Blackstone N W, Green D R
Department of Biological Sciences, Northern Illinois University, DeKalb 60115, USA.
Bioessays. 1999 Jan;21(1):84-8. doi: 10.1002/(SICI)1521-1878(199901)21:1<84::AID-BIES11>3.0.CO;2-0.
In the vertebrates, programmed cell death or apoptosis frequently involves the relocalization of mitochondrial cytochrome c to the cytoplasm. This prominent role in the regulation of apoptosis is in addition to the primary function of cytochrome c in the mitochondrial electron transport chain. These seemingly divergent roles become plausible when considering the symbiotic origin of the mitochondrion. Symbiosis involves conflicts between levels of selection, in this case between the primitive host cell and the protomitochondria. In an aerobic environment, selection on the protomitochondria may have favored routine manipulations of the host cell's phenotype using products and by-products of oxidative phosphorylation, in particular reactive oxygen species (ROS). Blocking the mitochondrial electron transport chain by removing cytochrome c enhances the production of ROS; thus cytochrome c release by protomitochondria may have altered the host cell's phenotype via enhanced ROS production. Subsequently, this signaling pathway may have been refined by selection so that cytochrome c itself became the trigger for changes in the host's phenotype. A mechanism of apoptosis in metazoans may thus be a vestige of evolutionary conflicts within the eukaryotic cell.
在脊椎动物中，程序性细胞死亡或凋亡常常涉及线粒体细胞色素c重新定位到细胞质中。细胞色素c在凋亡调控中的这一突出作用，是其在线粒体电子传递链中的主要功能之外的。当考虑线粒体的共生起源时，这些看似不同的作用就变得合理了。共生涉及选择水平之间的冲突，在这种情况下是原始宿主细胞和原始线粒体之间的冲突。在有氧环境中，对原始线粒体的选择可能有利于利用氧化磷酸化的产物和副产物，特别是活性氧（ROS），对宿主细胞的表型进行常规操纵。通过去除细胞色素c来阻断线粒体电子传递链会增强ROS的产生；因此，原始线粒体释放细胞色素c可能通过增强ROS的产生改变了宿主细胞的表型。随后，这种信号通路可能通过选择得到了优化，使得细胞色素c本身成为宿主表型变化的触发因素。因此，后生动物中的凋亡机制可能是真核细胞内进化冲突的遗迹。
