Volkert M R, Hartke M A
J Bacteriol. 1984 Feb;157(2):498-506. doi: 10.1128/jb.157.2.498-506.1984.
Suppressors of recF (srfA) were found by selection for resistance to mitomycin C and UV irradiation in a recB21 recC22 sbcB15 recF143 strain. srfA mutations map in recA and are dominant to srfA+. They suppress both the DNA repair and the recombination deficiencies due to recF mutations. Therefore, RecA protein which is altered by the srfA mutation can allow genetic recombination to proceed in the absence of recB, recC, and recF functions. recF is also required for induction of the SOS response after UV damage. We propose that recF+ normally functions to allow the expression of two recA activities, one that is required for the RecF pathway of recombination and another that is required for SOS induction. The two RecA activities are different and are separable by mutation since srfA mutations permit recombination to proceed but have not caused a dramatic increase in SOS induction in recF mutants. According to this hypothesis, one role for recF in DNA repair and recombination is to modulate RecA activities to allow RecA to participate in these recF-dependent processes.
通过在recB21 recC22 sbcB15 recF143菌株中筛选对丝裂霉素C和紫外线照射的抗性，发现了recF的抑制子（srfA）。srfA突变定位于recA基因，且对srfA+呈显性。它们能抑制由于recF突变导致的DNA修复和重组缺陷。因此，因srfA突变而改变的RecA蛋白能够在缺乏recB、recC和recF功能的情况下使基因重组得以进行。recF对于紫外线损伤后SOS应答的诱导也是必需的。我们提出，recF+通常发挥作用，使两种RecA活性得以表达，一种是重组的RecF途径所必需的，另一种是SOS诱导所必需的。这两种RecA活性是不同的，并且可通过突变分离，因为srfA突变允许重组进行，但并未导致recF突变体中SOS诱导的显著增加。根据这一假说，recF在DNA修复和重组中的一个作用是调节RecA活性，以使RecA能够参与这些依赖recF的过程。
