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Juvenile hormone membrane signaling phosphorylates usp and thus potentiates 20-hydroxyecdysone action in Drosophila

Science Bulletin 2022年第2期67卷 186-197,M0004页

作者： Yue Gao Suning Liu Qiangqiang Jia Lixian Wu Dongwei Yuan Emma Y.Li Qili Feng Guirong Wang Subba R.Palli Jian Wang Sheng Li Guangdong Provincial Key Laboratory of Insect Developmental Biology and Applied Technology Institute of Insect Science and Technology&School of Life SciencesSouth China Normal UniversityGuangzhou 510631China Guangmeiyuan R&D Center Guangdong Provincial Key Laboratory of Insect Developmental Biology and Applied TechnologySouth China Normal UniversityMeizhou 514779China International Department The Afﬁliated High School of South China Normal UniversityGuangzhou 510631China Lingnan Guangdong Laboratory of Modern Agriculture Genome Analysis Laboratory of the Ministry of AgricultureAgricultural Genomics Institute at ShenzhenChinese Academy of Agricultural SciencesShenzhen 518120China Department of Entomology College of AgricultureFood and EnvironmentUniversity of KentuckyLexington 40546USA Department of Entomology University of MarylandCollege Park 20742USA

Juvenile hormone(JH) and 20-hydroxyecdysone(20 E) coordinately regulate development and metamorphosis in insects. Two JH intracellular receptors, methoprene-tolerant(Met) and germ-cell expressed(Gce), have been identified in the fruit fly Drosophila melanogaster. To investigate JH membrane signaling pathway without the interference from JH intracellular signaling, we characterized phosphoproteome profiles of the Met gce double mutant in the absence or presence of JH in both chronic and acute *** through a potential receptor tyrosine kinase and phospholipase C pathway, JH membrane signaling activated protein kinase C(PKC) which phosphorylated ultraspiracle(usp) at Ser35, the PKC phosphorylation site required for the maximal action of 20 E through its nuclear receptor complex Ec Rusp. The usp;mutant, in which Ser was replaced with Ala at position 35 by genome editing, showed decreased expression of Halloween genes that are responsible for ecdysone biosynthesis and thus attenuated 20 E signaling that delayed developmental timing. The usp;mutant also showed lower Yorkie activity that reduced body size. Altogether, JH membrane signaling phosphorylates usp at Ser35 and thus potentiates 20 E action that regulates the normal fly development. This study helps better understand the complex JH signaling network.

关键词： Juvenile hormone Receptor tyrosine kinase Phosphoproteomics usp 20-hydroxyecdysone action Yorkie activity

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