Galactose-N/Gr11 inhibits AMPK phosphorylation byactivating the PI3K-AKT-PKF-ATPsignaling cascade viainsulin receptor and Gβγ

摘要

As ligands of the sugar gustatory receptors,sugars have been known to activatethe insulin/insulin-like growth factor signaling pathway;however,the precise pathways thatare 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 re-ceptor in the brown planthopper Nilaparvata lugens(Stal),and its ligand.Galactose-boundNGrl1(galactose-NIGr11)activated the-phosphatidylinositol 3-kinase(PI3K)-AKT signaling cascade via insulin receptor(InR)and Gβγin vitro.In addition,galactose-NlGr11inhibited the adenosine monophosphate-activated protein kinase(AMPK)phosphorylationby activating the AKT-phosphofructokinase(PFK)-ATP signaling cascade in vitro.Impor-tantly,the InR-PI3K-AKT-PFK-AKT signaling cascade was activated and the AMPKphosphorylation was inhibited after feeding the brown planthoppers with galactose solu-tion.Collectively,these findings confirm that NIGr1l can inhibit AMPK phosphorylationby activating the PI3K-AKT-PFK-ATP signaling cascades via both InR and GBy whenbound to galactose.Thus,our study provides novel insights into the signaling pathwaysregulated by the sugar gustatory receptors in insects.