Summations Only

Simpson is defining adaptive mutations as increasing the random mutation rate in times of stress. The mutations are still random with respect to fitness, the opposite of guided mutations. Here is some background on adaptive mutations.One of the important experiments dealing with adaptive mutations was on lac revertants. They were trying to use the Luria-Delbruck experimental design in a situation where the challenge was not immediately lethal. They chose a bacterial strain that had a knockout mutation in the lac gene which is responsible for the metabolism of lactose. Then then put this strain on plates where the only carbon source was lactose. They then looked for mutations in the lac gene which resotored lactase activity.When the counted the number of lac revertants they found that there were many more than they expected. This opened up the possibility that the bacteria were specifically mutating the lac gene in order to fix that gene. Further experiments disproved this notion, and these experiments led to the discovery of the SOS response. The response is triggered by DNA damage, not by the presence of lactose. This response upregulates the production of error prone polymerases and increases the rate of gene duplication and recombination. The random mutation rate increases, but the mutations are not guided to the lac gene. Nowhere in the process does the bacteria sense the presence of lactose and then specifically mutate the lac gene.This is the type of system that Simpson is talking about. He is talking about the non-random nature of the random mutation rate. Nowhere is Simpson supporting your idea of guided mutations.

I was assuming that Simpson was using the modern term which is probably a bad assumption to make.If Simpson is merely talking about phenotype plasticity then Zi ko is really barking up the wrong tree.

They demonstrate that mutations are random with respect to fitness, the very thing you are trying to deny. Or it could be filtered through natural selection, just as we observe. I think you should reread that quote and think about it.

This thread is about your theory of evolution. Where are those predictions? Random mutations is the rule. It is the only mechanism for producing heritable variation that I am aware of. If you disagree, then now would be the time to cite evidence. You need more than concepts. You need evidence. Where is it?

It is a matter of fact and observation. We observe that mutations are random with respect to fitness. We observe that these random mutations filter through natural selection.

Evidence please. It applies to all DNA based life. All life is exposed to mutagens, random mistakes by polymerases, indels, recombination events, and exogenous insertion of repetitive elements (e.g. transposons). We can see this in the divergence of non-coding DNA between species. The process of mutation in ALL life produces deleterious, neutral, and beneficial effects.Also, I have yet see evidence of any god or a plan set by this unevidenced god. Why would I include something for which there is no evidence? So says the person who thinks, without evidence, that there is a supernatural plan at work in evolution. You are projecting.

Here is one done in humans:

quote:

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Direct estimates of human per nucleotide mutation rates at 20 loci causing Mendelian diseases.
Kondrashov AS.
SourceNational Center for Biotechnology Information, NIH, Bethesda, Maryland 20892, USA. Kondrashov@ncbi.nlm.nih.gov

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Abstract
I estimate per nucleotide rates of spontaneous mutations of different kinds in humans directly from the data on per locus mutation rates and on sequences of de novo nonsense nucleotide substitutions, deletions, insertions, and complex events at eight loci causing autosomal dominant diseases and 12 loci causing X-linked diseases. The results are in good agreement with indirect estimates, obtained by comparison of orthologous human and chimpanzee pseudogenes. The average direct estimate of the combined rate of all mutations is 1.8x10(-8) per nucleotide per generation, and the coefficient of variation of this rate across the 20 loci is 0.53. Single nucleotide substitutions are approximately 25 times more common than all other mutations, deletions are approximately three times more common than insertions, complex mutations are very rare, and CpG context increases substitution rates by an order of magnitude. There is only a moderate tendency for loci with high per locus mutation rates to also have higher per nucleotide substitution rates, and per nucleotide rates of deletions and insertions are statistically independent on the per locus mutation rate. Rates of different kinds of mutations are strongly correlated across loci. Mutational hot spots with per nucleotide rates above 5x10(-7) make only a minor contribution to human mutation. In the next decade, direct measurements will produce a rather precise, quantitative description of human spontaneous mutation at the DNA level.
Direct estimates of human per nucleotide mutation rates at 20 loci causing Mendelian diseases - PubMed

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This study calculated the human mutation rate by measuring the occurence of deleterious mutations in a well defined population. They compared their results to mutation rate needed to produce the divergence seen in chimp and human pseudogenes (i.e. neutral mutations). If mutations are random with respect to fitness in humans then the two values should be close, and they are.On top of this, there is no known system by which metazoans can specifically mutate their DNA in response to a specific stimuli. All of the sources of mutation that we know of are random with respect to fitness. Polymerases are incapable of determining which mutations will affect fitness. Repair mechanisms are incapable of determining the same. Environmental mutagens can not tell which mutations will increase or decrease fitness. You claim that there are such systems, but you fail to even describe them, much less evidence them. Is it any wonder why scientists conclude that mutations are random? They are following the evidence, and the evidence clearly indicates random mutations with respect to fitness. Why do you insist that it exists when you have no evidence that it exists? We need evidence, not suggestions. Anyone can play make-believe. Anyone can make stuff up. What we are interested in is what is real. Surely you know this? Says the person unwilling to present evidence to back their claims.

The indirect measurement is more than enough to test the hypothesis.You claim that mutations are guided in metazoans. Where are your direct measurements?

I am presenting random mutations as a conclusion drawn from evidence. I have given you this evidence.You claim mutations are guided. You have offered zero evidence.It appears that your attempts to "fiddle with" the scientific community is rather feeble, and incompetent at that.Please present evidence for your claims or withdraw the claims. It is as simple as that.