V-ATPase C Acts as a Receptor for Bacillus thuringiensis Cry2Ab and Enhances Cry2Ab Toxicity to Helicoverpa armigera

Abstract

Currently, identified receptors do not fully elucidate the mechanism of action for Cry2Ab. Here, the results showed that Cry2Ab decreased HaV-ATPase C expression, and there was a confirmed interaction between them. The knockdown of HaV-ATPase C reduces Cry2Ab cytotoxicity, while its overexpression enhances it. Additionally, enhanced effects against H. armigera result from the combination of Cry2Ab and V-ATPase C. These findings demonstrate that V-ATPase C acts as a functional receptor for Cry2Ab in Helicoverpa armigera, and the synergistic interaction between them offers a promising strategy to enhance Cry2Ab toxicity.