Joined: Jan. 2007
It appears as though I have been banned from UD for my posts here: http://www.uncommondescent.com/archives/1968#comment-86064
One post of mine in responce to DaveScot, that I posted prior to the one that got me kicked out, but has yet to appear is below. I spent some time on it, so didn't want it to dissapear without making at least one appearance in cyberspace....
<i>But they’re not undeterministic in relation to fitness. They’re never or almost never positive fitness changes.</i>
I think that those are two contradictory statements. Say that 1*10^-10% of all mutations are beneficial, and 1-1*10^-10% of mutations are negative. This is still a random distribution, and the mutations are therefore random.
<i>That wasn’t what I claimed. What I claimed was that orthodox evolution predicts that environmental factors such as these will produce a random distribution of mutations by location in the genome.</i>
Technically, even in location in the genome certain areas are more likely than others to have mutations. So I think that these aren't "random" according to your definition.
<i>In fact what has been found to happen is that environmental stresses such as these are not randomly distributed but occur at at a higher rate in genes where change is needed. [...] In this case evolution isn’t driven by random mutations but is rather driven by directed mutations.</i>
I didn't see that in the Scripps paper. I saw that the net mutation rate was effected - and that the evolution would be slowed, but not fully stopped -
<blockquote>The evolution of clinically significant resistance requires the stepwise accumulation of several mutations . [...] The “second step” mutation rate was 1.9 (± 0.21) × 10-4 mutants/viable cell/d in the control strain and 5.5 (± 4.9) × 10-7 mutants/viable cell/d in the lexA(S119A) strain (Figure S3). Assuming that the first and second step mutations are independent, the LexA mutant strain evolves resistance to 650 ng/ml ciprofloxacin in vitro with a rate that is approximately 104-fold lower than the control strain. Because clinical resistance typically requires three to five independent mutations , the data imply that in the absence of efficient LexA cleavage, E. coli would evolve clinical resistance at least 106-fold slower.</blockquote>
So it seems to me that even without the increased mutation rate from the LexA the same mutation still occurs.