A novel mutation in mitochondrial cytochrome b conferring resistance to bifenazate in two‐spotted spider mite Tetranychus urticae Koch (Acarina: Tetranychidae)

BACKGROUND

The two‐spotted spider mite Tetranychus urticae causes significant damage to ornamental, cotton, sugarcane, and horticultural crops in Australia. It has a long history of developing resistance to many acaricides including bifenazate. A mutation in the conserved cd1‐ and ef‐helices of the Qo pocket of cytochrome b is recognized as the primary mechanism of bifenazate resistance. To investigate the resistance mechanisms against bifenazate in Australian two‐spotted spider mite we sequenced the complete mitochondrion genome of five mite strains including a susceptible and bifenazate‐resistant strain.

RESULTS

We identified a novel mutation D252N in the G126S background at cytochrome b being the cause of bifenazate resistance in a bifenazate‐resistant strain, Bram. We validated the role of this mutation combination by reciprocal crosses between a bifenazate resistant and susceptible strain. By doing these crosses we confirmed the pattern of inheritance was maternal. Also, mitochondrial heteroplasmy was not observed by single mite genotyping of the mutations in cytb in a known bifenazate‐resistant strain Bram. The phylogenetic analysis with the complete mitochondrion genome sequences revealed that Australian two‐spotted spider mite strains are closely related to the green form of T.urticae found in China.

CONCLUSIONS

The novel mutation D252N found in the cytochrome b in the G126S background was revealed to be the main cause of bifenazate resistance in the Australian T. urticae strain Bram.

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