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首页> 外文期刊>American Zoologist >Signaling pathways for ecdysteroid hormone synthesis in crustaceanY-organs
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Signaling pathways for ecdysteroid hormone synthesis in crustaceanY-organs

机译：甲壳类器官中蜕皮甾类激素合成的信号通路

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The Y-organs of crustaceans secrete steroid hormones (ecdysteroids) which are responsible for molting and regeneration. The Y-organs in turn are controlled (negatively) by the eyestalk peptide, molt-inhibiting hormone (MIH). We are exploring the signaling paths in Y-organ cells that lead to ecdysteroid generation when activated by the absence of MIH. The objective is to understand the connections between MIH-receptor occupancy and the depression of genes that express ecdysteroidogenic enzymes. MIH action is mediated by a rise in cyclic 5' adenosine monophosphate (cAMP); cGMP also is involved in some species. That a cyclic nucleotide is a central regulatory component is indicated by the following selection of results: dibutyryl cAMP, activators of adenylyl cyclase or inhibitors of cyclic nucleotide phosphodiesterase each mimic the inhibitory action of MIH. Cyclic AMP inhibits the receptor-mediated uptake of cholesterol (the obligate ecdysteroid precursor), by decreasing the number of receptor sites for the lipoprotein carrier of cholesterol. MIH via cAMP also depresses de novo protein synthesis upon which ecdysteroidogenesis depends in part. A role for cellular free calcium (Ca++) is indicated by the ability of Ca++ (or a Ca++ ionophore) to stimulate ecdysteroid production, thereby antagonizing MIH action. The mechanism involves lowering cAMP levels by enhancing phosphodiesterase activity via calmodulin, not by affecting adenylate cyclase activity. Ca++ counters the suppressive action of MIH or cAMP on protein synthesis. Consistent with the MIH-Ca++ mutual antagonism, MIH increases Ca++ efflux from Ca-45-preloaded cells. Y-Organ cells contain protein kinase C (PKC), the activation of which increases ecdysteroid production PKC activity is not affected by MIH, but is stimulated by Ca++, These and related experiments indicate that the PKC-activated increase in ecdysteroidogenesis involves events downstream from the production of cAMP and the degradation of cAMP by Ca++. In relation to the latter, specific and non-specific inhibitors of protein tyrosine kinases (PTK) inhibit ecdysteroid synthesis dose-dependently. The relationship of PTK with MIH-cAMP and Ca++-PKC;C systems is under study.
机译：甲壳类动物的Y器官分泌类固醇激素（蜕皮类固醇），它们负责蜕皮和再生。反过来，Y器官由视线肽，抑制蜕皮的激素（MIH）控制。我们正在探索Y器官细胞中的信号通路，当缺少MIH时，这些信号通路会导致蜕皮类固醇生成。目的是了解MIH受体占用与表达蜕皮甾类生成酶的基因抑制之间的联系。 MIH作用是由环状5'腺苷单磷酸（cAMP）的增加介导的; cGMP也与某些物种有关。下列结果选择表明环状核苷酸是一个中心调节成分：二丁酰基cAMP，腺苷酸环化酶激活剂或环状核苷酸磷酸二酯酶抑制剂均模拟MIH的抑制作用。环状AMP通过减少胆固醇脂蛋白载体的受体位点数量来抑制受体介导的胆固醇（专性蜕皮甾类前体）摄取。通过cAMP的MIH还抑制了蜕皮甾类生成部分依赖的从头蛋白质合成。 Ca ++（或Ca ++离子载体）刺激蜕皮类固醇生成（从而拮抗MIH作用）的能力表明了细胞游离钙（Ca ++）的作用。该机制涉及通过钙调蛋白增强磷酸二酯酶活性而不是通过影响腺苷酸环化酶活性来降低cAMP水平。 Ca ++抵消了MIH或cAMP对蛋白质合成的抑制作用。与MIH-Ca ++的相互拮抗作用一致，MIH可增加Ca-45预载细胞的Ca ++外排。 Y-器官细胞包含蛋白激酶C（PKC），其激活增加蜕皮类固醇的产生PKC活性不受MIH的影响，但受Ca ++刺激。这些及相关实验表明，PKC激活的蜕皮类固醇生成的增加涉及下游的事件Ca ++产生cAMP和降解cAMP。关于后者，蛋白酪氨酸激酶（PTK）的特异性和非特异性抑制剂可剂量依赖性地抑制蜕皮甾类合成。 PTK与MIH-cAMP和Ca ++-PKC; C系统的关系正在研究中。

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