Spinosad resistance of melon thrips, Thrips palmi, is conferred by G275E mutation in α6 subunit of nicotinic acetylcholine receptor and cytochrome P450 detoxification

• Partial nAChR α6 subunit gene sequences were determined for three Thrips palmi strains.
• The G275E mutation in nAChR α6 subunit was detected in resistant strains.
• Resistance to spinosad is conferred by target insensitivity of nAChR.
• Synergism tests using PBO showed reduced resistance to spinosad in resistant strains.
• CYP450-mediated detoxification caused spinosad resistance.

To examine the resistance mechanisms of Thrips palmi against spinosad, we cloned partial nucleotide sequences of the nicotinic acetylcholine receptor α6 subunit (TPα6) gene from susceptible (OK) and resistant (TS1 and TS5) strains and compared the deduced amino acid sequences among the three strains. The OK, TS1, and TS5 strains respectively showed LC50 values of 3.4 mg/L, 2838.5 mg/L, and 6655.5 mg/L. The deduced amino acid sequence of TPα6 gene showed 96% identity with that of Frankliniella occidentalis. Comparison of the deduced amino acid sequences of TPα6 gene among the three strains showed that the TS1 and TS5 strains had a resistant amino acid, Glu, at amino acid position 275. On the other hand, a susceptible amino acid, Gly, was encoded at the corresponding amino acid position for the OK strain. The synergist, piperonyl butoxide, respectively caused 1.1-fold , 5.8-fold , and 9.0-fold decreases in the resistance ratios of the OK, TS1, and TS5 strains. These results suggest that spinosad resistance of T. palmi is conferred by reduced sensitivity of TPα6 and cytochrome P450-mediated detoxification.

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