Vacuole membrane fusion: V0 functions after trans-SNARE pairing and is coupled to the Ca2+-releasing channel.
Vacuole membrane fusion: V0 functions after trans-SNARE pairing and is coupled to the Ca2+-releasing channel.
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DOI：
10.1083/jcb.200212004
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发表时间：
2003-07-21
期刊：
影响因子：
--
通讯作者：
Mayer A
中科院分区：
文献类型：
--
作者：
Bayer MJ;Reese C;Buhler S;Peters C;Mayer A
膜融合的孔道模型假定，完整的膜蛋白圆柱体在孔亚基构象重排后可以启动融合孔道。在酵母液泡的融合中，V-ATPase V0区段包含一个膜完整蛋白脂亚单位的中央圆柱体，形成一个跨复合体，可能类似于一些孔道模型中假设的中间体。我们测试了V0区段在空泡融合中的作用。V0在融合和质子转移中的功能可以通过突变和抑制性抗体的不同作用进行实验分离。V0亚基Vph1p的失活阻止了与质子梯度无关的末端反应阶段的融合。Δvph1突变体能够对接和跨SNAR配对，并随后释放腔内钙离子，但它们不能融合。钙释放通道似乎与V0紧密相连，因为抗体使Vph1p失活阻止了钙释放。仅在一个融合伙伴上缺失Vph1就足以严重降低融合活性。Vph1p的功能需求与V0跨复合体的形成相关，因为两者都发生在对接和钙离子释放之后。这些观察证实，V0是作用于反式SNARE配对下游的空泡融合的关键因素。
Pore models of membrane fusion postulate that cylinders of integral membrane proteins can initiate a fusion pore after conformational rearrangement of pore subunits. In the fusion of yeast vacuoles, V-ATPase V0 sectors, which contain a central cylinder of membrane integral proteolipid subunits, associate to form a transcomplex that might resemble an intermediate postulated in some pore models. We tested the role of V0 sectors in vacuole fusion. V0 functions in fusion and proton translocation could be experimentally separated via the differential effects of mutations and inhibitory antibodies. Inactivation of the V0 subunit Vph1p blocked fusion in the terminal reaction stage that is independent of a proton gradient. Δvph1 mutants were capable of docking and trans-SNARE pairing and of subsequent release of lumenal Ca2+, but they did not fuse. The Ca2+-releasing channel appears to be tightly coupled to V0 because inactivation of Vph1p by antibodies blocked Ca2+ release. Vph1 deletion on only one fusion partner sufficed to severely reduce fusion activity. The functional requirement for Vph1p correlates to V0 transcomplex formation in that both occur after docking and Ca2+ release. These observations establish V0 as a crucial factor in vacuole fusion acting downstream of trans-SNARE pairing.
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DOI：
10.1083/jcb.124.3.351
发表时间：
1994-02
期刊：
The Journal of cell biology
影响因子：
--
作者：
Cunningham KW;Fink GR
通讯作者：
Fink GR
影响因子：
11.4
作者：
Haas, A;Wickner, W
通讯作者：
Wickner, W
酵母CDC42在胞吐作用的后期发挥作用，特别是在新兴芽的极化生长过程中。
影响因子：
7.8
作者：
Adamo, JE;Moskow, JJ;Gladfelter, AS;Viterbo, D;Lew, DJ;Brennwald, PJ
通讯作者：
Brennwald, PJ
DOI：
10.1083/jcb.200204089
发表时间：
2002-08-19
期刊：
The Journal of cell biology
影响因子：
--
作者：
Eitzen G;Wang L;Thorngren N;Wickner W
通讯作者：
Wickner W
影响因子：
64.8
作者：
Fernández-Chacón, R;Königstorfer, A;Südhof, TC
通讯作者：
Südhof, TC