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Molecular Mechanism of Rhodopsin Synthesis and Transport in Drosophila Phatoreceptor Cell.

果蝇噬菌体细胞视紫红质合成和运输的分子机制。

基本信息

批准号：
05640766
负责人：
OZAKI Koichi
金额：
$ 1.34万
依托单位：
Osaka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1993
资助国家：
日本
起止时间：
1993 至 1994
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-05640766/
关键词：
Drosophia Visual Pigment Rhodopsin Vesicle Transport Sorting Retinal Glycosylation Rab 光受容視細胞 rab

项目摘要

In order to elucidate the molecular mechanism of rhodopsin synthesis and transport in the Drosophila photoreceptor cells, investigations were carried out with special reference to the following points : (1) importance of molecular conformation of opsin, (2) identification of Drosophila Rab proteteins, and (3) interaction between opsin transport and signal transduction system. The present research then elucidated that : (1) when normal forlding of opsin molecule was prohibited by the amino acid substitution of opsin or chromophore starvation, processing of the glycosylated opsin (immature form of opsin) was inhibited, and opsin bearing large (highmannose) oligosaccharide chain was accumulated. Both in vitro and in vivo experiments indicated that single oligosaccharide chain was attached at the N-terminal region of opsin immediately after translation. The sugar chain was essential to stabilize the immature opsin, but must be processed before forming a functional rhodopsin. (2) Carotenoid deprivation affected the transcription of drosophila Rab genes. In this study, 14 kinds of Rab proteins were identified in the Drosophila retinal. Four of them (including one novel member of Rab) showed carotenoid-depandent mRNA expression. Since the similar regulation of Rab expression with carotenoid was also found in the brain, this regulation may run widely in the nervous system. (3) Retinal degeneration caused by the irradiation with strong light was resulted from the inhibition of opsin synthesis, as well as abnormal invagination of microvillar membrane into cytosol. The inhibition of opsin syntheisi was caused by blocking of opsin transport from rER to microvillar membrane, which was induced by the hyper-activation of phototransduction system. Based upon these results, a rough model for opsin synthesis was constructed.

为了阐明果蝇光感受器细胞视紫红质合成和转运的分子机制，本文从以下几个方面进行了研究：(1)视紫质分子构象的重要性；(2)果蝇视紫红质蛋白的鉴定；(3)视紫红质转运与信号转导系统的相互作用。本研究进一步阐明：(1)当视蛋白的氨基酸取代或发色团饥饿抑制视蛋白分子的正常构筑时，糖基化视蛋白(视蛋白的未成熟形式)的加工被抑制，并积聚含有大(高甘露糖)寡糖链的视蛋白。体外和体内实验均表明，视蛋白翻译后的N-末端立即连接了单链低聚糖。糖链对稳定未成熟的视黄素是必不可少的，但在形成功能性视紫红质之前必须进行加工。(2)类胡萝卜素剥夺影响果蝇Rab基因的转录。在本研究中，在果蝇视网膜中鉴定了14种Rab蛋白。其中4个(包括1个Rab新成员)显示类胡萝卜素依赖的mRNA表达。由于类胡萝卜素对Rab表达的类似调节也在大脑中发现，这种调节可能在神经系统中广泛存在。(3)强光照射引起的视网膜变性是由于视素合成受到抑制，微绒毛膜异常内陷胞浆所致。视素合成的抑制是由于光传导系统的过度激活导致视素从RER到微绒毛膜的运输受阻所致。在此基础上，建立了一个粗略的视蛋白合成模型。