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Mss51p促进线粒体细胞色素c氧化酶亚基1(Cox1p)的合成,并与新合成的Cox1p相互作用。

Mss51p promotes mitochondrial Cox1p synthesis and interacts with newly synthesized Cox1p.

作者信息

Perez-Martinez Xochitl, Broadley Sarah A, Fox Thomas D

机构信息

Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853-2703, USA.

出版信息

EMBO J. 2003 Nov 3;22(21):5951-61. doi: 10.1093/emboj/cdg566.

Abstract

The post-transcriptional role of Mss51p in mitochondrial gene expression is of great interest since MSS51 mutations suppress the respiratory defect caused by shy1 mutations. SHY1 is a Saccharomyces cerevisiae homolog of human SURF1, which when mutated causes a cytochrome oxidase assembly defect. We found that MSS51 is required for expression of the mitochondrial reporter gene ARG8(m) when it is inserted at the COX1 locus, but not when it is at COX2 or COX3. Unlike the COX1 mRNA-specific translational activator PET309, MSS51 has at least two targets in COX1 mRNA. MSS51 acts in the untranslated regions of the COX1 mRNA, since it was required to synthesize Arg8p when ARG8(m) completely replaced the COX1 codons. MSS51 also acts on a target specified by the COX1 coding region, since it was required to translate either COX1 or COX1:: ARG8(m) coding sequences from an ectopic COX2 locus. Mss51p was found to interact physically with newly synthesized Cox1p, suggesting that it could coordinate Cox1p synthesis with insertion into the inner membrane or cytochrome oxidase assembly.

摘要

Mss51p在线粒体基因表达中的转录后作用备受关注,因为MSS51突变可抑制shy1突变导致的呼吸缺陷。SHY1是人类SURF1在酿酒酵母中的同源物,其突变会导致细胞色素氧化酶组装缺陷。我们发现,当线粒体报告基因ARG8(m)插入COX1位点时,MSS51是其表达所必需的,但当它位于COX2或COX3位点时则不是。与COX1 mRNA特异性翻译激活因子PET309不同,MSS51在COX1 mRNA中至少有两个作用靶点。MSS51在COX1 mRNA的非翻译区发挥作用,因为当ARG8(m)完全取代COX1密码子时,合成Arg8p需要MSS51。MSS51还作用于由COX1编码区指定的一个靶点,因为从异位COX2位点翻译COX1或COX1::ARG8(m)编码序列需要MSS51。研究发现Mss51p与新合成的Cox1p存在物理相互作用,这表明它可能将Cox1p的合成与插入内膜或细胞色素氧化酶组装过程协调起来。

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