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PMID: 17248905 Published · ppublish English Journal Article

A mutant killer plasmid whose replication depends on a chromosomal "superkiller" mutation.

Genetics ·Vol. 91 ·No. 4 ·1979-04-00 ·Pages 673-82

Toh-E A, Wickner RB

Abstract

Yeast strains carrying a 1.5 x 10(6) molecular weight linear double-stranded RNA in virus-like particles (M dsRNA, the killer plasmid or virus) secrete a toxin that is lethal to strains not carrying this plasmid. Recessive mutations in any of four chromosomal genes (called ski1-ski4) result in increased production of toxin activity. We report here a mutation of the killer plasmid (called [KIL-sd] for ski-dependent) that makes the killer plasmid dependent for its replication on the presence of a chromosomal mutation in any ski gene. Thus, the [KIL-sd] plasmid is lost from SKI(+) strains. When the wild-type killer plasmid, [KIL-k], is introduced into a ski2-2 [KIL-o] strain, the killer plasmid changes to a [KIL-sd] plasmid. This may represent a specific form of mutagenesis or selective replication in the ski2-2 strain of [KIL-sd] variants (mutants) in the normal [KIL-k] population. The ski2-1 and ski2-3 mutations do not convert [KIL-k] to [KIL-sd], but ski2-3 does allow maintenance of the [KIL-sd] plasmid. The [KIL-sd] plasmid thus lacks a plasmid site or product needed for replication in wild-type cells.

Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Toh-E A
Laboratory of Biochemical Pharmacology, National Institute of Arthritis, Metabolism and Digestive Diseases, National Institutes of Health, Bethesda, Maryand 20014.
Wickner R B
References (11)
11 references, click to expand
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Article Info
Journal
Genetics
Abbr.
Genetics
ISSN
0016-6731
Published
1979-04-00
Pages
673-82
Language
English
Region
United States
NLM ID
0374636
PMCID
PMC1216859
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