State Key Laboratory of Microbial Technology, Shandong University, Jinan, China.
FEBS Lett. 2011 Aug 4;585(15):2507-12. doi: 10.1016/j.febslet.2011.06.034. Epub 2011 Jul 2.
Here we report that budding yeast mitochondrial DNA protects against salt stress-induced apoptosis. Yeast cells lacking mitochondrial DNA (ρ(0)) are hypersensitive to salt stress-induced apoptosis, which is mediated by mitochondrial cytochrome c release. In addition, cytochrome c expression is downregulated upon salt stress, suggesting a transcriptionally regulated, homeostatic protection mechanism. The repression of cytochrome c transcription is mediated by transcription factor Mig1. Consistently, deletion of MIG1 induces cytochrome C transcription and yields ρ(0) cells that are more sensitive to salt stress. In summary, deletion of mitochondrial function leads to salt stress-induced transcriptional deregulation of cytochrome C, causing apoptosis in yeast.
在这里，我们报告酵母线粒体 DNA 可抵御盐胁迫诱导的细胞凋亡。缺乏线粒体 DNA（ρ(0)）的酵母细胞对盐胁迫诱导的细胞凋亡高度敏感，这种凋亡是由线粒体细胞色素 c 释放所介导的。此外，盐胁迫会导致细胞色素 c 的表达下调，提示存在转录调控的、维持内稳态的保护机制。细胞色素 c 转录的抑制是由转录因子 Mig1 介导的。一致地，Mig1 的缺失会诱导细胞色素 C 的转录，导致 ρ(0)细胞对盐胁迫更为敏感。总之，线粒体功能的缺失会导致盐胁迫诱导的细胞色素 C 转录失调，从而导致酵母细胞凋亡。
