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首页> 外文期刊>Developmental biology >Short neuropeptide F (sNPF) is a stage-specific suppressor for juvenile hormone biosynthesis by corpora allata, and a critical factor for the initiation of insect metamorphosis
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Short neuropeptide F (sNPF) is a stage-specific suppressor for juvenile hormone biosynthesis by corpora allata, and a critical factor for the initiation of insect metamorphosis

机译:短神经肽F(sNPF)是一种特定阶段的抑制物,可以通过语料库生物合成幼体激素,并且是引发昆虫变态的关键因素

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Molting and metamorphosis are essential events for arthropod development, and juvenile hormone (JH) and its precursors play critical roles for these events. We examined the regulation of JH biosynthesis by the corpora allata (CA) in Bombyx mori, and found that intact brain-corpora cardiaca (CC)-CA complexes produced a smaller amount of JH than that in CC-CA complexes and CA alone throughout the 4th and 5th (last) instar stadium. The smaller amount of synthesis was due to allatostatin-C (AST-C) produced by the brain. The CC synthesized short neuropeptide F (sNPF) that also suppressed the JH synthesis, but only in day 3 4th stadium and after the last larval ecdysis. For the suppression, both peptides prevented the expression of some of the distinct JH biosynthetic enzymes in the mevalonate pathway. Allatotropin (AT) stimulated sNPF expression in the CC of day 1 5th instar stadium, not of day 3 4th; therefore the stage-specific inhibition of JH synthesis by sNPF was partly due to the stimulative action of AT on the sNPF expression besides the stage-specific expression of the sNPF receptors in the CA, the level of which was high in day 2 4th and day 0 5th instar larvae. The cessation of JH biosynthesis in the last instar larvae is a key event to initiate pupal metamorphosis, and both sNPF and AST-C are key factors in shutting down JH synthesis, along with the decline of ecdysone titer and dopamine. (C) 2014 Elsevier Inc. All rights reserved.
机译:蜕皮和变态是节肢动物发育必不可少的事件,少年激素(JH)及其前体在这些事件中起关键作用。我们检查了家蚕体内的体集(CA)对JH生物合成的调节,发现完整的脑体-心脏cardiac门(CC)-CA复合体产生的JH量要比CC-CA复合体和整个CA中单独的CA少。第4和第5(最后一个)青年体育场。较少的合成是由于大脑产生的阿托伐他汀-C(AST-C)。 CC合成了短神经肽F(sNPF),它也抑制了JH的合成,但仅在第3天第4场和最后一次幼虫蜕皮之后。为了抑制,两种肽均阻止了甲羟戊酸途径中某些截然不同的JH生物合成酶的表达。 Allatotropin(AT)在第1天第5龄体育场的CC中刺激sNPF表达,而不是第3天第4天;因此,sNPF对JH合成的阶段特异性抑制部分归因于AT对sNPF表达的刺激作用,除了CA中sNPF受体的阶段特异性表达外,其水平在第2天,第4天和第2天较高0 5龄幼虫。末龄幼虫中JH生物合成的停止是引发p变态的关键事件,并且sNPF和AST-C都是关闭JH合成的关键因素,同时蜕皮激素滴度和多巴胺的下降也是如此。 (C)2014 Elsevier Inc.保留所有权利。

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