Summations Only

Just a few posts ago you were claiming there was no evidence for random mutations so I guess this represents progress of a sort. Including the ones that render an animal infertile or produce embryos which will never develop into a viable organism?You seem to have decide to not only redefine randomness without telling anyone what your new definition means, but also fitness so as to allow deleterious mutations to be beneficial. Its an incredibly poor analogy, other than saying that both obey the laws of nature you have provided nothing suggesting that they are analogous.TTFN,WK

And then you accepted that there was evidence for random mutations as they are commonly understood. How could the Luria-Delbruck experiments "show only that "random" mutations exist", as you concede, and yet not also be evidence for the existence of random mutations? I'm sure it isn't intentional but nearly every time you endeavor to make your position more clear you instead make it even more incoherent and impenetrable.Perhaps once again it is time to ask you to actually coherently define some terms, in this case it appears that your definition of 'Random' is required so we can know exactly hat you think you are saying.If you insist on 'Random' to mean that all outcomes are equiprobable then no one will quibble that mutation is not random in that sense, but in that case you are using it in a sense rarely used in the biological sciences where it principally means a stochastic phenomenon which can be described with a probability distribution.You seem to be essentially making a philosophical claim that the apparent randomness is not truly fundamentally random, but since your hypothesis does not include any criteria on which the two could be told apart it is entirely worthless in scientific terms. Many creationists and IDists have a similar approach claiming that the apparent randomness of mutations serves to mask subtle interventions to direct evolution by the Intelligent Designer/ God. You haven't proven it once, not even close. You have certainly claimed it ad nauseam but that isn't the same thing at all. Your supposedly logical inference is radically flawed.TTFN,WKEdited by Wounded King, : No reason given.

I made this very point to you previously and you blew it off as irrelevant because people could believe that any type of information could affect the genome. Similarly anyone could believe that telephone numbers can affect the genome.So why should anyone accept your hypothesis on empathy affecting the genome over Panda's hypothesis that telephone numbers can? You later added the addendum that it was "in cases being essential to survival" but even then an argument could be made that a phone number is sometimes essential for survival. It might be avery weak argument but that only serves to strengthen the analogy with your position.Your definition of random seems to be one wholly disconnected to how it is used in evolutionary biology, which explains quite a lot.If you wanted to approach the question scientifically of course then the answer to determining whether empathy affects the genome or phone numbers do would be to look for evidence and come up with plausible mechanism. In the absence of that both hypotheses are equally plausible.TTFN,WK

It seems strange then that absolutely none of the evidence presented in favour of an actual mechanism for guided mutations seems to have been in the metazoa. The only putative mechanisms that been put forward, i.e. Wright's de-repression based system, only seem to work in the context of unicellular organisms and have no readily apparent way to apply to multicellular organisms where there is a separation of the germ line from the somatic cells. And welcome back to evolutionary genetics 101! This is absolutely basic stuff Zi Ko, and if you aren't familiar with it then you just don't understand evolutionary theory at all.The simple answer is that the disparities are principally the result of natural selection. There are other factors, such as mutational hotspots and previously discussed sequence and higher chromosomal organisational effects on mutation rates which can affect the disparities, but in the main when we are discussing interspecies genetic diversity we are talking about distinguishing between nonselective diversity, which is the product of random mutation and maintained in the population through genetic drift, and selective differences which show evidence of having tended to increase or maintain their presence in the population as the result of selection in the case of positive selection or to have been reduced beyond what would be expected in the case of negative selection.Positive selection on a particularly beneficial functional trait will drive fixation far quicker than genetic drift would and will counteract the tendency of drift to eliminate the trait if it is at a low frequency in the population.Some genes are more important to an organisms viability and reproductive success and therefor allow less variability in their sequence while remaining functional and are therefore more prone to stringent selection, these will tend to show less diversity.Other genes have less stringent structural.sequence requirements or are not as vital to the organisms survival and reproductive success, these will support a higher degree of genetic diversity.Once again you seem to have decided to ignore the fact that evolutionary theory is not a theory of random mutation alone but of the patterns of genetic diversity, or morphological diversity, we see as the result of the interplay between random mutation and natural selection operating on populations over many generations.I find it hard to believe you can make these sweeping statements about the predictions of evolutionary theory when you so clearly have little or no understanding of evolutionary theory.TTFN,WK

