Vesicular calcium regulates coat retention, fusogenicity, and size of pre-Golgi intermediates.
Vesicular calcium regulates coat retention, fusogenicity, and size of pre-Golgi intermediates.
复制标题
DOI：
10.1091/mbc.e09-10-0914
复制
发表时间：
2010-03-15
影响因子：
3.3
通讯作者：
Hay JC
中科院分区：
文献类型：
--
作者：
Bentley M;Nycz DC;Joglekar A;Fertschai I;Malli R;Graier WF;Hay JC
This study establishes a role for luminal Ca2+ in ER/Golgi transport organelles and elucidates an effector mechanism involving the EF-hand protein ALG-2 and regulation of COPII coat retention. The significance and extent of Ca2+ regulation of the biosynthetic secretory pathway have been difficult to establish, and our knowledge of regulatory relationships integrating Ca2+ with vesicle coats and function is rudimentary. Here, we investigated potential roles and mechanisms of luminal Ca2+ in the early secretory pathway. Specific depletion of luminal Ca2+ in living normal rat kidney cells using cyclopiazonic acid (CPA) resulted in the extreme expansion of vesicular tubular cluster (VTC) elements. Consistent with this, a suppressive role for vesicle-associated Ca2+ in COPII vesicle homotypic fusion was demonstrated in vitro using Ca2+ chelators. The EF-hand–containing protein apoptosis-linked gene 2 (ALG-2), previously implicated in the stabilization of sec31 at endoplasmic reticulum exit sites, inhibited COPII vesicle fusion in a Ca2+-requiring manner, suggesting that ALG-2 may be a sensor for the effects of vesicular Ca2+ on homotypic fusion. Immunoisolation established that Ca2+ chelation inhibits and ALG-2 specifically favors residual retention of the COPII outer shell protein sec31 on pre-Golgi fusion intermediates. We conclude that vesicle-associated Ca2+, acting through ALG-2, favors the retention of residual coat molecules that seem to suppress membrane fusion. We propose that in cells, these Ca2+-dependent mechanisms temporally regulate COPII vesicle interactions, VTC biogenesis, cargo sorting, and VTC maturation.
登录
查看更多内容
影响因子：
4.8
作者：
Appenzeller-Herzog, C;Roche, AC;Hauri, HP
通讯作者：
Hauri, HP
影响因子：
4
作者：
Malli R;Naghdi S;Romanin C;Graier WF
通讯作者：
Graier WF
影响因子：
2.9
作者：
GUAN, KL;DIXON, JE
通讯作者：
DIXON, JE
影响因子：
4
作者：
Hughes, Helen;Budnik, Annika;Stephens, David J.
通讯作者：
Stephens, David J.
本地化，动力学和蛋白质相互作用揭示了ER和高尔基人的不同作用。
DOI：
10.1083/jcb.141.7.1489
发表时间：
1998-06-29
期刊：
The Journal of cell biology
影响因子：
--
作者：
通讯作者：
--