上海生科所PLoS Genetics解析保幼激素

　　

　　3月16日，PLoS Genetics 发表了中国科学院上海生命科学研究院植物生理生态研究所研究员李胜研究组题为Methyl farnesoate plays a dual role in regulating Drosophila metamorphosis 的研究论文。

　　昆虫的变态发育受蜕皮激素（20E）和保幼激素（JH）的协同调控：20E主导幼虫蜕皮和幼虫-蛹-成虫变态；JH则在幼虫蜕皮期拮抗20E作用而维持幼虫性状，从而阻止变态提前发生。经过20多年的努力，20E信号传导途径已被基本阐明。而发现JH虽然至今已近80年，但是“JH受体”之谜和JH信号传导途径直到近几年才被揭示。甲基法尼酯（MF）是JH III的前体，较JH III少一个环氧基团。MF被认为是甲壳动物的JH，但在昆虫中是否具有JH作用一直没有定论。

　　李胜实验室长期研究JH，以果蝇和家蚕作为模式昆虫，之前在鉴定JH受体、阐明JH信号传导、剖析JH-20E互作等方面取得了一系列研究成果。研究人员结合昆虫生理生化方法和果蝇遗传学技术，证明果蝇中MF以两种形式发挥JH功能、调控果蝇的变态发育：一方面直接与JH受体Met结合诱导Kr-h1表达，另一方面在周边组织中转化为JHB3等活性更高的JH形式。推断MF作为一种古老的JH在昆虫中保持下来，但功能已经弱化，而在昆虫中不同的JH是在自然选择下逐步进化而来。

　　该研究得到了先导专项B、科技部“973”项目、自然科学基金委国家杰出青年基金和重点项目的经费支持。研究论文由博士毕业生文狄经7年辛勤研究完成，得到了University of Maryland教授王建（共同通讯作者）、University of Kentucky教授Subba R. Palli、Florida International University教授Fernando G. Noriega、University of Toronto教授Stephen S. Tobe、Queen’s University教授William G. Bendena及其团队的大力支持。

MF以两种形式发挥JH功能，调控果蝇的变态发育

原文摘要：

Methyl farnesoate plays a dual role in regulating Drosophila metamorphosis

Corpus allatum (CA) ablation results in juvenile hormone (JH) deficiency and pupal lethality in Drosophila. The fly CA produces and releases three sesquiterpenoid hormones: JH III bisepoxide (JHB3), JH III, and methyl farnesoate (MF). In the whole body extracts, MF is the most abundant sesquiterpenoid, followed by JHB3 and JH III. Knockout of JH acid methyl transferase (jhamt) did not result in lethality; it decreased biosynthesis of JHB3, but MF biosynthesis was not affected. RNAi-mediated reduction of 3-hydroxy-3-methylglutaryl CoA reductase (hmgcr) expression in the CA decreased biosynthesis and titers of the three sesquiterpenoids, resulting in partial lethality. Reducing hmgcr expression in the CA of the jhamt mutant further decreased MF titer to a very low level, and caused complete lethality. JH III, JHB3, and MF function through Met and Gce, the two JH receptors, and induce expression of Kr-h1, a JH primary-response gene. As well, a portion of MF is converted to JHB3 in the hemolymph or peripheral tissues. Topical application of JHB3, JH III, or MF precluded lethality in JH-deficient animals, but not in the Met gce double mutant. Taken together, these experiments show that MF is produced by the larval CA and released into the hemolymph, from where it exerts its anti-metamorphic effects indirectly after conversion to JHB3, as well as acting as a hormone itself through the two JH receptors, Met and Gce.