Jiangsu Key Laboratory for Microbes and Functional Genomics, College of Life Sciences, Nanjing Normal University, 1 Wen Yuan Rd, Nanjing, 210023, China.
FEMS Microbiol Lett. 2020 Oct 21;367(19). doi: 10.1093/femsle/fnaa170.
The mitochondrial genome encodes key components of the oxidative phosphorylation (OXPHOS) system, whose expression is essential for mitochondrial functions. We have previously shown that deletion of the Schizosaccharomyces pombe ppr10 encoding a pentatricopeptide repeat protein severely reduces the mature levels of intron-containing mitochondrial transcripts cox1 and cob1, and severely impairs mitochondrial translation. In this study, we examined the possibility that the reduced levels of Cox1 and Cob1 proteins in cells were due to lowered levels of cox1 and cob1 mRNAs. We found that deletion of ppr10 did not affect the levels of mature cox1 and cob1 mRNAs in a mitochondrial intronless background. However, synthesis of Cox1 and Cob1 proteins were still severely affected by deletion of ppr10 in a mitochondrial intronless background. Consistent with this, we found that deletion of mitochondrial introns could not rescue the respiratory growth defect of Δppr10 cells. Our results reveal that Ppr10 is not required for the stability of cox1 and cob1 mRNAs, and provide further support for the idea that Ppr10 plays a critical role in mitochondrial translation.
线粒体基因组编码氧化磷酸化（OXPHOS）系统的关键组成部分，其表达对于线粒体功能至关重要。我们之前已经表明，缺失编码五肽重复蛋白的裂殖酵母 ppr10 严重降低了包含内含子的线粒体转录物 cox1 和 cob1 的成熟水平，并严重损害了线粒体翻译。在这项研究中，我们研究了细胞中 Cox1 和 Cob1 蛋白水平降低是否是由于 cox1 和 cob1 mRNA 水平降低所致。我们发现，在没有线粒体内含子的背景下，ppr10 的缺失并不影响成熟 cox1 和 cob1 mRNA 的水平。然而，在没有线粒体内含子的背景下，ppr10 的缺失仍然严重影响 Cox1 和 Cob1 蛋白的合成。与此一致，我们发现线粒体内含子的缺失不能挽救 Δppr10 细胞的呼吸生长缺陷。我们的结果表明 Ppr10 不参与 cox1 和 cob1 mRNA 的稳定性，并且进一步支持 Ppr10 在线粒体翻译中起关键作用的观点。
