Evolutionary succession of pyrethroid resistance mutations in a sodium channel of Heliothis virescens F

Abstract

Evolution of new adaptations in response to novel environmental selection pressures is often associated with negative pleiotropic costs. Fitness costs may be ameliorated by further evolutionary processes if selection pressure is maintained. Modifier mutations that ameliorate the fitness costs of resistance mutation may arise. Alternatively, resistance mutations that incur lower fitness costs at the same locus or other loci will replace the resistance mutations with high fitness costs. Taylor and Feyereisen (1996) proposed a hypothesis of genetic "succession" for such a mechanism in the evolution of resistance to toxins. Numerous disruptive mutations in the target of a toxin may confer resistance, but with the likelihood of high fitness costs at an early stage in the evolution of resistance. Rare specific mutation(s) with less fitness costs will replace the early resistance allele(s) at a later stage and form a genetic succession. The genetic succession hypothesis is examined in this dissertation. Theory and modeling predicts that genetic succession is likely a process involved in resistance evolution against stimulatory toxins. Thus, numerous disruptive mutations on the target site will confer resistance with high fitness costs initially, but later will be replaced by rare specific mutation(s) with lower fitness costs. Genetic succession is also investigated in the case of sodium channel mutations for pyrethroid resistance in Heliothis virescens. Three distinct resistance mutations in or near the H. virescens sodium channel gene hscp have been determined by sequence comparisons; Val 421 to Met (V421M), Leu1029 to His (L1029H), and the third factor linked to Hpy5 allele that involves neither of the mutations V421M or L1029H. Frequency changes in these mutations during the time of sampling (1990 to 1997) suggest a successional replacement of both V421M and an unknown Hpy5-linked mutation by L1029H in Louisiana H. virescens populations. Further information on relative fitness costs of the mutations is necessary before we can conclude with confidence that the apparent replacement of the V421M and Hpy5 linked resistance by L1029H H. virescens represents a genuine successional event.