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首页> 外文期刊>Journal of bacteriology >Metabolic suppressors of trimethoprim and ultraviolet light sensitivities of Saccharomyces cerevisiae rad6 mutants.
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Metabolic suppressors of trimethoprim and ultraviolet light sensitivities of Saccharomyces cerevisiae rad6 mutants.

机译：甲氧苄啶的代谢抑制剂和酿酒酵母rad6突变体的紫外线敏感性。

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摘要

Dominant mutations at two newly identified loci, designated SRS1 and SRS2, that metabolically suppress the trimethoprim sensitivity of rad6 and rad18 strains, have been isolated from trimethoprim-resistant mutants arising spontaneously in rad6-1 rad18-2 strains of the yeast Saccharomyces cerevisiae. The SRS2 mutations also efficiently suppress the ultraviolet light sensitivity of the parent strains. They do not, however, suppress their sensitivity to ionizing radiation or their deficiency with respect to induced mutagenesis and sporulation. Such observations support the hypothesis that RAD6-dependent activities can be separated into two functionally distinct groups: a group of error-free repair activities that are responsible for a large amount of the radiation resistance of wild-type strains and also for their resistance to trimethoprim, and a group of error-prone activities that are responsible for induced mutagenesis and are also important in sporulation, but which account at best for only a very small amount of wild-type recovery.
机译：从两个新发现的基因位点SRS1和SRS2的显性突变，其代谢抑制了rad6和rad18菌株的甲氧苄啶敏感性，已从在啤酒酵母rad6-1 rad18-2菌株中自发产生的耐甲氧苄啶的突变体中分离出来。 SRS2突变还有效抑制了亲本菌株的紫外线敏感性。但是，它们不会抑制其对电离辐射的敏感性或在诱变和孢子形成方面的不足。这些观察结果支持以下假设，即RAD6依赖的活性可以分为两个功能上不同的组：一组无错误的修复活性，这些活性导致野生型菌株的大量辐射抗性以及它们对甲氧苄啶的抗性，以及一组容易引起错误的活动，这些活动导致诱变，并且在孢子形成中也很重要，但充其量只能解释非常少量的野生型恢复。

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