Abstract：
DEAD-box helicases are important players in mitochondrial gene expression, which is necessary for mitochondrial respiration. In this study, we characterized Schizosaccharomyces pombe Mss116 (spMss116), a member of the family of DEAD-box RNA helicases. Deletion of spmss116 in a mitochondrial intron-containing background significantly reduced the levels of mitochondrial DNA (mtDNA)-encoded cox1 and cob1 mRNAs and impaired mitochondrial translation, leading to a severe respiratory defect and a loss of cell viability during stationary phase. Deletion of mitochondrial introns restored the levels of cox1 and cob1 mRNAs to wide-type (WT) levels but could not restore mitochondrial translation and respiration in Δspmss116 cells. Furthermore, deletion of spmss116 in both mitochondrial intron-containing and intronless backgrounds impaired mitoribosome assembly and destabilization of mitoribosomal proteins. Our findings suggest that defective mitochondrial translation caused by deletion of spmss116 is most likely due to impaired mitoribosome assembly.
摘要：
DEAD-box解旋酶是线粒体基因表达的重要参与者,这是线粒体呼吸所必需的。在这项研究中,我们表征了裂殖酵母PombeMss116（spMss116），DEAD-boxRNA解旋酶家族的成员。在含有线粒体内含子的背景中缺失spmss116显着降低了线粒体DNA（mtDNA）编码的cox1和cob1mRNA的水平，并损害了线粒体翻译，导致严重的呼吸缺陷和静止期细胞活力的丧失。线粒体内含子的缺失将cox1和cob1mRNA的水平恢复到宽型（WT）水平，但无法恢复Δspmss116细胞的线粒体翻译和呼吸。此外，线粒体内含子和无内含子背景中spmss116的缺失损害了线粒体体组装和线粒体蛋白的不稳定。我们的发现表明，由spmss116缺失引起的线粒体翻译缺陷很可能是由于线粒体组装受损。
