Posted on 06/08/2009 4:41:47 PM PDT by GodGunsGuts
Biomimicry: why the world is full of intelligent design
Forget human ingenuity - the best source of ideas for cutting-edge technology might be in nature, according to experts in 'biomimicry'
We humans like to think we're pretty good at design and technology – but we often forget that Mother Nature had a head start of 3.6 million years. Now, the way that geckoes climb walls, or hummingbirds hover, is at the centre of a burgeoning industry: biomimicry, the science of "reverse-engineering" clever ideas from the natural world....
(Excerpt) Read more at telegraph.co.uk ...
I have insisted no such thing. I have related the results of an experiment. What you insist is that the mutations are not targeted, therefore there should be more than just the two which restored an ability to metabolize lactose using a gene whose function was something else.
You have repeatedly failed to show that the mutations brought about by using error prone DNA polymerase to replicate the genome produce anything other than genome wide genetic variability.
There are two and only two mutations in a gene, ebgA, which restore lactose metabolism in the bacteria. Other experiments or papers argue that the mutation rate required to produce those results would require other effects on the whole genome which are not observed. These papers therefore argue that there is no adaptive mutation. But to address more papers by the author.
Spectra of Spontaneous Growth-Dependent and Adaptive Mutations at ebgR
The large contribution of IS30 insertions at the hot spot in late-arising mutants raises the question of whether that hot spot alone accounts for those highly significant differences. It does not. Elimination of those mutants with IS30 inserted at the hot spot still results in a highly significant difference (P = 0.0065) between early and late arising in terms of the relative frequencies with which the different IS elements cause those mutations, and a significant difference (P = 0.04) between growth-dependent and adaptive mutants in terms of the contributions of IS elements to the mutational spectrum. It is emphasized that there is neither a good statistical reason nor a good biological reason to eliminate those hot spot IS30 mutants from consideration.
I must also add this for you.
Adaptive mutations are spontaneous mutations that occur in microorganisms during periods of prolonged stress in nondividing (2) or very slowly dividing (8) populations. The key feature that distinguishes adaptive mutations from growth-dependent mutations is that the former are specific to the selective challenge that is imposed, i.e., the selective conditions are not generally mutagenic and the only mutations that are recovered are mutations in the site that is under selection (10, 12) (but see reference 3 for an exception to this rule). The phrase "only mutations that are recovered" was chosen carefully to avoid implying that other mutations do not occur. A variety of experiments have looked very hard for mutations at sites that are not under selection and have failed to find such mutations (9, 10), but that does not rule out the possibility that mutations occur but are lost before they can be recovered. One possibility that has gained increasing acceptance over the last few years is that mutations do occur at other sites, but that the cells that suffer those mutations die (because the mutations confer no advantage), and thus the mutations are not recovered (6).
“The phrase “only mutations that are recovered” was chosen carefully to avoid implying that other mutations do not occur.”
Having trouble with reading comprehension?
Once again you have repeatedly failed to show that the mutations brought about my using error prone DNA polymerase to replicate the genome produce anything other than genome wide genetic variability.
Also...
“Adaptive mutations are spontaneous”
Spontaneous, i.e. they are not the direct planned result of some sort of directed mutation.
You should be asking yourself that question. I posted that portion for a reason, mainly due to the fact that you apparently do not do much reading, but I do understand what it means. I also understand what this means .... A variety of experiments have looked very hard for mutations at sites that are not under selection and have failed to find such mutations
The fact remains that no other mutations were found despite looking hard for them and despite any apologetic explanation for not finding them.
Spontaneous, i.e. they are not the direct planned result of some sort of directed mutation.
You left out this important notation.
The key feature that distinguishes adaptive mutations from growth-dependent mutations is that the former are specific to the selective challenge that is imposed
Plus again this....
The large contribution of IS30 insertions at the hot spot in late-arising mutants raises the question of whether that hot spot alone accounts for those highly significant differences. It does not.
Genetic variation from using error prone DNA polymerase introduces mutation throughout the genome.
That this particular screen found two mutations that restored function does not in any way imply that..
a) the mutations were anything other than spontaneous, as the authors clearly state
b) that somehow a “computing” cell knew which regions of DNA needed to be mutated and directed mutagenesis to that region.
Error prone DNA polymerase is not the only DNA polymerase used in the SOS response.
The SOS response is a tightly controlled response involving many repressive and de-repressive controls.
And other experiments show the start differences between "normal" and adaptive mutagenic responses.
stark=start
The SOS response leads to an increase in genetic diversity. The vast majority of that genetic diversity is eliminated by selection. Only those mutations that are amenable to the stress survive and contribute to the resulting population.
An elegant example of evolution through natural selection of genetic variation.
That is not what that chart shows. In "normal" mutations the "hotspot" at location 400 shows a mutation making up around 8 percent of the isolates. When subjected to SOS diversity goes down. It becomes more specific and the mutation at 400 makes up around 25 percent of the isolates and is of a different form of insertion. That is not genetic diversity. That is a targeted response.
[[That is not genetic diversity. That is a targeted response.]]
Almost as though they were....Designed to do this.... Eeeek- the ugly ‘D’ word!
I saw a whole bunch of ‘ifs’ in your proof ...
Good for you-
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