Disturbance of the secretory pathway in Micrasterias denticulata by tunicamycin and cyclopiazonic acid
Disturbance of the secretory pathway in Micrasterias denticulata by tunicamycin and cyclopiazonic acid
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DOI：
10.1007/bf01280171
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发表时间：
1995-01-01
期刊：
影响因子：
2.9
通讯作者：
Meindl, U
中科院分区：
文献类型：
--
作者：
Hoftberger, M;Url, T;Meindl, U
衣霉素（一种蛋白质N-连接糖基化的抑制剂）和环匹阿尼酸（一种抑制ER中Ca ~（2+）依赖性ATP酶的抑制剂）都影响ER水平上的分泌途径，并导致微星藻细胞生长的停止。电子显微镜调查显示，这两种抑制剂的作用方式不同。虽然衣霉素处理导致高尔基体崩解成小泡，但cyclopiazonic acid阻止了ER提供的产物，导致ER池扩张和高尔基体池数量减少，同时丧失了高尔基体活性。衣霉素作用下细胞壁的形成受到干扰，表明微星藻细胞的正常生长需要蛋白质的N-连接糖基化。此外，我们的研究表明，细胞质游离钙浓度的变化，作为环匹阿尼酸在ER中的ATP酶抑制的结果，可能会通过中断正常的ER-网质体协会抑制壁物质分泌。
Both tunicamycin, an inhibitor of N-linked glycosylation of proteins, and cyclopiazonic acid, which inhibits the Ca2+-dependent ATPase in the ER, influence the secretory pathway al the ER level and lead to a cessation of cell growth in Micrasterias. Electron microscopical investigations reveal that the mode of action of the two inhibitors differs. While tunicamycin treatment results in a disintegration of the Golgi bodies into small vesicles, cyclopiazonic acid prevents products being supplied from the ER, resulting in the dilatation of ER cisternae and a reduction in the number of Golgi cisternae, combined with a loss of dictyosomal activity. The disturbed cell wall formation under tunicamycin indicates that N-linked glycosylation of proteins is required for normal cell growth in Micrasterias. Moreover, our studies reveal that changes in cytoplasmic free calcium concentration, as a consequence of ATPase inhibition in the ER by cyclopiazonic acid, may inhibit wall material secretion by interrupting the normal ER-dictyosome association.