A series of conserved mutations in the acetylcholinesterase (AChE) confer resistance to organophosphorous and carbamate insecticides in most arthropod pests. However, the mutations associated with the reduced sensitivity to insecticides usually resulted in the reduction of catalytic efficiency, being responsible for the fitness disadvantage. To compensate for the reduced catalytic activity, overexpression of neuronal AChE appears to be necessary, which is achieved by a relatively recent duplication of AChE gene (ace) as observed in the two-spotted spider mite and other insects. Unlike the cases of the overexpression of neuronal AChE, extensive generation of soluble AChE is observed in some insects either from a distinct non-neuronal ace locus or from a single ace locus via alternative splicing, which is induced by a chemical stress. Such a soluble AChE acts as a potential bioscavenger and provides a typical non-neuronal function of tolerance to xenobiotics, suggesting its role in chemical adaptation during evolution.

Duplication and mutation of arthropod acetylcholinesterase: Implications for the pesticide resistance and tolerance

248th National Meeting (2014)

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