how fast are they evolving? Or, anytime intelligence is involved (e.g., drugs), you get to declare it not applicable?  Do other organisms include in this subset, since you presume they were designed by God, you must conclude that even things evolving far from man's reach are ID'd... and on it goes...

Yes, that is the question I ask.


No, selection pressure is selection pressure regardless of the source.  At what rate are parasites, bacteria and insects evolving in response to the selection pressure of drugs and chemicals?  Experimental analaysis shows it is not very fast and not very far.  But don't take my word.  Research it and then tell me, how fast is it?


Show me any organism you wish and tell us what rate is it evolving?

Thank you tej, that was interesting.  Your job sounds fascinating to me.  And thanks for pointing out that the restatement barney offered was vague, I should not have accepted it. That was my fault.  I was asking about selection.  Specifically I was challenging those who view drug resistance as good examples of how evolution accounts for observed diversity to estimate the rate that these evolutionary processes are generating new biological information, the kind required for new form and function.


Fair enough.  I should have asked for an average over an observed period.  I also once again intended to ask about accumulating new function and the corresponding new biological information.

Right, It appears that some conserved proteins are critical for biological function in many organisms.  Any modification of these genes cause failure so they don't carry forward.  Other sections of the genome are not critical and are subject to modification without significant effect.  It is consistent with my original premise that you would see evolutionary modification in genes involved in pathogen interaction since these pathogen pathway blocking techniques that damage or degrade function but block out the even larger threat seem to be one thing evolution is quite proficient at accomplishing.

Returning to your previous example of bacteria exposed to (high energy) UV radiation which is also known to damage genes should have a similar effect.  UV is completely random in its damage and some of the billions of organisms will have just the right genes damaged to block the antibiotic pathway but still allow the weakend bacteria to survive and duplicate in an environment now free of competition.

These are all good examples of the evidence that evolution damages function to block pathogen and damaging chemical pathways but does not seem to build new function.  If evolution also built new function we would predict the conserved genes to also show evolutionary characteristics and also they should be identified as sources for evolved genes but they don't. 

Once again analysis from probability provides the basis to explain why we don't see behavior.  Evolution can and does successfully mutate to alternate functional forms when the probability involved in the alteration is greater than the inverse of the number of probabilistic resources available (organism count is the primary resource) but does not when the probability involved in a new or alternate functional protein is less than the inverse of the resources.  Bacteria counts on this earth are estimated at 10^35 or so but the probability of obtaining a functional protein from random change is less than 10^-55 for even the shortest ones.

Indeed.  We have a different view about what counts for evidence for a pathway.  You seem to count the outcome as evidence of a specific path, but the outcome is explained by many possible paths.


By this I take it to mean that the reason we don't observe the expected behavior is because it is obscured by the large number of posible pathways and potential starting points in attempting to recreate history from a narrative.  Instead let's stick with what we can and do observe and test.  We observe mutations occuring and we even know how to accellerate mutation rates, but we don't observe a progression of changes building on each other to produce new functional components.


Have we confirmed that these protiens have new function with no loss of old function?  My understanding is that function is lost (or reduced) and in the process the antibiotic pathway is also lost.