期刊
MOLECULAR BIOLOGY OF THE CELL
卷 17, 期 1, 页码 213-226出版社
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.e05-06-0585
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资金
- NATIONAL HUMAN GENOME RESEARCH INSTITUTE [R01HG002432] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM062368, T32GM007445, R01GM046803] Funding Source: NIH RePORTER
- NHGRI NIH HHS [HG02432, R01 HG002432] Funding Source: Medline
- NIGMS NIH HHS [R01 GM046803, 5T32GM07445, GM46803, T32 GM007445, GM62368, R01 GM062368] Funding Source: Medline
Unlike many other organisms, the yeast Saccharomyces cerevisiae can tolerate the loss of mitochondrial DNA (mtDNA). Although a few proteins have been identified that are required for yeast cell viability without mtDNA, the mechanism of mtDNA-independent growth is not completely understood. To probe the relationship between the mitochondrial genome and cell viability, we conducted a microarray-based, genomewide screen for mitochondrial DNA-dependent yeast mutants. Among the several genes that we discovered is MGR1, which encodes a novel subunit of the i-AAA protease complex located in the mitochondrial inner membrane. mgr1 Delta mutants retain some i-AAA protease activity, yet mitochondria lacking Mgr1p contain a misassembled i-AAA protease and are defective for turnover of mitochondrial inner membrane proteins. Our results highlight the importance of the i-AAA complex and proteolysis at the inner membrane in cells lacking mitochondrial DNA.
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