A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosis
A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosis
复制标题
DOI：
10.1016/s1534-5807(01)00116-2
复制
发表时间：
2002-01-01
影响因子：
11.8
通讯作者：
Korsmeyer, SJ
中科院分区：
文献类型：
--
作者：
Scorrano, L;Ashiya, M;Korsmeyer, SJ
在没有线粒体肿胀的情况下，细胞色素c在细胞凋亡过程中迅速完全释放的机制尚不确定。在这里，我们展示了两种不同的途径。一个介导细胞色素c在线粒体外膜的释放，另一个，在本研究中表征，负责细胞色素c储存在线粒体嵴内的重新分配。我们发现“仅bh3”分子tBID通过动员嵴中细胞色素c储存（约85%）诱导线粒体结构的显著重塑。这种重组不需要tBID的BH3结构域，并且独立于BAK，但被CsA抑制。在这个过程中，单个嵴融合，嵴与膜间隙之间的连接处被打开。
The mechanism during apoptosis by which cytochrome c is rapidly and completely released in the absence of mitochondrial swelling is uncertain. Here, we show that two distinct pathways are involved. One mediates release of cytochrome c across the outer mitochondrial membrane, and another, characterized in this study, is responsible for the redistribution of cytochrome c stored in intramitochondrial cristae. We have found that the "BH3-only" molecule tBID induces a striking remodeling of mitochondrial structure with mobilization of the cytochrome c stores (similar to85%) in cristae. This reorganization does not require tBID's BH3 domain and is independent of BAK, but is inhibited by CsA. During this process, individual cristae become fused and the junctions between the cristae and the intermembrane space are opened.