Galactose-NlGr11 inhibits AMPK phosphorylation by activating the PI3K-AKT-PKF-ATP signaling cascade via insulin receptor and Gβγ.

Abstract

As ligands of the sugar gustatory receptors, sugars have been known to activate the insulin/insulin-like growth factor signaling pathway; however, the precise pathways that are activated by the sugar-bound gustatory receptors in insects remain unclear. In this study, we aimed to investigate the signaling cascades activated by NlGr11, a sugar gustatory receptor in the brown planthopper Nilaparvata lugens (Stål), and its ligand. Galactose-bound NlGr11 (galactose-NlGr11) activated the -phosphatidylinositol 3-kinase (PI3K)-AKT signaling cascade via insulin receptor (InR) and Gβγ in vitro. In addition, galactose-NlGr11 inhibited the adenosine monophosphate-activated protein kinase (AMPK) phosphorylation by activating the AKT-phosphofructokinase (PFK)-ATP signaling cascade in vitro. Importantly, the InR-PI3K-AKT-PFK-AKT signaling cascade was activated and the AMPK phosphorylation was inhibited after feeding the brown planthoppers with galactose solution. Collectively, these findings confirm that NlGr11 can inhibit AMPK phosphorylation by activating the PI3K-AKT-PFK-ATP signaling cascades via both InR and Gβγ when bound to galactose. Thus, our study provides novel insights into the signaling pathways regulated by the sugar gustatory receptors in insects.