Molecular mechanisms of resistance to spirodiclofen and spiromesifen in Tetranychus urticae

Abstract

Ketoenol acaricides have been widely used to control Tetranychus urticae populations across the world. However, control failure due to resistance development is an increasing concern. To sustain resistance management, it is therefore important to understand the molecular mechanisms underlying resistance, as well as understand the level of cross-resistance they convey between different ketoenol acaricides, such as spirodiclofen or spiromesifen. A T. urticae population with moderate levels of resistance to ketoenols was collected from a carnation greenhouse and further selected in the laboratory with spirodiclofen and spiromesifen, separately, until high levels of resistance were achieved. Synergism assays indicated the involvement of P450 monooxygenases and, to a lesser extent, carboxyl/cholinesterases in resistance. Genome-wide gene expression analysis of ketoenol-selected populations compared to the initial field-collected population and a susceptible reference laboratory population further supported the hypothesis of P450-mediated resistance to ketoenols. In addition to metabolic resistance, target-site resistance was also investigated, but no amino acid substitutions in the carboxyl-transferase (CT) domain of the acetyl-CoA carboxylase (ACCase), the target-site of ketoenols, were found in the studied populations. However, increased expression of ACCase was found in the spiromesifen-selected, but not in the spirodiclofen-selected population. Finally, changes in resistance levels of some commonly used acaricides were identified after selection with spiromesifen or spirodiclofen.