Association of novel mutations in a sodium channel gene with fluvalinate resistance in the mite, Varroa destructor

Varroa (Varroa destructor) has recently become resistant to Apistan, a pyrethroid pesticide with tau-fluvalinate as its active ingredient. In many insect pests, resistance to pyrethroid insecticides is due to reduced target-site (sodium channel) sensitivity to pyrethroids in the nervous system, a phenomenon called knockdown resistance (kdr). A number of studies showed that kdr and kdr-type resistance is a result of point mutations in the para family of sodium channel genes. To investigate the molecular mechanism of resistance to fluvalinate in varroa, we have cloned and sequenced a large cDNA fragment corresponding to segment 3 of domain II (IIS3) to segment 6 of domain IV (IVS6) of a para-homologous sodium channel gene (VmNa) from susceptible and resistant mite populations. The deduced amino acid sequence from this cDNA shares 71%, 60%, and 50% identity with the corresponding region of the para-homologous protein of the Southern cattle tick, Boophilus microplus, Drosophila melanogaster Para, and rat brain type II sodium channel α-subunit, respectively. Sequence analysis revealed that four amino acid changes, F758L in IIIS6, L826P in the linker connecting domains III and IV, 1982V in IVS5 and M1055I in IVS6, were correlated with fluvalinate resistance in both Florida and Michigan populations. Interestingly, the kdr or super-kdr (which confers much higher level resistance than kdr) mutation previously identified in insects was not detected in the resistant mites. These results support the emerging notion that distinct sodium channel gene mutations are selected in different insects and arachnids in response to pyrethroid selection.

Duke Scholars

Author Ke Dong Biology