Abstract
Ecm10p was initially identified as a cell wall synthesis-related gene product [Genetics 147 (1997) 435] and also reported as a mitochondrial protein which was partially capable of compensating the phenotypic defect by SSC1 gene mutation [FEBS Lett. 487 (2000) 307]. Here we report that ecm10p is localized in mitochondrial nucleoids as its major component and the targeting signal resides between amino acid residues 161 and 240. Overexpression of ecm10p induces extensive mitochondrial DNA aggregations, which might be due to aberrant mitochondrial DNA cleavages through an altered endonuclease activity in mitochondrial nucleoids.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphatases / chemistry
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Cell Nucleus / metabolism
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DNA, Mitochondrial / chemistry*
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Electrophoresis, Polyacrylamide Gel
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HSP70 Heat-Shock Proteins / biosynthesis*
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HSP70 Heat-Shock Proteins / chemistry
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Heat-Shock Proteins / metabolism
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Microscopy, Fluorescence
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Mitochondria / metabolism*
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Mutation
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Phenotype
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Plasmids / metabolism
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Promoter Regions, Genetic
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Protein Structure, Tertiary
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Saccharomyces cerevisiae / metabolism
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Saccharomyces cerevisiae Proteins / biosynthesis*
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Saccharomyces cerevisiae Proteins / chemistry
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Time Factors
Substances
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DNA, Mitochondrial
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ECM10 protein, S cerevisiae
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HSP70 Heat-Shock Proteins
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Heat-Shock Proteins
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Saccharomyces cerevisiae Proteins
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Adenosine Triphosphatases