Fitness effects for Ace insecticide resistance mutations are determined by ambient temperature

Background Insect pest control programs often use periods of insecticide
treatment with intermittent breaks, to prevent fixing of mutations
conferring insecticide resistance. Such mutations are typically costly in
an insecticide free environment, and their frequency is determined by the
balance between insecticide treatment and cost of resistance. Ace, a key
gene in neuronal signaling, is a prominent target of many insecticides and
across several species three amino acid replacements (I161V, G265A and
F330Y) provide resistance against several insecticides. Because
temperature disturbs neuronal signaling homeostasis, we reasoned that the
cost of insecticide resistance could be modulated by ambient temperature.
Results Experimental evolution of a natural Drosophila simulans population
at hot and cold temperature regimes uncovered a surprisingly strong effect
of ambient temperature. In the cold temperature regime, the resistance
mutations were strongly counter selected (s= -0.055), but in a hot
environment the fitness costs of resistance mutations were reduced by
almost 50% (s=-0.031). We attribute this unexpected observation to the
advantage of the reduced enzymatic activity of resistance mutations in hot
environments. Conclusion We show that fitness costs of insecticide
resistance genes are temperature-dependent, and suggest that duration of
insecticide-free periods need to be adjusted for different climatic
regions to reflect these costs. We suggest that such environment-dependent
fitness effects may be more common than previously assumed and pose a
major challenge for modeling climate change.