Abstract

The cAMP/PKA intracellular signaling pathway is launched by adenylyl cyclase (AC) conversion of adenosine triphosphate (ATP) to 3', 5'-cyclic AMP (cAMP) and cAMP-dependent activation of PKA. Although this pathway is very well known in insect physiology, there is little to no information on it in some very small pest insects, such as the brown planthopper (BPH), Nilaparvata lugens Stål. BPH is a destructive pest responsible for tremendous crop losses in rice cropping systems. We are investigating the potentials of novel pest management technologies from RNA interference perspective. Based on analysis of transcriptomic data, the BPH AC like-9 gene (NlAC9) was up-regulated in post-mating females, which led us to pose the hypothesis that NlAC9 is a target gene that would lead to reduced BPH fitness and populations. Targeting NlAC9 led to substantially decreased soluble ovarian protein content, yeast-like symbiont abundance, and vitellogenin gene expression, accompanied with stunted ovarian development and body size. Eggs laid were decreased and oviposition period shortened. Taken together, our findings indicated that NlAC9 exerted pronounced effects on female fecundity, growth and longevity, which strongly supports our hypothesis.

Highlights

  • Many extracellular signals, such as hormones, peptides, biogenic amines and prostaglandins, are transduced into intracellular second messengers via G-protein coupled receptors (GPCRs)

  • Because adenylyl cyclase (AC) operates in a very wide range of cell signaling processes, including those directly involved in reproduction, we posed the hypothesis that AC9 is a target gene that would lead to reduced brown planthopper (BPH) fitness and populations

  • The dietary dsNlAC9-unmated females treatment strongly suppressed mRNA accumulations in adult females, down 34% to 68% compared to untreated controls at 1, 3, 5 and 7 days post emergence (d PE). dsGFP-unmated femalestreatments led to mRNA accumulations similar to controls

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Summary

Introduction

Many extracellular signals, such as hormones, peptides, biogenic amines and prostaglandins, are transduced into intracellular second messengers via G-protein coupled receptors (GPCRs). As the receptors bind to their specific ligands they undergo a conformational change that leads to activation of their coupled G proteins, the heterotrimeric guanine nucleotide-binding proteins. The G proteins activate any of several downstream effectors, one of which is adenylyl cyclase (AC) [1]. Activated AC converts ATP into cyclic adenosine 3’,5’-monophosphate (cAMP), which stimulates cAMP-dependent protein kinase (PKA). PKA is one of the major kinases acting in reversible protein phosphorylation mechanisms in which protein functions.

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