Wu Zhongxia, Guo Wei, Xie Yingtian, Zhou Shutang
From the School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.
J Biol Chem. 2016 Mar 4;291(10):5418-27. doi: 10.1074/jbc.M115.698936. Epub 2016 Jan 4.
Although juvenile hormone (JH) is known to prevent insect larval metamorphosis and stimulate adult reproduction, the molecular mechanisms of JH action in insect reproduction remain largely unknown. Earlier, we reported that the JH-receptor complex, composed of methoprene-tolerant and steroid receptor co-activator, acts on mini-chromosome maintenance (Mcm) genes Mcm4 and Mcm7 to promote DNA replication and polyploidy for the massive vitellogenin (Vg) synthesis required for egg production in the migratory locust (Guo, W., Wu, Z., Song, J., Jiang, F., Wang, Z., Deng, S., Walker, V. K., and Zhou, S. (2014) PLoS Genet. 10, e1004702). In this study we have investigated the involvement of cell-division-cycle 6 (Cdc6) in JH-dependent vitellogenesis and oogenesis, as Cdc6 is essential for the formation of prereplication complex. We demonstrate here that Cdc6 is expressed in response to JH and methoprene-tolerant, and Cdc6 transcription is directly regulated by the JH-receptor complex. Knockdown of Cdc6 inhibits polyploidization of fat body and follicle cells, resulting in the substantial reduction of Vg expression in the fat body as well as severely impaired oocyte maturation and ovarian growth. Our data indicate the involvement of Cdc6 in JH pathway and a pivotal role of Cdc6 in JH-mediated polyploidization, vitellogenesis, and oogenesis.
尽管已知保幼激素(JH)可阻止昆虫幼虫变态并刺激成虫繁殖,但JH在昆虫繁殖中的作用分子机制仍 largely未知。此前,我们报道了由耐甲氧普烯和类固醇受体共激活因子组成的JH受体复合物作用于微小染色体维持(Mcm)基因Mcm4和Mcm7,以促进DNA复制和多倍体形成,从而实现飞蝗产卵所需的大量卵黄原蛋白(Vg)合成(郭,W.,吴,Z.,宋,J.,江,F.,王,Z.,邓,S.,沃克,V.K.,和周,S.(2014年)《公共科学图书馆·遗传学》10,e1004702)。在本研究中,我们研究了细胞分裂周期6(Cdc6)在JH依赖的卵黄发生和卵子发生中的作用,因为Cdc6对于复制前复合物的形成至关重要。我们在此证明,Cdc6在JH和耐甲氧普烯的作用下表达,且Cdc6转录受JH受体复合物直接调控。敲低Cdc6会抑制脂肪体和卵泡细胞的多倍体化,导致脂肪体中Vg表达大幅降低,以及卵母细胞成熟和卵巢生长严重受损。我们的数据表明Cdc6参与JH信号通路,且在JH介导的多倍体化、卵黄发生和卵子发生中起关键作用。