The Ghost of Paley
Posts: 1703
Joined: Oct. 2005
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Avocationist:
Here's a few preliminary comments on your post.
1) Be suspicious about any claims about mathematicians proving neodarwinism "impossible". Most of these claims can be traced back to the Wistar Institute symposia during the 60's. These papers didn't account for Ohno's pivotal discussion of the importance of gene duplication in the evolutionary process.
2) Don't take Spetner's claims at face value. This paper, for instance, argues that double mutations might be more likely than experimenters previously realised:
| Quote | The probability of one or more double mutants in a particular colony by day 10 is 5.7 x 10-8, but the probability increases to 0.0028 by day 30. Fig 1 depicts the time course of the process, which bears a striking resemblance to actual experimental data (HALL 1991 , Figure 1B).
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3) Are you certain that your sources say what you think they do? For example, Wright provides several naturalistic mechanisms that create the appearance of "directed" mutations:
| Quote | A number of events initiated by carbon source starvation can facilitate the evolution of a new catabolic pathway. Under these circumstances, cells with gene duplication and higher enzyme levels have a selective advantage (87, 95). In some systems, duplicated segments are specifically subject to higher mutation rates (93), providing ideal and expendable material for mutations representing minor modifications of existing genes (58). These new genes can encode modified enzymes catalyzing reactions closely related and/or complementary to those in existence (56). An additional consequence of starvation is the removal of feedback controls, resulting in the derepression of genes previously inhibited by the now absent metabolite. Increased rates of mutation in these derepressed genes increase the probability of creating a new gene-enzyme system. A number of examples exist in which derepression of a gene has enabled an enzyme to use a new substrate. For example, altros-galactoside can be used by â-galactosidase after it is derepressed (53); other examples are â-glycerolphosphate via alkaline phosphatase (100), putrescine via diamine-á-ketoglutarate transaminase (44), and d-mannitol via d-arabitol dehydrogenase (55).
[....]
Presumably, feedback mechanisms existing today evolved in the past to prevent unnecessary and wasteful metabolic activities by coordinating these activities with the presence or absence of nutrients in the environment. High mutation rates in derepressed genes prepare cells to respond rapidly to new challenges should the stress become more severe. As will become apparent, genetic derepression may be the only mechanism by which particular environmental conditions of stress target specific regions of the genome for higher mutation rates (hypermutation). Although this direct avenue for increasing variability is probably not available to multicellular organisms in which germ cells and somatic cells are separated, the derepression of biosynthetic pathways is essential to increased longevity in mammals subjected to caloric restriction (54), and amino acid limitation in rats can also induce gene expression (9).
[all bolding mine -- Paley]
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Nonrandom? Certainly. Directed? Perhaps, but by purely mechanistic feedback loops, as environmental changes relax regulatory controls on certain genes, causing higher transcription rates and thereby higher mutation rates. Note the importance of gene duplication, because duplicated sections of the genome are more likely to mutate, partly due to relaxed selection pressures caused by functional redundancy*.
Here's another paper:
| Quote | The mechanisms of evolution have been the subject of many controversies and speculations for some 200 years (1, 2). Clearly, selection of the fittest occurs, but does the environment also play a role in generating the fittest? Do all of the variants selected result from mutations that are completely “random”? Background mutations are loosely referred to as random even though they do not occur with equal probability, but at different and characteristic rates because of DNA context and variables such as the intrinsic instability of cytosine, giving rise to the (most frequent) C-to-T transition mutations (3, 4) or the presence of tandem repeats, resulting in frameshift mutations (5). Moreover, environmental conditions such as thymidine starvation can selectively increase the rate of particular kinds of mutation (6). However, in an evolutionary context, “random” has a very specific meaning: Neo-Darwinism holds that the spectrum of background mutations and the frequency with which they occur are random (undirected) with respect to selective conditions of the environment. Another ambiguous word, “mechanism,” can mean one thing when applied to evolution and another when applied to mutations. There are mechanisms by which particular kinds of mutations occur (e.g., base substitution, deletion, frameshift), and there are mechanisms by which the rates of many kinds of background mutations are stimulated (e.g., replication, UV irradiation, defective repair, transcription). It is the latter sort of mechanism that applies to evolution because stimulating mutation rates increases the availability of variants on which evolution depends. Our data indicate that transcription (starvation-induced derepression) is unique in augmenting variant availability in a specific manner, i.e., by stimulating rates of transcription (and associated phenomena such as RNA polymerase pausing) in targeted operons, thereby increasing the concentration of single-stranded DNA (ssDNA), which is more vulnerable to mutations than double-stranded DNA. Although the mutations per se are random, as described above for background mutations, the mechanisms that target operons for increased rates of transcription are highly specific. This specificity is not compatible with current neo-Darwinian dogma. And yet, evidence in the literature supports the two major assumptions on which our hypothesis is based: (i) ssDNA is more vulnerable to mutagenesis than double-stranded DNA; increased rates of transcription will, therefore, increase rates of mutation; and (ii) derepression and activation of an amino acid biosynthetic operon occur specifically in response to starvation for that amino acid.
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More later.
*[Edit -- I don't think that's quite right.....relaxed selection pressures would lead to higher fixation of mutations...but the paralogues produced from gene duplications are more likely to duplicate again. So the process can feed on itself, leading to gene families.]
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Dey can't 'andle my riddim.
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