Esposti M D, Erler J T, Hickman J A, Dive C
Cancer Research Campaign Molecular Pharmacology Group, School of Biological Sciences, University of Manchester, Manchester M13 9PT, United Kingdom.
Mol Cell Biol. 2001 Nov;21(21):7268-76. doi: 10.1128/MCB.21.21.7268-7276.2001.
Bid is an abundant proapoptotic protein of the Bcl-2 family that is crucial for the induction of death receptor-mediated apoptosis in primary tissues such as liver. Bid action has been proposed to involve the relocation of its truncated form, tBid, to mitochondria to facilitate the release of apoptogenic cytochrome c. The mechanism of Bid relocation to mitochondria was unclear. We report here novel biochemical evidence indicating that Bid has lipid transfer activity between mitochondria and other intracellular membranes, thereby explaining its dynamic relocation to mitochondria. First, physiological concentrations of phospholipids such as phosphatidic acid and phosphatidylglycerol induced an accumulation of full-length Bid in mitochondria when incubated with light membranes enriched in endoplasmic reticulum. Secondly, native and recombinant Bid, as well as tBid, displayed lipid transfer activity under the same conditions and at the same nanomolar concentrations leading to mitochondrial relocation and release of cytochrome c. Thus, Bid is likely to be involved in the transport and recycling of mitochondrial phospholipids. We discuss how this new role of Bid may relate to its proapoptotic action.
Bid是Bcl-2家族中一种丰富的促凋亡蛋白,对诱导肝脏等原代组织中死亡受体介导的细胞凋亡至关重要。Bid的作用被认为涉及其截短形式tBid转移至线粒体,以促进凋亡细胞色素c的释放。Bid转移至线粒体的机制尚不清楚。我们在此报告新的生化证据,表明Bid在线粒体与其他细胞内膜之间具有脂质转移活性,从而解释了其向线粒体的动态转移。首先,当与富含内质网的轻膜一起孵育时,生理浓度的磷脂(如磷脂酸和磷脂酰甘油)会诱导全长Bid在线粒体中积累。其次,天然Bid和重组Bid以及tBid在相同条件下和相同纳摩尔浓度下均表现出脂质转移活性,导致线粒体转移和细胞色素c的释放。因此,Bid可能参与线粒体磷脂的运输和循环利用。我们讨论了Bid的这一新作用可能与其促凋亡作用有何关联。