Sure and it doesn't mean that magical faeries aren't directing evolution, but at the moment your neural hypothesis and the magical faery hypothesis have the same evidentiary footing. Except we would expect some evidence because even if the idea is new the mechanism shouldn't be, this should be a mechanism that has operated for millions of years. So far there hasn't been any evidence presented for directed mutation in the metazoa. So not only is there no evidence of a mechanism there is no data which requires such a mechanism to explain it.If all you have is a theory which is mechanically indistinguishable from current theories based on random mutation and has no coherent and tenable mechanism then you have nothing that anyone should care two hoots about. Maybe you don't deny it but when you ask why there are differences in the divergences of different genes between chimps and humans then you make it very clear that you ignore it, meaning that you are ignoring one of the central features of evolutionary theory. This seems incoherent to me. Why should random mutations themselves have a predictive value? Why should it concern you?Random mutations occur, they generated functional diversity and natural selection acts upon that functional diversity so as to over time shape the genomes of a population.We can measure the rates and nature of these mutations and learn things about their probabilistic distribution. For a large enough population this may allow us to make certain predictions, such as in bacterial experiments where we can have a good idea of the size and number of generations required to have a diverse enough population that almost every single step nucleotide mutation will have probably occurred.TTFN,WK

I came across a paper recently and I find it hard to believe that it isn't one Zi Ko has brought to our attention. The paper is 'Neural Control of Gene Recruitment in Metazoans' by Nelson Cabej (2011) who also has a website http://www.epigeneticscomesofage.com .It seems that Zi Ko and Dr. Cabej may be long lost soul mates. Despite Cabej's emphasis on the CNS' role in the 'processing of information' most of his examples are developmental and are more related to the CNS' development and how that interacts with other developing systems than to the nervous system's role as a mediator of environmental information, and certainly not the direct result of neural activity.TTFN,WK

That paper is also pretty light on the evidence, as the author himself states ... He has an idea and because the nervous system is an important factor during metazoan development and acts as an organising center for various other systems he thinks it should be able to do what he proposes. But there is not any solid evidence of it and all the examples he gives really come down to standard evolution acting upon developmental systems that just happen to involve the CNS as part of their development.As Taq pointed out the paper doesn't propose the sort of directed genetic changes you have been proposing. Instead it is a more like some of Waddington's epigenetic scenarios where the CNS interaction with the environment tends to channel selection in a particular direction through changes in gene expression patterns controlled or initiated by the CNS.TTFN,WK

Sure Ace, you stump up the ~$150 dollars that Cabej's book costs and I'll be happy to read it. This is pretty vague, I'm quite happy to stipulate that the CNS has direct involvement in evolution in many ways represented in the examples in the paper, I just don't think that there is much evidence for the more speculative way Cabej describes in his paper. Cabej himself states that his examples of genee recruitment are not examples of a neural mechanism of gene recruitment but simply of gene recruitment in which the nervous system was involved. In at least 2 of the examples, Pax6 and Neural Crest Cells I'd say it was the role of the developing nervous system as an organising centre that was the cause of that involvement since the key developmental timepoints involved are well before the CNS starts acting as a central interpreter of environmental information.Even in the introduction he only cites his book as a reference for examples of metazoans directly controlling their own gene expression instead of actually giving any examples or details, so it is hard to know exactly what sort of thing he is thinking of. There are plenty of environmental stimuli that change gene expression, some of these are mediated through the nervous system, what Cabej seems to be proposing is a more complex phenomenon than simply that observation and the fact it is a suitable substrate for heritable variation and natural selection surely? I don't think he does either, in fact that was pretty much exactly what I said in the last paragraph of the post you were replying too.I doubt that Zi Ko considers that Cabej's thesis either, that is more what Zi Ko's own theory is about.TTFN,WK

Actually, this thread is about Zi Ko's 'neurogenic theory' and in one of his several OP variants he included epigenetics as one of the factors he was interested in.Maybe you are getting mixed up with the thread about the Wright paper. That would be fairly understandable since there are currently 2 parallel subthreads going on, one titled "Re: Are there ONLY RANDOM MUTATIONS?" and the other "Re: Are there RANDOM MUTATIONS?"TTFN,WK

