In former studies it was found that the ERV1 gene is essential for cell viability and for the biogenesis of functional mitochondria. A temperature-sensitive nuclear mutant exhibits a severe reduction in all the mitochondrial transcripts. Elimination of the gene leads to growth arrest after a few cell divisions. The putative gene product bears the characteristics of a regulatory factor since it has low expression rate and a high content of charged amino acids. In this study it is further verified that the ERV1 gene alone is responsible for the observed cellular and mitochondrial defects. The 5' region of the gene is analysed by DNA deletions and complementation studies. Expression of the gene under the control of the GAL1-10 promoter in a disruption strain of ERV1 allows a more detailed specification ot its influence on mitochondrial and cellular functions. Immediate and complete loss of mitochondrial genomes is observed after the promoter has been shut off, whereas the yeast cells are still able to grow for a limited time under these conditions. Analysis of the cells by in-vivo DNA fluorescence demonstrates a specific arrest in the cell-division cycle as the terminal phenotype. To further characterize the temperature-sensitive allele of ERV1 the mutated gene has been isolated and sequenced. A single point mutation which leads to the exchange of a single amino acid is found in the reading frame.

• PMID: 7954891
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Journal Article | Research Support, Non-U.S. Gov't

Authors

Lisowsky T

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