Mode of inheritance and biochemical mechanisms underlying lambda-cyhalothrin and bifenthrin resistance in the laboratory-selected two-spotted spider mite, Tetranychus urticae

Tetranychus urticae (Koch) (Acari: Tetrancyhidae) is one of the most economically important pests among spider mites, due to the number of hosts that it harms in agricultural fields and greenhouses, and to its remarkable ability to develop resistance to chemicals applied in a short time. Pyrethroids are among the most widely used insecticides to control this pest. In this study, the biochemical mechanisms and inheritance mode of lambda cyhalothrin and bifenthrin resistance in T. urticae were investigated. A greenhouse population (BEYDOM) of T. urticae was selected for eight cycles in the laboratory with lambda cyhalothrin and bifenthrin by a spray tower-Petri dish method using the LC90 of a standard susceptible population (GSS). After eight selection cycles, the BEYDOM population was found 18.24-fold resistant to lambda cyhalothrin and 74.23-fold resistant to bifenthrin compared with the GSS based on LC50 values. Reciprocal and backcross studies revealed that the inheritance of lambda cyhalothrin resistance was sex-linked, incompletely dominant, and was probably under the control of more than one gene at lower doses and a single gene at higher doses, while inheritance to bifenthrin resistance was autosomal and incompletely recessive and may be controlled by one gene. Biochemical and synergism experiments suggested that monooxygenases and carboxylesterase enzymes play an essential role in the resistance to these pyrethroids, whereas glutathione S-transferases were not found to have a significant effect. These results provide valuable information in terms of designing an effective resistance management strategy to retard or avoid the development of resistant T. urticae populations. •Synthetic pyrethroid resistance is a very common in T. urticae.•Inheritance of lambda-cyhalothrin resistance is sex-linked and incompletely dominant.•Inheritance to bifenthrin resistance is autosomal and incompletely recessive.•P450 MOs and esterases are the major components of resistance to the pyrethroids in T. urticae.