| 19165831 |
Van Nieuwenhuyse P, Van Leeuwen T, Khajehali J, Vanholme B, Tirry L: Mutations in the mitochondrial cytochrome b of Tetranychus urticae Koch (Acari: Tetranychidae) confer cross-resistance between bifenazate and acequinocyl. Pest Manag Sci. 2009 Apr;65(4):404-12.
BACKGROUND: Resistance of Tetranychus urticae Koch to bifenazate was recently linked with mutations in the mitochondrial cytochrome b Q (o) pocket, suggesting that bifenazate acts as a Q (o) inhibitor (Q (o) I). Since these mutations might cause cross-resistance to the known acaricidal Q (o) I acequinocyl and fluacrypyrim, resistance levels and inheritance patterns were investigated in several bifenazate-susceptible and bifenazate-resistant strains with different mutations in the cd1 and ef helices aligning the Q (o) pocket. RESULTS: Cross-resistance to acequinocyl in two bifenazate-resistant strains was shown to be maternally inherited and caused by the combination of two specific mutations in the cytochrome b Q (o) pocket. Although most investigated strains were resistant to fluacrypyrim, resistance was not inherited maternally, but as a monogenic autosomal highly dominant trait. As a consequence, there was no correlation between cytochrome b genotype and fluacrypyrim resistance. CONCLUSIONS: Although there is no absolute cross-resistance between bifenazate, acequinocyl and fluacrypyrim, some bifenazate resistance mutations confer cross-resistance to acequinocyl. In the light of resistance development and management, high prudence is called for when alternating bifenazate and acequinocyl in the same crop. Maternally inherited cross-resistance between bifenazate and acequinocyl reinforces the likelihood of bifenazate acting as a mitochondrial complex III inhibitor at the Q (o) site. |
93(1,1,3,3) |