Wow Zi Ko, your nested quoting there make that whole thing fairly hard to interpret.The article (Wilkins, 1997)doesn't really show much doubt about randomness, what it does is describe and discuss a common misconception of the role of randomness in evolution and the distinction between random in a scientific sense and its more common usage.It is a shame you didn't include the mentioned Gould quote since it eloquently addresses your recent line of enquiry about the predictive value of random mutations ... At this point you seem to have retreated to a position where you refuse to defend or provide any evidence to support your theory's more novel features about the role of the nervous system in directing evolution and are now just trying to create a new terminology to just describe evolution as it is commonly understood. You perseverance of life looks little different from the evolutionary concept of fitness taken up to the higher level of the whole global ecosystem as a system for regulating and producing variant ecosystems to account for changes in the environment, perhaps you should move onto quoting gigantic chunks of James Lovelock now.TTFN,WKEdited by Wounded King, : No reason given.Edited by Wounded King, : No reason given.Edited by Wounded King, : No reason given.

Looking back at Wilkins' article I see that Zi Ko is being tricksy in his quoting. From the section of material from GG Simpson he cut out, without any indication he had done so, the following sections ( the ellipses are all from the original Wilkins article) ... This suggests very strongly that what Simpson means by adaptive mutation is not a directed mutation in response to a specific environmental stimulus but rather simply a beneficial mutation, one that helps the organism adapt to its new environment. The opposite being an inadaptive mutation that doesn't contribute to such adaptation.TTFN,WKP.S. I still have no idea what you are trying to say when you talk about the predictive value of mutations, it seems to be an essentially meaningless term as you use it.

Yes, we do, but Simpson was writing this in 1953. The structure of DNA was only elucidated that year, Cairns wouldn't publish his research on 'adaptive' mutation for another 35 years and the Lederbergs had only just demonstrated very clearly that adaptive, as in beneficial, mutations for one environment arose in environments for which they were not adaptive/beneficial.Indeed the Lederbergs' paper consistently (Lederberg and Lederberg, 1951 PDF) refers to the mutations as adaptive and does not use the term beneficial once. The distinction they draw is between pre-adaptive mutations and directed adaptive mutations.I don't think a single part of the rest of the quote argues against this interpretation and indeed it is much more consistent with this interpretation than that of Simpson meaning directed mutation. It has, in fact the Lederberg plate experiment has been presented as an example of just such a case where the assumption of mutations random for fitness predicts that resistant colonies will be discreet and clonal with representation in both the selected and non-selected replicates while an adaptive response would predict a random distribution of resistant cells/colonies arising on the selected plate and not the un-selected. The fact that you are monumentally ignorant is not any sort of argument.As I've said before your theory only differs from the standard one in its uniquely insane regions which you seem to have chosen to no longer discuss. The rest of it seems to be made up of this sort of meaningless semantic drivel where you insist of confusing different usages of the term random. It is remarkable since the Wilkins article you are quoting so extensively is specifically designed to counter such confusion.TTFN,WK

I think you are ceding too much to Zi Ko's interpretation.What Simpson draws a distinction between is adaptation utilising already existant heritable standing variation including in the population and heritable variation that arises after some environmental challenge as a de novo adaptive mutation, what Lederberg differentiated as pre- and post-adaptive mutations. He stipulates that he thinks both exist but I'm not sure there is anything more to be drawn from the quoted material here.He never suggests anywhere that there is any sort of change in mutation rate due to stress. I'd be interested to know where you think he does.TTFN,WK

No, it doesn't. Just repeating something that isn't true doesn't magically make it true. It is easier to demonstrate in unicellular organisms because they have very short generation time and can be cultured very simply but there are no studies in metazoa that support directed mutation and all the existing studies seem consistent with mutation being random in terms of their phenotypic/fitness effects.The real problem is that except in very extreme selective environments it is hard to detect any signature of something like directed evolution. It isn't impossible that there is a tiny signal of directed mutation lost in the vast ocean of random mutational noise, but there is no evidence in the metazoa to support it. No it wouldn't, it would be lying. Now I believe I have pointed out before that somewhere where it would be germane to suggest that all the evidence, and there isn't much of it, comes from bacterial/unicellular examples is for the sort of directed mutations you have been promoting.You have yet to articulate even the most sketchy outline for how your theoretical system could overcome the germ/soma division in more complex multicellular animals. That you see things that aren't there is unlikely to surprise anyone at this late stage in the debate.TTFN,WK