Here's some more:
"Spontaneous beneficial mutations are the fuel for adaptation, the source of evolutionary novelty, and one of the least understood aspects of biology. Although adaptation is everywhere—cancer invading tissues, bacteria escaping drugs, viruses switching from livestock to humans—beneficial mutations are notoriously difficult to study (1, 2). Theoretical and experimental advances have been made in recent years by focusing on the distribution of fitness effects of spontaneous beneficial mutations (3–8). Mapping the options for improvement available to single organisms, however, is insufficient for understanding the adaptive course of an entire population, especially in asexual populations of microorganisms or cancer cells where multiple mutations often spread simultaneously (9–16). Here, we use modeling and experimental results to show that the seeming additional complication of having multiple lineages competing within a population leads in fact to a drastic simplification: Regardless of the distribution of mutational effects available to individuals, a population's adaptive dynamics can be approximated by an equivalent model in which all favorable mutations confer the same fitness advantage, which we call the effective selection coefficient. We provide experimental estimates of the effective selection coefficient and the corresponding effective rate of beneficial mutations for laboratory populations of Escherichia coli, and we demonstrate the predictive power of these effective parameters. "
But if you really want to get into it, read the paper. I don't want Science mad at me.
Thanks, I would if it were free, but I can't subscribe to every Tom, Dick, and Hairy :) publication that wants my money. "Spontaneous beneficial mutations" and "in which all favorable mutations confer the same fitness advantage" sure looks like something Shapiro would write.
These examples make it clear that natural genetic engineering occurs episodically and non-randomly in response to stress events that range from DNA damage to the inability to find a suitable mating partner. One important consequence of such episodic activation is that multiple connected genetic changes can occur at different genome locations within a brief period of time. Studies of hybrid dysgenesis in the fruit fly (49) have documented such temporally coordinated changes within a single cell during the mitotic development of the germ line. Since these multiple changes occur several cell divisions before gametes are formed, multiple sperm or eggs (and, consequently, multiple individuals) can be produced which share a constellation of related genome alterations.
In addition to temporal specificity, it turns out that many natural genetic engineering functions show intriguing degrees of selectivity in where they act within the genome. This selectivity appears to be chiefly related to interactions between natural genetic engineering systems and the cellular systems controlling transcription and chromatin formatting. The examples we have of target selection include the action of localized point mutagenesis, retrotransposons and DNA transposons (see 9, 10 for specific references):
Seems like (for this case), one can describe the results in terms of averages rather than having to analyze each individual bacterium. In stochastic® terms, the weak solution is sufficient.