Recent advances in the molecular genetics of insecticide resistance have id
entified the point mutations associated with target site insensitivity in t
he genes encoding the three major insecticide targets: the Rdl GABA recepto
r, the para voltage gated sodium channel and insect acetylcholinesterase. H
owever central questions relating to the origin, selection and fitness of t
hese mutations in natural populations remain. This review examines the exte
nt to which we understand how a specific subset of potential resistance ass
ociated mutations are selected, how often they may arise and/or recombine,
and whether we can explain any potential fitness disadvantages based on our
knowledge of the molecular mechanisms of resistance involved. (C) 1999 Els
evier Science Ltd. All rights reserved.