Specificity and frequency of ultraviolet-induced reversion of an iso-1-cytochrome c ochre mutant in radiation-sensitive strains of yeast.
Specificity and frequency of ultraviolet-induced reversion of an iso-1-cytochrome c ochre mutant in radiation-sensitive strains of yeast.
复制标题
辐射敏感酵母菌株中 iso-1-细胞色素 c 赭石突变体的紫外线诱导回复的特异性和频率。
DOI：
10.1016/0022-2836(74)90134-x
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发表时间：
1974
影响因子：
5.6
通讯作者：
R. Christensen
中科院分区：
文献类型：
--
作者：
C. Lawrence;J. Stewart;F. Sherman;R. Christensen
cyc1-9（iso-1-细胞色素c结构基因的赭色等位基因）紫外线诱导回复的特定模式的基础已在辐射敏感酵母菌株中进行了检查。先前使用RAD+菌株的分析表明，紫外线诱导的23cyc1-9回复体中的21个是由UAA密码子中第一个位置的A·T到G·C的转换引起的，其余两个是由第二个位置的A·T到T·A的转换引起的（Stewartet al.，1972；Sherman＆Stewart，1974）。所有可能的碱基对取代都可以借助其他诱变剂获得。现在已经表明，这种特异性很大程度上取决于RAD6基因座的作用，因为紫外线诱导的cyc1-9回复体是通过携带therad6-1等位基因的菌株中的各种碱基对取代产生的。携带该等位基因的菌株中的诱导回复频率虽然显着高于自发频率，但远低于正常频率，并且菌株对紫外线和 X 射线的致死作用更加敏感。表型相似的rad18-2突变似乎会阻断与rad6-1相同的修复途径，对回复特异性也有一定影响，但其作用取决于其他未识别突变的存在。然而，在携带 therad1-2 等位基因的切除缺陷菌株中，特异性完全没有改变。该菌株中cyc1-9的诱导回复频率远高于正常菌株。光再激活研究表明，嘧啶二聚体是造成 RAD+、rad1 和 rad6 菌株中大部分回复体的原因。这些实验表明RAD6+基因座与易错修复密切相关，并表明切除修复基本上没有错误。
The basis for the specific pattern of ultraviolet-induced reversion ofcyc1-9, an ochre allele of the structural gene for iso-1-cytochromec, has been examined in radiation-sensitive strains of yeast. Previous analysis, usingRAD+strains, showed that 21 out of 23cyc1-9 revertants induced by ultraviolet light arose by A · T to G · C transition at the first position in the UAA codon, the remaining two occurring by A · T to T · A transversion at the second position (Stewartet al., 1972; Sherman & Stewart, 1974). All possible base-pair substitutions could be obtained with the aid of other mutagens.It has now been shown that this specificity depends largely on the action of theRAD6 locus, since ultraviolet-induced revertants ofcyc1-9 arose by a variety of base-pair substitutions in a strain carrying therad6-1 allele. Induced reversion frequencies in strains carrying this allele are much lower than normal, though significantly higher than the spontaneous frequency, and the strains are more sensitive to the lethal effects of both ultraviolet and X-irradiation. The phenotypically similarrad18-2 mutation, which appears to block the same repair pathway asrad6-1, also has some effect on the reversion specificity, but its action depends on the presence of other, unidentified, mutations. Specificity was, however, completely unaltered in an excision-defective strain carrying therad1-2 allele. Induced reversion frequency ofcyc1-9 was much higher than normal in this strain. Photoreactivation studies indicated that pyrimidine dimers were responsible for most of the revertants inRAD+, rad1 andrad6 strains. These experiments show that theRAD6+ locus is intimately concerned witherror-pronerepair, and suggest that excision repair is substantiallyerror-free.