Chasserot-Golaz S, Vitale N, Sagot I, Delouche B, Dirrig S, Pradel L A, Henry J P, Aunis D, Bader M F
Institut National de la Santé et de la Recherche Médicale U-338, Biologie de la Communication Cellulaire, Strasbourg, France.
J Cell Biol. 1996 Jun;133(6):1217-36. doi: 10.1083/jcb.133.6.1217.
Annexin II is a Ca(2+)-dependent membrane-binding protein present in a wide variety of cells and tissues. Within cells, annexin II is found either as a 36-kD monomer (p36) or as a heterotetrameric complex (p90) coupled with the S-100-related protein, p11. Annexin II has been suggested to be involved in exocytosis as it can restore the secretory responsiveness of permeabilized chromaffin cells. By quantitative confocal immunofluorescence, immunoreplica analysis and immunoprecipitation, we show here the translocation of p36 from the cytosol to a subplasmalemmal Triton X-100 insoluble fraction in chromaffin cells following nicotinic stimulation. A synthetic peptide corresponding to the NH2-terminal domain of p36 which contains the phosphorylation sites was microinjected into individual chromaffin cells and catecholamine secretion was monitored by amperometry. This peptide blocked completely the nicotine-induced recruitment of p36 to the cell periphery and strongly inhibited exocytosis evoked by either nicotine or high K+. The light chain of annexin II, p11, was selectively expressed by adrenergic chromaffin cells, and was only present in the subplasmalemmal Triton X-100 insoluble protein fraction of both resting and stimulated cells. p11 can modify the Ca(2+)- and/or the phospholipid-binding properties of p36. We found that loss Ca2+ was required to stimulate the translocation of p36 and to trigger exocytosis in adrenergic chromaffin cells. Our findings suggest that the translocation of p36 to the subplasmalemmal region is an essential event in regulated exocytosis and support the idea that the presence of p11 in adrenergic cells may confer a higher Ca2+ affinity to the exocytotic pathway in these cells.
膜联蛋白II是一种依赖钙离子的膜结合蛋白,存在于多种细胞和组织中。在细胞内,膜联蛋白II以36-kD单体(p36)或与S-100相关蛋白p11结合的异源四聚体复合物(p90)的形式存在。由于膜联蛋白II能够恢复透化嗜铬细胞的分泌反应性,因此有人认为它参与了胞吐作用。通过定量共聚焦免疫荧光、免疫复型分析和免疫沉淀,我们在此展示了烟碱刺激后嗜铬细胞中p36从胞质溶胶向质膜下Triton X-100不溶性部分的转位。将一段对应于p36含磷酸化位点的NH2末端结构域的合成肽显微注射到单个嗜铬细胞中,并通过安培法监测儿茶酚胺的分泌。该肽完全阻断了烟碱诱导的p36向细胞周边的募集,并强烈抑制了烟碱或高钾离子诱发的胞吐作用。膜联蛋白II的轻链p11由肾上腺素能嗜铬细胞选择性表达,并且仅存在于静息和刺激细胞的质膜下Triton X-100不溶性蛋白质部分。p11可以改变p36的钙离子和/或磷脂结合特性。我们发现,在肾上腺素能嗜铬细胞中,钙离子的流失是刺激p36转位和触发胞吐作用所必需的。我们的研究结果表明,p36向质膜下区域的转位是调节性胞吐作用中的一个重要事件,并支持这样一种观点,即肾上腺素能细胞中p11的存在可能赋予这些细胞的胞吐途径更高的钙离子亲和力。