1) Genetically variable bacteria are attacked by an antibiotic which kills off all but one gene type which is resistant to it. This type then proliferates and becomes a new headache for the human race who have been trying to get rid of the whole species for some time now. What happens? The program calls this an example of evolution. What it is, and Mark24 acknowledged this, is merely natural selection working in pre-existing genetic types.
This may well be the case in the wild but it is possible to perform similar selection for antibiotic resistance artificially on a population grown from a single bacterium which is known not to have antibiotic resistance. Fora an example see...
Evolution of drug resistance in experimental populations of Candida albicans.Cowen LE, Sanglard D, Calabrese D, Sirjusingh C, Anderson JB, Kohn LM.
J Bacteriol. 2000 Mar;182(6):1515-22.
Adaptation to inhibitory concentrations of the antifungal agent fluconazole was monitored in replicated experimental populations founded from a single, drug-sensitive cell of the yeast Candida albicans and reared over 330 generations. The concentration of fluconazole was maintained at twice the MIC in six populations; no fluconazole was added to another six populations. All six replicate populations grown with fluconazole adapted to the presence of drug as indicated by an increase in MIC; none of the six populations grown without fluconazole showed any change in MIC. In all populations evolved with drug, increased fluconazole resistance was accompanied by increased resistance to ketoconazole and itraconazole; these populations contained ergosterol in their cell membranes and were amphotericin sensitive. The increase in fluconazole MIC in the six populations evolved with drug followed different trajectories, and these populations achieved different levels of resistance, with distinct overexpression patterns of four genes involved in azole resistance: the ATP-binding cassette transporter genes, CDR1 and CDR2; the gene encoding the target enzyme of the azoles in the ergosterol biosynthetic pathway, ERG11; and the major facilitator gene, MDR1. Selective sweeps in these populations were accompanied by additional genomic changes with no known relationship to drug resistance: loss of heterozygosity in two of the five marker genes assayed and alterations in DNA fingerprints and electrophoretic karyotypes. These results show that chance, in the form of mutations that confer an adaptive advantage, is a determinant in the evolution of azole drug resistance in experimental populations of C. albicans.
It also depends upon what definition of evolution you are working under, if you are simply thinking in terms of changes in allelic frequency then selection on 'pre-existent'variation is a perfectly legitimate example of evolution. You are obviously thinking of evolution as something generating novelty, but even with that point of view the experimental evidence shows that antibiotic resistance can arise as a novel mutation in a non-resistant population.
What is very important is not to make the mistaken assumption that this is neccessarily being put forward as a response to the antibiotic. Even in the experiment I referenced the antibiotic is added after the single progenitor has expanded over many generations, to introduce variation to the population, before the antibiotic is introduced. Depending on the type of antibiotic it is certainly not impossible for resistance to arise de-novo in the presence of the antibiotic, but such a demonstration is not required to show evolution in action.
The genetic capacity for a poison type was already present in the species, but natural selection brought it out in response to environmental threat.
This is a tricksy statement, from an evolutionary perspective simply using DNA as its genetic material is sufficient to produce the 'genetic capacity' for poison no matter what the species.
TTFN,
WK
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