Journal
PEST MANAGEMENT SCIENCE
Volume 65, Issue 4, Pages 404-412Publisher
JOHN WILEY & SONS LTD
DOI: 10.1002/ps.1705
Keywords
bifenazate; acequinocyl; fluacrypyrim; cytochrome b; Q(o)I; genetics; acaricide; cross-resistance
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Funding
- Special Research Fund (BOF) of Ghent University, Ghent, Belgium
- Institute for the Promotion of Innovation by Science and Technology in Flanders (IWT Vlaanderen) [IWT/SB/071454, IWT/OZM/05079]
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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. (C) 2009 Society of Chemical Industry
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