Weiss-Brummer B, Hüttenhofer A
Institut für Genetik und Mikrobiologie, Universität München, Federal Republic of Germany.
Mol Gen Genet. 1989 Jun;217(2-3):362-9. doi: 10.1007/BF02464905.
The leaky expression of the yeast mitochondrial gene oxi1, containing a framshift mutation (+1), is caused by natural frameshift suppression, as shown previously (Fox and Weiss-Brummer 1980). A drastic decrease in the natural level of frameshifting is found in the presence of the parr-454 mutation, localized at the 3' end of the 15 S rRNA gene. This mutation causes resistance to the antibiotic paromomycin in the yeast strains D273-10B and KL14-4A (Li et al. 1982; Tabak et al. 1982). The results of this study imply that in the yeast strain 777-3A this mutation alone is sufficient for restriction of the level of natural frameshifting but is insufficient to confer resistance to paromomycin. A second mutation, arising spontaneously with a frequency of 10(-4) leads, in combination with the parr-454 mutation, to full paromomycin resistance in strain 777-3A.
酵母线粒体基因oxi1存在移码突变(+1),其渗漏性表达是由自然移码抑制引起的,如先前所示(福克斯和魏斯 - 布鲁默,1980年)。在位于15 S rRNA基因3'端的parr - 454突变存在的情况下,发现移码的自然水平急剧下降。该突变导致酵母菌株D273 - 10B和KL14 - 4A对抗生素巴龙霉素产生抗性(李等人,1982年;塔巴克等人,1982年)。本研究结果表明,在酵母菌株777 - 3A中,仅这种突变就足以限制自然移码水平,但不足以赋予对巴龙霉素的抗性。另一个自发产生频率为10(-4)的突变,与parr - 454突变一起,导致菌株777 - 3A对巴龙霉素完全抗性。