uvrD和recB基因参与大肠杆菌K-12 uvrB5和B/r uvrA155中不同的诱变脱氧核糖核酸修复途径。
Involvement of genes uvrD and recB in separate mutagenic deoxyribonucleic acid repair pathways in Escherichia coli K-12 uvrB5 and B/r uvrA155.
作者信息
Sargentini N J, Smith K C
出版信息
J Bacteriol. 1980 Jul;143(1):212-20. doi: 10.1128/jb.143.1.212-220.1980.
Abstract
We compared the ultraviolet radiation-induced reversion of nonsense (lacZ53) and missense (leuB19) mutations in uvrB5, uvrB5 uvrD3, uvrB5 recB21, and uvrB5 uvrD3 recB21 strains of Escherichia coli K-12. Nonsense (trpE65) reversion was also compared in similar derivatives of E. coli B/r uvrA155. The uvrD mutation reduced mutagenesis in very case, but had its main effect in cells ultraviolet irradiated with low fluences (< 0.6 J m-2). The effect of the recB mutation varied; it decreased Leu and Trp reversion, but had little effect on Lac reversion. The effect of the uvrD recB combination was a gross reduction in mutagenesis. Only in the case of Lac reversion was appreciable mutagenesis detected (at fluences > 0.3 J m-2). These results indicate that separate uvrD- and recB-controlled pathways exist for ultraviolet radiation mutagenesis.
摘要
我们比较了紫外线辐射诱导的大肠杆菌K-12的uvrB5、uvrB5 uvrD3、uvrB5 recB21和uvrB5 uvrD3 recB21菌株中无义突变（lacZ53）和错义突变（leuB19）的回复突变。还比较了大肠杆菌B/r uvrA155的类似衍生物中无义突变（trpE65）的回复突变。uvrD突变在每种情况下均降低了诱变作用，但其主要作用体现在低通量（<0.6 J m-2）紫外线照射的细胞中。recB突变的影响各不相同；它降低了Leu和Trp的回复突变，但对Lac回复突变影响很小。uvrD recB组合的作用是使诱变作用大幅降低。仅在Lac回复突变的情况下检测到明显的诱变作用（在通量>0.3 J m-2时）。这些结果表明，紫外线辐射诱变存在uvrD和recB分别控制的途径。
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