Rothman R H, Margossian L J, Clark A J
Mol Gen Genet. 1979 Feb 1;169(3):279-87. doi: 10.1007/BF00382274.
W-reactivation is reduced by recF143 and recF144 mutations and is undetectable if a second mutation at either the uvrA or uvrB locus is combined with recF143. The uvrA and uvrB mutations alone block W-reactivation partially. A recL152 mutation also partially blocks W-reactivation by itself. In combination with a uvrB5 mutation, recL125 blocks W-reactivation completely but in combination with recF143, significant residual W-reactivation ability remains. We suggest that the phenomenon of W-reactivation is the result of at least two modes or pathways. The observation that recF143 uvrB5 and recF143 uvrA6 strains permit normal levels of mutagenesis (Kato et al., 1977) but completely block all W-reactivation leads us to suggest further that the mechanism(s) of W-reactivation is at least partly different from that of UV mutagenesis.
recF143和recF144突变可降低W再活化，若uvrA或uvrB位点的第二个突变与recF143组合，则无法检测到W再活化。单独的uvrA和uvrB突变会部分阻断W再活化。recL152突变自身也会部分阻断W再活化。与uvrB5突变组合时，recL125会完全阻断W再活化，但与recF143组合时，仍存在显著的残余W再活化能力。我们认为W再活化现象是至少两种模式或途径的结果。recF143 uvrB5和recF143 uvrA6菌株允许正常水平的诱变（加藤等人，1977年）但完全阻断所有W再活化，这一观察结果使我们进一步认为，W再活化的机制至少部分不同于紫外线诱变的机制。
