Over-expression of the solute carrier gene SLC23A1 as a novel mechanism contributing to imidacloprid resistance in Nilaparvata lugens.

Solute carriers (SLCs), the largest human transmembrane transporter family regulating cellular metabolism, mediate drug resistance in mammals but remain understudied in insects. While several SLCs are known to contribute to drug resistance evolution in mammals, their functions are comparatively underexplored in insects. The brown planthopper (Nilaparvata lugens) is a major sucking mouthparts rice pest and causes severe damage to rice growth and food production in Asia. Presently, field populations of N. lugens have developed resistance to many insecticides. However, the underlying resistance mechanisms are complex and variable, and elucidating them is essential for effective management of resistant populations. In this study, we show that NlSLC23A1 overexpression confers resistance to insecticides in field N. lugens populations. Its expression is significantly induced by neonicotinoids; transgenic Drosophila melanogaster expressing NlSLC23A1 exhibit reduced neonicotinoid susceptibility. Knocking down NlSLC23A1 increases N. lugens' sensitivity to imidacloprid (but not other neonicotinoids), and imidacloprid specifically upregulates NlSLC23A1 in the pest's brain. These findings identify NlSLC23A1 as a key mediator of imidacloprid resistance, providing mechanistic insights and a potential target for pest management.