Mentors: Funmilayo Egunjobi, Milena Jankowska Ph.D.
P.I.: Ke Dong Ph.D.
Pyrethroid insecticides are synthetic versions of the naturally occurring insecticide pyrethrum, which is found in Chrysanthemum species. They target voltage-gated sodium channels (VGSCs), prolonging the opening and inhibiting the closing of the channels in excitable cells. The continuous depolarization of the cells causes paralysis and death and is known as the knockdown mechanism. The continuous use of pyrethroids has resulted in mutations in the VGSC gene reducing the sensitivity of the channels to pyrethroids. This mechanism of pyrethroid resistance is known as knockdown resistance. Functional studies of VGSC mutations have been made possible through heterologous expression of channels in Xenopus oocytes (frog egg cells). Several VGSC mutations, conferring pyrethroid resistance in Xenopus oocytes, have been identified; however, this study focuses on the mutation F174I. We hypothesize that mutation F174I induces pyrethroid insensitivity in the oocytes. We compare wild-type clones to mutated clones of insect sodium channels using Xenopus oocytes expression system. Electrophysiological techniques are used to record the sodium currents from both the wild-type and mutated clones before and after they are exposed to pyrethroids.
