ABSTRACT
Elevenin is a newly discovered novel neuropeptide. Knockdown of either elevenin or orphan receptor NlA42 transcript expression by RNA interference caused severe cuticle melanization in the brown planthopper (BPH). Injection of a synthetic elevenin peptide not only rescued the body color phenotype in dselevenin-pretreated individuals but also suppressed melanization of black insects grown in natural conditions. Real-time quantitative PCR results revealed that elevenin expression levels were highest in the brain and salivary gland. Immunohistochemistry analysis confirmed that a precursor peptide of elevenin was generated in the salivary gland, suggesting that the salivary gland might be an important neurosecretory tissue in addition to the brain in BPH. Furthermore, double-strand RNA-mediated silencing of elevenin and NlA42 resulted in down-regulation of arylalkylamine-N-acetyltransferase and up-regulation of tyrosine hydroxylase, whereas elevenin peptide injection resulted in up-regulation of N-ß-alanyldopamine synthase and aspartate 1-decarboxylase, indicating a complex regulation network for cuticle pigmentation. In addition, functional characterization demonstrated that NlA42 is a cognate receptor for elevenin, and couples to Gq and Gs proteins, triggering both PLC/Ca2+/PKC and AC/cAMP/PKA signaling pathways in response to elevenin treatment. These findings suggest that the elevenin signaling functions control BPH body color through the tyrosine-mediated cuticle melanism pathway.-Wang, S.-L., Wang, W.-W., Ma, Q., Shen, Z.-F., Zhang, M.-Q., Zhou, N.-M., Zhang, C.-X. Elevenin signaling modulates body color through the tyrosine-mediated cuticle melanism pathway.
Subject(s)
Hemiptera/metabolism , Insect Proteins/metabolism , Neuropeptides/metabolism , Pigmentation/genetics , Animals , Depsipeptides/pharmacology , Gene Expression Regulation/drug effects , Gene Expression Regulation, Developmental , HEK293 Cells , Hemiptera/genetics , Humans , Insect Proteins/genetics , Neuropeptides/genetics , Pigmentation/physiology , Sf9 Cells , Signal TransductionABSTRACT
Most animals are oviparous. However, the genes regulating egg shell formation remain not very clear. In this study, we found that Nilaparvata lugens Forkhead box transcription factor L2 (NlFoxL2) directly activated follicle cell protein 3C (NlFcp3C) to regulate chorion formation. NlFoxL2 and NlFcp3C had a similar expression pattern, both highly expressed in the follicular cells of female adults. Knockdown of NlFoxL2 or NlFcp3C also resulted in the same phenotypes: obesity and female infertility. RNA interference (RNAi) results suggested that NlFcp3C is a downstream gene of NlFoxL2 Furthermore, transient expression showed that NlFoxL2 could directly activate the NlFcp3C promoter. These results suggest that NlFcp3C is a direct target gene of NlFoxL2. Depletion of NlFoxL2 or NlFcp3C prevented normal chorion formation. Our results first revealed the functions of Fcp3C and FoxL2 in regulation of oocyte maturation in an oviparous animal.
