutionary biology and it is spread throughout the literature of all the fields he mentions.TTFN,WK

Well it could arguably have confounded it in the case of prokaryotes, but even then this doesn't really seem to be the case. Sure if we trace particular prokaryotic lineages back far enough we might hit up against the sort of non-darwinian event horizon that Carl Woese characterised as the Darwinian threshold, beyond which HGT is so prevalent that we can't trace common ancestry for an organismal lineage (Woese, 2000; Woese, 2002). This certainly may present an insuperable barrier for ever reconstructing a genetic model of the Latest Universal Commmon Ancestor (LUCA), but beyond that most of our current genetic models work well enough as long as the possibility of HGT is borne in mind.So yeah, if we go back far enough it presents a problem for prokaryotic lineages and if we got back really far it presents a problem for the putative common origins of all life.As for epigenetic inheritance, the current evidence is that these traits are transitory rarely lasting more than 1 or 2 generations in the absence of a maintainence of some outside environmental factor, usually diet in experimental settings (Waterland et al., 2007).So I don't see much reason to throw out our current models, containing a heavy dose of darwinian theory, certainly not for some nebulous and incohate creationist alternative which you claim may be more parsimonious. Can you give us an example of how such a model would be more parsimonious?TTFN,WKEdited by Wounded King, : No reason given.

Yawwwn, indeed as we have all agreed from the start because the MS is a series of mathematical formulations describing population genetics almost a century old. Could you stop repeating the same thing over and over again? What am I, psychic? I'd suggest pragmatically that one possible reason is that coining a term that then goes into popular usage can be a good way to get your names in the textbooks and ongoing citations. Maybe he thinks a catchy title will encourage people to focus on the specific areas of research he considers most important. Maybe he wanted to write some sort of overall precis of current evolutionary theory and the direction he sees it going for those outside the field.TTFN,WK

I think this runs into a definitional issue of what exactly everyone means by macroevolution.Obviously when one goes out to a large enough perspective of life 'microevolution', in this case lets say that means random mutation coupled to traditional modern synthesis style population genetics, is insufficient to describe the diversification of life on Earth. We only need to look at endosymbiosis to see this is clearly the case.If that sort of large scale event is what is meant by macroevolution then I'd agree. If what is meant by macroevolution is speciation then I would disagree in as much as speciation certainly can come about through 'microevolution', as I previously defined it, in two isolated populations.However I can also see situations where other mechanisms, not covered by the strict definition of 'microevolution' I am using, could play a role in speciation and subsequent divergence of the lineages after speciation.But this doesn't require a change to the Modern Synthesis (MS) because it isn't what the modern synthesis was formulated to deal with. That is why Pigliucci talks about extension and emphasises the fact that there is no overthrow of MS required.To hark back to the topic title, when you ask if MS should be modified that is quite different from asking whether 'Darwinian Theory', which would certainly encompass a large swathe of Pigliucci's 'extended synthesis', requires modification or replacement.TTFN,WKEdited by Wounded King, : No reason given.

Sanford original, srsly? He's just put a shiny patina of academic respectability on Walter Remine's tired old Haldane's dilemma schtick which he's been pounding out since at least the 90s.They've even collaborated together on the "Mendel's accountant" software.TTFN,WK

Wow you just won't get the message will you no matter how many people tell you how many times. The answer is no because the MS is a very specific thing. There is no way to modify the population genetic basis of the MS to accomodate some of the events that have occurred during the diversification of life on Earth.What is required is the information and models from the other relevant fields that encompass those mechanisms distinct from microevolutionary ones and a framework on which to identify when these mechanisms have been in operation. That is why Pigliucci calls it an extended synthesis, because we need additional mechanism to explain those situations for which a molecular pop. gen. model is insufficient. In the majority of cases it probably is, but as I said in my earlier post there are obviously some evolutionary events, such as the endosymbiotic origins of mitochondria and chloroplasts, which are necessary to explain the diversity of life on earth and for which the MS is insufficient.All you have really done is change the question to what you mean by transpecific evolution. There is a very wide range of things this could encompass, from changes in recently isolated sister species to differences between the animal and plant kingdoms.So rather than quoting Mayr why don't you actually tell me what you understand transpecific evolution to mean.TTFN,WK

NB means nota bene it is latin for 'note well', in this case Dr. A is drawing our attention once again to your preference for using authority figures as mouthpieces for your own position.TTFN,WK

Please settle on one term and use it, do you mean the modern synthesis here or something else?TTFN,WKEdited by Wounded King, : No reason given.

