Adaptation to the cost of resistance: a model of compensation, recombination, and selection in a haploid organism.
Populations of pathogenic organisms often evolve resistance in response to the use of pesticides or antibiotics. This rise of resistance may be followed by a fall when chemical control is suspended and resistance alleles carry a fitness cost. Another possibility is that mutations at secondary loci compensate for the cost, usually without loss of resistance. This enables resistant types to withstand invasion by the susceptible wild-type; resistance then persists in the population, which reduces the efficacy of future pesticide or antibiotic use. We examined a two-locus model of a haploid organism that adapts to the cost of resistance by a single compensatory mutation. We addressed the question how different combinations of cost and compensation and different levels of recombination affect the consequences of a single pesticide application. Resistance will become fixed in the population when the fraction of the population exposed to pesticide exceeds the cost of resistance. Compensatory mutations reduce the cost of resistance and therefore this threshold level of pesticide use. In the absence of pesticide, recombination promotes stability of equilibria. In the presence of pesticide, recombination accelerates the fixation of resistance and compensating alleles; recombination may also enable the persistence of compensated resistant types after pesticide use.
Wijngaarden
Pieter J
PJ
Laboratory of Genetics, Wageningen University, Arboretumlaan 4, NL-6703 BD Wageningen, The Netherlands. pieter_wijngaarden@yahoo.com
van den Bosch
Frank
F
Jeger
Michael J
MJ
Hoekstra
Rolf F
RF
D000220:Adaptation, Biological / Q000235:genetics*; D004351:Drug Resistance / Q000235:genetics*; D005828:Genetics, Population; D006238:Haploidy; D008957:Models, Genetic; D009154:Mutation / Q000235:genetics; D012641:Selection, Genetic; D013997:Time Factors