首页> 美国卫生研究院文献>The Journal of Biological Chemistry >Juvenile Hormone Prevents 20-Hydroxyecdysone-induced Metamorphosis by Regulating the Phosphorylation of a Newly Identified Broad Protein
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Juvenile Hormone Prevents 20-Hydroxyecdysone-induced Metamorphosis by Regulating the Phosphorylation of a Newly Identified Broad Protein

机译:少年激素通过调节新鉴定的宽蛋白的磷酸化作用来防止20-羟基蜕皮激素诱导的变态

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摘要

The steroid hormone 20-hydroxyecdysone (20E) initiates insect molting and metamorphosis. By contrast, juvenile hormone (JH) prevents metamorphosis. However, the mechanism by which JH inhibits metamorphosis remains unclear. In this study, we propose that JH induces the phosphorylation of Broad isoform Z7 (BrZ7), a newly identified protein, to inhibit 20E-mediated metamorphosis in the lepidopteran insect Helicoverpa armigera. The knockdown of BrZ7 in larvae inhibited metamorphosis by repressing the expression of the 20E response gene. BrZ7 was weakly expressed and phosphorylated during larval growth but highly expressed and non-phosphorylated during metamorphosis. JH regulated the rapid phosphorylation of BrZ7 via a G-protein-coupled receptor-, phospholipase C-, and protein kinase C-triggered pathway. The phosphorylated BrZ7 bound to the 5′-regulatory region of calponin to regulate its expression in the JH pathway. Exogenous JH induced BrZ7 phosphorylation to prevent metamorphosis by suppressing 20E-related gene transcription. JH promoted non-phosphorylated calponin interacting with ultraspiracle protein to activate the JH pathway and antagonize the 20E pathway. This study reveals one of the possible mechanisms by which JH counteracts 20E-regulated metamorphosis by inducing the phosphorylation of BrZ7.
机译:类固醇激素20-羟基蜕皮激素(20E)启动昆虫蜕皮和变态。相比之下,少年激素(JH)可以防止变态。但是,JH抑制变态的机制仍不清楚。在这项研究中,我们建议JH诱导宽泛亚型Z7(BrZ7),一种新鉴定的蛋白质的磷酸化,以抑制鳞翅目昆虫棉铃虫Helicoverpa armigera中20E介导的变态。幼虫中BrZ7的敲低通过抑制20E反应基因的表达来抑制变态。 BrZ7在幼虫生长过程中弱表达和磷酸化,但在变态过程中高表达而没有磷酸化。 JH通过G蛋白偶联受体,磷脂酶C和蛋白激酶C触发的途径调节BrZ7的快速磷酸化。磷酸化的BrZ7结合到钙蛋白的5'调节区域,以调节其在JH途径中的表达。外源JH诱导BrZ7磷酸化,通过抑制20E相关基因的转录来防止变态。 JH促进非磷酸化钙钙蛋白与超细气管蛋白相互作用,以激活JH途径并拮抗20E途径。这项研究揭示了JH通过诱导BrZ7磷酸化来抵消20E调控的变态的一种可能机制。

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