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Cytoplasmic tyrosyl-tRNA synthetase rescues the defect in mitochondrial genome maintenance caused by the nuclear mutation mgm104-1 in the yeast Saccharomyces cerevisiae.

作者信息

Guan M X

机构信息

Molecular and Population Genetics Group, Research School of Biological Sciences, The Australian National University, Canberra.

出版信息

Mol Gen Genet. 1997 Aug;255(5):525-32. doi: 10.1007/s004380050525.

Abstract

The yeast nuclear mutation mgm104-1, which leads to slow growth on glucose medium and temperature-sensitive (ts) loss of mitochondrial DNA (mtDNA), has been identified by screening a collection of temperature-sensitive mutants on glycerol medium. A nuclear gene was isolated from a genomic DNA library by complementation of the mgm104-1 allele and was found to be identical to TTS1, which encodes the cytoplasmic tyrosyl-tRNA synthetase required for cytoplasmic protein synthesis. A gene disruption in a diploid strain demonstrated that the TTS1 gene is essential for cell viability. The lack of mutations in TTS1 in the mgm104-1 mutant indicates that TTS1 and MGM104 are different genes. The ability to rescue the mgm104-1 phenotype with a single additional copy of TTS1 suggests that TTS1 has an additional function that is directly or indirectly involved in the maintenance of the mitochondrial genome.

摘要

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