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首页> 外文期刊>Molecular biology of the cell >Mitochondrial Outer Membrane Proteins Assist Bid in Bax-mediated Lipidic Pore Formation
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Mitochondrial Outer Membrane Proteins Assist Bid in Bax-mediated Lipidic Pore Formation

机译：线粒体外膜蛋白协助Bax介导的脂质孔形成中的出价。

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Mitochondrial outer membrane permeabilization (MOMP) is a critical step in apoptosis and is regulated by Bcl-2 family proteins. In vitro systems using cardiolipin-containing liposomes have demonstrated the key features of MOMP induced by Bax and cleaved Bid; however, the nature of the “pores” and how they are formed remain obscure. We found that mitochondrial outer membranes contained very little cardiolipin, far less than that required for liposome permeabilization, despite their responsiveness to Bcl-2 family proteins. Strikingly, the incorporation of isolated mitochondrial outer membrane (MOM) proteins into liposomes lacking cardiolipin conferred responsiveness to cleaved Bid and Bax. Cardiolipin dependence was observed only when permeabilization was induced with cleaved Bid but not with Bid or Bim BH3 peptide or oligomerized Bax. Therefore, we conclude that MOM proteins specifically assist cleaved Bid in Bax-mediated permeabilization. Cryoelectron microscopy of cardiolipin-liposomes revealed that cleaved Bid and Bax produced large round holes with diameters of 25–100 nm, suggestive of lipidic pores. In sum, we propose that activated Bax induces lipidic pore formation and that MOM proteins assist cleaved Bid in this process in the absence of cardiolipin.
机译：线粒体外膜通透性（MOMP）是细胞凋亡的关键步骤，并受Bcl-2家族蛋白的调节。使用含有心磷脂的脂质体的体外系统已经证明了Bax和裂解的Bid诱导的MOMP的关键特征。但是，“孔”的性质及其形成方式仍然不清楚。我们发现，尽管线粒体外膜对Bcl-2家族蛋白有反应性，但其心磷脂却很少，远远少于脂质体通透性所需的心磷脂。令人惊讶的是，将分离的线粒体外膜（MOM）蛋白掺入到缺乏心磷脂的脂质体中，赋予了对裂解的Bid和Bax的响应能力。仅当切割的Bid引起通透性时才观察到心磷脂依赖性，而Bid或Bim BH3肽或寡聚的Bax则不引起通心化。因此，我们得出结论，MOM蛋白在Bax介导的通透性中特异性协助切割的Bid。心磷脂脂质体的冷冻电子显微镜检查显示，裂解的Bid和Bax产生直径为25–100 nm的大圆形孔，提示存在脂质孔。总之，我们建议活化的Bax诱导脂质孔的形成，并且在没有心磷脂的情况下，MOM蛋白在此过程中有助于裂解Bid。

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