I guess this depends exactly what you consider 'Classical Darwinism', But I doubt you'll find anyone in evolutionary biology who would say that Darwin's original work, or even the modern synthesis of the first half of the 20th century entirely explained the diversity of life on Earth that we see.That is one reason why the Discovery Institute's list of dissenting scientists is a bit dodgy. The actual statement ... Is one that very few evolutionary biologists, even those who might consider themselves hardcore Darwinists, should object to. Darwin certainly wouldn't have had a problem with it given that he himself suggested other mechanism than natural selection would contribute to evolution. But the implications the DI chooses to hang on it are dubious in the extreme, it certainly doesn't suggest the need to throw out the modern evolutionary biology we have.TTFN,WK

As has been pointed out, this isn't what he says. Once again you fail on comprehension. What he actually says is what I already told you, that microevolution is insufficient to explain all macroevolutionary changes, that is why he says ... I hope you understand the difference between not always and never, though given the creationist/IDist propensity to mistake rare for impossible I understand that you might not.TTFN,WK

Hi Percy,I think you've done a pretty good job of summarising what the review paper says about the CRISPR system in terms of anti-viral defence. One bit that I thought was a bit unclear was when you were discussing the non-random selection of sequences. The actual non-randomness is due to the preference for elements of the CRISPR system to target specific nucleotide sequences, these sequences are termed proto-spacer adjacent motifs (PAMS). These PAMS are not actually part of the proto-spacer sequence but rather appear to be the sites targeted by whatever mechanism incorporates the viral sequence into the CRISPR locus. These aren't highly specific sequences, one recognition motif is NNAGAAW (where N represents any nucleotide and W represents an A or T) another is NGGNG. These different recognition sites seem to be associated with distinct CRISPR loci.I'm not sure from your description if you were saying that the viral sequences had any specific function in the virus, there doesn't seem to be anything suggesting that in the paper.So the sequences are non-random in that they are both targeted to specific motifs for picking up proto-spacer sequences and also in as much as the sequences are reincorporated into the appropriate CRISPR locus on the bacterial genome.This all seems to suggest that there must be something in the CRISPR associated genes around a specific CRISPR locus or in the leader sequence which provides both the motif template for PAM recognition and also identifies that CRISPR locus as the point of insertion for newly incorporated spacer sequences. Mutation of PAM sites shows that they are also required to be present in the phage for the resistance mechanism to operate.The selection of the sequences itself is much less interesting in terms of non-randomness, since it is simply based on not very rare recurrent sequence motifs, than the way the system inserts the corresponding spacer sequences back into the right CRISPR loci.TTFN,WK

I don't think the question of fitness for any particular CRISPR incorporation event can be evaluated on the basis of the papers discussed so far. Certainly it is easy to appreciate how a defence system against bacteriophages in general should be beneficial to a bacterial population.It isn't clear however to what extent any particular protospacer sequence will be an effective substrate for the CRISPR system to combat bacteriophage infection. The sequences the review discusses are ones already established in various bacterial populations, in other words they are ones that have already passed through several rounds of natural selection.It may be that when a bacterial population is subject to a challenge from bacteriophage infection its constituent bacteria will incorporate dozens or hundreds of different spacer sequences depending on the prevalence of the particular PAM motifs that the CRISPR loci in the population targets. If a particular spacer sequence confers immunity to the bacteriophage challenge we would expect it to proliferate in the population. But we can't simply assume that all spacer sequences confer the same degree of immunity or even any immunity at all.I'll have a look in some of the other CRISPR papers and see if there is anything about this. As it stands though I don't think we can say that every CRISPR locus spacer incorporation is a beneficial mutation even though we have specific instances where they have been.TTFN,WK