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一种依赖于染色体“超级杀手”突变进行复制的突变杀手质粒。

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

机构信息

Laboratory of Biochemical Pharmacology, National Institute of Arthritis, Metabolism and Digestive Diseases, National Institutes of Health, Bethesda, Maryand 20014.

出版信息

Genetics. 1979 Apr;91(4):673-82. doi: 10.1093/genetics/91.4.673.

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.

摘要

携带 1.5 x 10(6)分子量线状双链 RNA 于病毒样颗粒中的酵母菌株(M dsRNA,杀伤质粒或病毒)会分泌一种毒素,对不携带该质粒的菌株具有致命性。任何四个染色体基因(称为 ski1-ski4)中的隐性突变都会导致毒素活性的产生增加。我们在这里报告了一个杀伤质粒(称为 ski 依赖性 [KIL-sd])的突变,该突变使杀伤质粒的复制依赖于任何 ski 基因中的染色体突变的存在。因此,[KIL-sd]质粒从 SKI(+)菌株中丢失。当野生型杀伤质粒 [KIL-k] 被引入 ski2-2 [KIL-o]菌株时,杀伤质粒会转变为 [KIL-sd]质粒。这可能代表了 ski2-2 菌株中 [KIL-sd]变体(突变体)的特定形式的诱变或选择性复制,在正常的 [KIL-k]群体中。ski2-1 和 ski2-3 突变不会将 [KIL-k] 转化为 [KIL-sd],但 ski2-3 确实允许 [KIL-sd]质粒的维持。因此,[KIL-sd]质粒缺乏在野生型细胞中复制所需的质粒位点或产物。

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