Thursday, June 21, 2007

Downhill from here...

GilDodgen at uncommondescent is making some complaints about mutations (June 20th, 2007). Writes he:
Mutations break things. However, on occasion, with huge probabilistic resources, a broken thing can promote survival in a specific environment (e.g., bacterial antibiotic resistance).
I would like to analyze this comment in the light of a paper entitled "The biological cost of antibiotic resistance" (downloadable for free). This paper sums up the experimental results of quite a few papers and gives quite a good picture of the fitness costs associated with antibiotic resistance. As the paper says:
In the majority of studies performed, resistance caused by target alterations has been found to engender some cost tofitness (Table 1),
This would seem to support GilDodgen's point that mutations break things, but
but mutants with no measurable costs have also been observed. One example of a ‘no cost’ resistance mutation is the 42nd codon AAA (Lys)®AGA (Arg) substitution of the rpsL gene, responsible for resistance to high concentrations of streptomycin in S. typhimurium and other enteric bacteria
flat out contradicts his argument. Mutations don't have to "break" things. Even if a mutation does "break" something to confer resistance, this will not necessarily mean that the antibiotic resistant bacterium will be less fit forever. Other mutations might restore fitness while maintaining resistance:
Although occasionally, in the absence of antibiotics, drugsensitive revertants have evolved in most cases, adaptation to the costs of chromosomal resistance in vitro and in vivo has been through compensatory mutations (Table 2). In the majority, but not all cases, the second site mutations compensating for the cost of resistance have been identified. These occur by additional (or alternative) mutations at the same locus as the resistance gene, intragenic suppression, or at other loci, extragenic suppression.
So, mutations don't always "break" things, even when they yield a selective advantage, and even if they do, they can "unbreak" them while still maintaining the advantage. GilDodgen is nothing short of wrong. Do these mutations "require huge probabilistc resources"? Well, typically 1 in 10^8 cells acquire the required mutations, so they are fairly unlikely. But why does that matter? With lots of cells mutating and there being long amounts of time for them to do so, this is not necessarily a problem (unless you are a young earth creationist).

GilDodgen continues:
But broken things represent a downhill process, informationally, and cannot account for an uphill, information-creating process, not to mention the machinery required to process that information.
Well, by his own definition he is right I suppose. But then mutations don't necessarily mean broken, so his point is moot. GilDodgen finishes:
Understanding this is not difficult, unless one has a nearly pathological commitment to the notion that design in the universe and living systems cannot possibly exist.
It is diffcult understanding because it is WRONG. And who, exactly, claims that design cannot possibly exist? ID is rejected because it is unscientific and useless.

2 Comments:

At 9:00 PM, Blogger RBH said...

You wrote Mutations don't have to "break" things. Even if a mutation does "break" something to confer resistance, this will not necessarily mean that the antibiotic resistant bacterium will be less fit forever. Other mutations might restore fitness while maintaining resistance:

I have to comment. "Fitness" cannot be defined in the absence of a description of the selective environment. In an antibiotic-laden selective environment in which a mutation for antibiotic resistance occurs and comes to dominate the population via natural selection, the mutated critters are more fit, regardless of whether in the non-antibiotic environment their ancestors would out-compete them. If a mutation "breaks" something to confer resistance, and the bearers of the "break" are more reproductively successful than their unmutated cousins, in the antibiotic-containing selective environment they are more fit than their unmutated cousins and ancestors.

The definition and measurement of "fitness" is inextricably bound to a selective context; it is not an intrinsic property of a lineage of critters that can be determined independent of the selective environment. Only mutations that are lethal pre-reproduction are intrinsically unfit (and I can imagine a scenario in which even they might be selectively advantageous to a lineage, say if the lethal mutation kills additional offspring that would otherwise make all offspring of that mother unsuccessful at subsequently reproducing). All other mutations require specification of the particular selective environment in order to determine their relative fitness.

RBH

 
At 2:52 PM, Blogger Hawks said...

The definition and measurement of "fitness" is inextricably bound to a selective context;

Indeed. IDists are, however, very keen on pointing out that increased fitness in one environment (e.g. in the presence of antibiotics) can be detrimental to the fitness in the "original" environment (i.e. no antibiotics present). For some reason they see this as a problem. What the paper I referenced did, was to show that a high level of fitness could be attained in both environments. So, even playing the IDists game and allowing for their definition of fitness, they would still be wrong.

 

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