Schmidt C, Söllner T, Schweyen R J
Institut für Genetik und Mikrobiologie, Universität München, Federal Republic of Germany.
Mol Gen Genet. 1987 Nov;210(1):145-52. doi: 10.1007/BF00337771.
A mitochondrial RNA splice defect in the first intron of the COB gene (bI1) can be suppressed by a dominant nuclear mutation SUP-101. Starting with a gene bank of yeast nuclear DNA from a SUP-101 suppressor strain cloned in the YEp13 plasmid, we have isolated a recombinant plasmid which exerts a suppressor activity similar to the SUP-101 allele. The N3(2) insert of this plasmid contains an open reading frame (ORF) of 1014 bp which is transcribed to a 12 S RNA. Deletion of the 5' end of this ORF and its upstream sequences abolishes the suppressor activity. The N3(2) insert thus carries a functional gene (called MRS3) which can suppress a mitochondrial splice defect. The chromosomal equivalent of the cloned gene has been mapped to chromosome 10. Disruption of this chromosomal gene has no phenotypic effect on wild-type cells.
细胞色素b基因(bI1)第一个内含子中的线粒体RNA剪接缺陷可被显性核突变SUP - 101抑制。从克隆于YEp13质粒的SUP - 101抑制菌株的酵母核DNA基因库开始,我们分离出了一种重组质粒,其发挥的抑制活性与SUP - 101等位基因相似。该质粒的N3(2)插入片段包含一个1014 bp的开放阅读框(ORF),转录为12 S RNA。该ORF 5'端及其上游序列的缺失消除了抑制活性。因此,N3(2)插入片段携带一个功能性基因(称为MRS3),其可抑制线粒体剪接缺陷。克隆基因的染色体对应物已定位到第10号染色体。该染色体基因的破坏对野生型细胞没有表型影响。