Genome complexity: what genes do and don't do (Introduction)

by David Turell @, Tuesday, February 12, 2019, 17:57 (6 days ago) @ dhw

DAVID: Again, I don't believe the large steps required in rearranging a species into a new one is simply cell adaptation. It requires a new design only a designer can create.

dhw: I have never said speciation was “simply cell adaptation”. But it is sometimes difficult to draw a borderline between adaptation and innovation, as in legs becoming flippers. And I have repeated ad nauseam that we do not know if cell communities can innovate (= take the necessary large steps), which is why my hypothesis is an unproven hypothesis, as is your own.

The problem for you is you accept the necessity for design but not the designer.

DAVID: The use of 'life' or 'living organisms' is all the same to me, although your quibble is technically correct. My point is living organisms run on information stored in the genome, much of which had to be pre-programmed for life to have formed at all. Inorganic matter does not have functional information, which means as life started from the inorganic, information had to be GIVEN from someone.

dhw: Once again you scurry back to the origin of life, whereas my point is that living organisms do NOT run on information stored in the genome but – in your own words – they run on their “own operating system” for interpreting that information and acting on it. Information without the means to interpret and act on it would be no use to any organism. But having told us that organisms must have their own operating system, you still insist that they don’t – all their actions are apparently the result of your God’s dabbles or their automatic, non-interpreting, non-decision-making obedience to instructions passed down by the first living cells through 3.8 billion years’ worth of innovations, lifestyles and natural wonders.

Just like Darwin (as usual) you avoid the origin of life, the worst problem for naturalism, which exists in a continuum with further evolution and most always be part of the discussion.

dhw: Under “Bacterial antibiotic resistance

QUOTES: “No research to date has explained the underlying mechanisms of heteroresistance. “

A range of genetic investigations also enabled the researchers to show that the underlying mechanism of heteroresistance was often spontaneous occurrence of gene amplifications of various antibiotic resistance genes.”

These gene amplifications are unstable, and as a result, antibiotic-resistant bacteria can rapidly revert to susceptibility again. This instability makes heteroresistance difficult to detect and study[…]. Accordingly, bacteria can be classified as susceptible although they are actually resistant, and this may lead to use of the wrong antibiotic and failure of the treatment."

DAVID: As I've previously noted, many bacterial populations have a variety of resistant and non-resistant individuals, so that group will survive on their own without gene transfer, which is another mechanism.

dhw: Maybe the mechanism is not “spontaneous”, and maybe resistance/non-resistance depends on what you would call each bacterium’s “own operating system” for interpreting information and acting on it, i.e. “single cells change their metabolic pathways"… and “learn” and “create instructions on the hoof”, as proposed in the article you initially agreed with. The expansion of resistant bacteria would then take time because those bacteria which work out the solution to the new problems would have to pass on the new information.

The one percent who have resistance multiply every 20 minutes. Not much time to take. Lenski's E.coli show this.

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