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  Topic: Official Uncommonly Dense Discussion Thread< Next Oldest | Next Newest >  

Posts: 160
Joined: Jan. 2007

(Permalink) Posted: Jan. 18 2007,13:50   


It appears as though I have been banned from UD for my posts here:

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 [1]. [...] 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 [1], 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.

  29999 replies since Jan. 16 2006,11:43 < Next Oldest | Next Newest >  

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