DELETION OF MITOCHONDRIAL DNA BYPASSING A CHROMOSOMAL GENE NEEDED FOR MAINTENANCE OF THE KILLER PLASMID OF YEAST
Author(s) -
Reed B. Wickner
Publication year - 1977
Publication title -
genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.792
H-Index - 246
eISSN - 1943-2631
pISSN - 0016-6731
DOI - 10.1093/genetics/87.3.441
Subject(s) - biology , plasmid , gene , mitochondrial dna , genetics , mutant , dna , mutation , extrachromosomal dna , saccharomyces cerevisiae , microbiology and biotechnology
Strains of Saccharomyces cerevisiae carrying a 1.4 × 106 dalton double-stranded (ds) RNA in virus-like particles (the killer plasmid or virus) secrete a toxin that is lethal to strains not carrying this plasmid (virus). The mak10 gene is one of 24 chromosomal genes (called pets, mak1, mak2,…) that are needed to maintain and replicate the killer plasmid. We report here isolation of spontaneous and induced mutants in which the killer plasmid is maintained and replicated in spite of a defect in the mak10 gene. The bypass (or suppressor) mutations in these strains are in the mitochondrial genome. Respiratory deficiency produced by various chromosomal pet mutations, by chloramphenicol, or by antimycin A, does not bypass the mak10-1 mutation. Several spontaneous mak10-1 killer strains have about 12-fold more of the killer plasmid ds RNA than do wild-type killers. Although the absence of mitochondrial DNA bypasses mak10-1, it does not bypass pets-1, mak1-1, mak3-1, mak4-1, mak5-1, mak6-1, mak7-1, or mak8-1.
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