Pyridaben resistance, inheritance and target site mutations in Neoseiulus californicus (McGregor) (Acari: Phytoseiidae)

The predatory mite Neoseiulus californicus (McGregor) (Acari: Phytoseiidae) is a key natural enemy applied in phytophagous mite control in agricultural production areas. This study is aimed at investigating the development of pyridaben resistance as a result of the selection pressure under laboratory conditions on N. californicus mites, the inheritance of pyridaben resistance in this predatory mite, and the relationship of resistance with target region mutations. Pyridaben resistance levels were evaluated using a leaf disc spraying tower method. As a result of seven selections, 270-fold pyridaben resistance was identified in N. californicus. As a result of inheritance studies, pyridaben resistance in F1 females resulted from incomplete dominance and sex. Neoseiulus californicus was resistant to pyridaben and there was no significant difference in the monooxygenase enzyme levels in respect to the initial population. No amino acid changes were detected in the PCR evaluations of target site mutations in the pyridaben-resistant and initial populations of N. californicus. Increased pyridaben resistance in the selected population was thought to be caused by more mechanisms other than target site mutations.

Automated summary

This study investigates the development of pyridaben resistance in the predatory mite N. californicus, the inheritance of this resistance, and its association with target region mutations. The researchers found that after seven selections, N. californicus exhibited a 270-fold increase in pyridaben resistance. Inheritance studies revealed that pyridaben resistance in F1 females was due to incomplete dominance and sex. The mites resistant to pyridaben did not show significant differences in monooxygenase enzyme levels compared to the initial population. No amino acid changes were detected in the target site mutations of pyridaben-resistant N. californicus populations. The researchers suggest that the increased pyridaben resistance may be caused by mechanisms other than target site mutations.