TORC1与神经肽AST相互拮抗调控保幼激素合成的分子机制

昆虫的保幼激素（JH）是促进雌性成虫生殖的重要促性腺激素。TORC1主导的营养信号能通过提高咽侧体中JH合成促进生殖，而神经肽（AST）可抑制咽侧体中JH的合成，暗示二者在JH合成调控中起拮抗的作用，然而二者如何介导JH合成的调控机制尚不清楚。申请人已在前期研究中证明，在美洲大蠊中TORC1信号通过诱导JH合成途径关键酶基因Jhamt和Cyp15a1的表达而促进JH合成，进而促进生殖。本项目拟在原有基础上，以第一个生殖周期的美洲大蠊雌虫为研究对象：1）阐释AST是否和如何通过抑制JH合成途径关键酶基因的表达而阻遏JH生物合成；2）筛选和鉴定TORC1和AST下游调控JH合成的关键转录因子，并阐明其对JH合成酶基因的转录调控机制；3）阐明TORC1与AST相互拮抗调控JH合成的分子机制。该研究将揭示不同上游信号如何互作调控昆虫JH的合成和生殖发育的具体作用机理。

Juvenile hormone (JH) is an important gonadotrophic hormone that promotes female insect reproduction. TORC1 mediated nutritional signal promotes reproduction by increasing JH biosynthesis in corpora allata, while neuropeptide (AST) inhibits JH biosynthesis, suggesting that they play opposite roles in JH biosynthesis regulation. However, the mechanism of how they mediate JH biosynthesis transcriptional regulation remains unclear, and whether they antagonize each other in JH biosynthesis regulation remains to be clarified. The applicant has proved in previous studies that TORC1 signal can induce the expression of Jhamt and Cyp15a1, the key enzyme genes of JH synthesis pathway, to promote JH synthesis in Periplaneta americana. In this project, the female cockroaches in the first reproductive cycle will be selected as the research object: 1) to explain whether and how AST inhibits JH biosynthesis by inhibiting the expression of key enzyme genes in JH biosynthesis pathway; 2) to screen and identify the key transcription factors downstream of TORC1 and AST that regulate JH biosynthesis, and to clarify their transcriptional regulation mechanism for JH biosynthase genes; 3) to elucidate the relationship between TORC1 and AST, how they antagonize with each other to regulate JH synthesis. This study will reveal how different upstream signals interact to regulate JH biosynthesis and reproductive development in insects.