酵母菌 DEAD-box 蛋白 Mss116 是 mitoribosome 组装和线粒体翻译的必需蛋白

IF 3.9 3区 生物学 Q2 CELL BIOLOGY
Yirong Wang, Gang Feng, Ying Huang
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引用次数: 0

摘要

DEAD-box 螺旋酶是线粒体基因表达的重要参与者,而线粒体基因表达是线粒体呼吸所必需的。在这项研究中,我们对 DEAD-box RNA 螺旋酶家族的成员 Schizosaccharomyces pombe Mss116(spMss116)进行了鉴定。在含有线粒体内含子的背景中缺失 spmss116 会显著降低线粒体 DNA(mtDNA)编码的 cox1 和 cob1 mRNA 的水平,并损害线粒体翻译,从而导致严重的呼吸缺陷和静止期细胞活力的丧失。删除线粒体内含子可将 cox1 和 cob1 mRNA 的水平恢复到宽型(WT)水平,但不能恢复 Δspmss116 细胞的线粒体翻译和呼吸。此外,在含线粒体内含子和无内含子背景中缺失 spmss116 会损害线粒体的组装和线粒体蛋白的不稳定性。我们的研究结果表明,缺失 spmss116 导致的线粒体翻译缺陷很可能是由于 mitoribosome 组装受损所致。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Schizosaccharomyces pombe DEAD-box protein Mss116 is required for mitoribosome assembly and mitochondrial translation

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.

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来源期刊
Mitochondrion
Mitochondrion 生物-细胞生物学
CiteScore
9.40
自引率
4.50%
发文量
86
审稿时长
13.6 weeks
期刊介绍: Mitochondrion is a definitive, high profile, peer-reviewed international research journal. The scope of Mitochondrion is broad, reporting on basic science of mitochondria from all organisms and from basic research to pathology and clinical aspects of mitochondrial diseases. The journal welcomes original contributions from investigators working in diverse sub-disciplines such as evolution, biophysics, biochemistry, molecular and cell biology, genetics, pharmacology, toxicology, forensic science, programmed cell death, aging, cancer and clinical features of mitochondrial diseases.
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