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肌抑制肽免疫反应性在烟草天蛾和家蚕中的定位,表明该肽在蜕皮和化蛹过程中起作用。

Localization of myoinhibitory peptide immunoreactivity in Manduca sexta and Bombyx mori, with indications that the peptide has a role in molting and ecdysis.

作者信息

Davis Norman T, Blackburn Michael B, Golubeva Elena G, Hildebrand John G

机构信息

Division of Neurobiology, University of Arizona, Box 210077, Tucson, AZ 85721-0077, USA.

出版信息

J Exp Biol. 2003 May;206(Pt 9):1449-60. doi: 10.1242/jeb.00234.

DOI:10.1242/jeb.00234
PMID:12654884
Abstract

For normal development of Manduca sexta larvae, the ecdysteroid titer must drop following its sudden rise at the start of the molting cycle; this sudden decline in titer may be due to myoinhibitory peptide I (MIP I), which has an inhibitory effect on the release of ecdysone by the prothoracic glands of Bombyx mori in vitro. Using an antiserum to MIP, we have demonstrated secretion of an MIP-like peptide by the epiproctodeal glands of Manduca sexta, which are located on each proctodeal nerve, just anterior to the rectum. These MIP-immunoreactive glands are also present in B. mori. In fourth-instar larvae of M. sexta, the epiproctodeal glands show a distinct cycle of synthesis and sudden release of MIP that coincides with the time of the rapid decline in ecdysteroid titer. The function of the epiproctodeal glands appears to be the timely release of MIP during the molting cycle, so as to inhibit the prothoracic glands and thus to facilitate the sudden decline in ecdysteroid titer. In addition, we have found that MIP immunoreactivity is co-localized with that of crustacean cardioactive peptide (CCAP) in the 704 interneurons; these peptides appear to be co-released at the time of ecdysis. It is known that CCAP can initiate the ecdysis motor program; our results suggest that MIP may also be involved in activating ecdysis behavior.

摘要

对于烟草天蛾幼虫的正常发育,蜕皮甾体滴度在蜕皮周期开始时突然升高后必须下降;滴度的这种突然下降可能是由于肌抑制肽I(MIP I),它在体外对家蚕前胸腺蜕皮激素的释放具有抑制作用。使用针对MIP的抗血清,我们已证明烟草天蛾的肛上腺可分泌一种MIP样肽,这些腺体位于每条直肠神经上,就在直肠前方。这些MIP免疫反应性腺体在家蚕中也存在。在烟草天蛾四龄幼虫中,肛上腺呈现出一个明显的MIP合成和突然释放周期,这与蜕皮甾体滴度快速下降的时间一致。肛上腺的功能似乎是在蜕皮周期中适时释放MIP,从而抑制前胸腺,进而促进蜕皮甾体滴度的突然下降。此外,我们发现MIP免疫反应性与甲壳类心脏活性肽(CCAP)在704个中间神经元中共定位;这些肽似乎在蜕皮时共同释放。已知CCAP可启动蜕皮运动程序;我们的结果表明MIP可能也参与激活蜕皮行为。

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