在Xenopus卵细胞中激活储存的Ca2+电流需要SNAP-25,而不是扩散信使
Y Yao1, A V Ferrer-Montiel, M Montal
1Department of Pharmacology, University of California, San Diego, La Jolla 92093-0647, USA.
Cell
|September 11, 1999
概括
在Xenopus卵细胞中 (Ca2+) 储存量的耗尽会触发血膜Ca2+的进入 (I(soc)). 这个过程涉及SNAP-25和可能的外细胞形成,而不是扩散信使.
科学领域:
- 细胞生物学 细胞生物学
- 离子通道生理学 离子通道生理学
- 分子信号传递是分子信号传递.
背景情况:
- (Ca2+) 信号传递对卵细胞功能至关重要.
- 储存运行的 (SOC) 进入是Ca2+流入的一个关键机制.
- 精确的调节SOC进入卵细胞的分子机制仍然不完全理解.
研究的目的:
- 为了研究 (Ca2+) 在Xenopus卵细胞中存储的 (I(soc)) 进入的机制.
- 确定Rho GTPase和SNAP-25在调节I(soc) 中的作用.
- 为了阐明I(soc) 是否通过扩散性信使或蛋白质介导的过程进行介导.
主要方法:
- 在Xenopus卵细胞中测量Ca2+电流 (I(soc)) 的补丁电生理学.
- 使用Clostridium C3转移酶对Rho GTPase活动的操纵和Rho突变的表达.
- 使用肉毒神经毒素A和SNAP-25突变体抑制与外细胞形成相关的蛋白质.
主要成果:
- 细胞内Ca2+储量的耗尽激活了I(soc) 在血上.
- I(soc) 通过Rho GTPase抑制得到增强,并通过Rho激活得到抑制.
- I(soc) 激活依赖于SNAP-25而不受brefeldin A的影响,这表明它对外细胞形成有作用.
结论:
- 施诺普斯卵细胞I ((soc) 并没有通过水性扩散信使进行介导.
- SNAP-25在激活I(soc) 中起着至关重要的作用.
- 这些发现表明,I(soc) 是通过膜通道或相关调节分子的外细胞分裂来调节的.
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