Sandler S J, Clark A J
Department of Molecular and Cell Biology, University of California, Berkeley 94720.
J Bacteriol. 1994 Jun;176(12):3661-72. doi: 10.1128/jb.176.12.3661-3672.1994.
The recF, recO, and recR genes form the recFOR epistasis group for DNA repair. recF mutants are sensitive to UV irradiation and fail to properly induce the SOS response. Using plasmid derivatives that overexpress combinations of the recO+ and recR+ genes, we tested the hypothesis that high-level expression of recO+ and recR+ (recOR) in vivo will indirectly suppress the recF mutant phenotypes mentioned above. We found that overexpression of just recR+ from the plasmid will partially suppress both phenotypes. Expression of the chromosomal recO+ gene is essential for the recR+ suppression. Hence we call this RecOR suppression of recF mutant phenotypes. RecOR suppression of SOS induction is more efficient with recO+ expression from a plasmid than with recO+ expression from the chromosome. This is not true for RecOR suppression of UV sensitivity (the two are equal). Comparison of RecOR suppression with the suppression caused by recA801 and recA803 shows that RecOR suppression of UV sensitivity is more effective than recA803 suppression and that RecOR suppression of UV sensitivity, like recA801 suppression, requires recJ+. We present a model that explains the data and proposes a function for the recFOR epistasis group in the induction of the SOS response and recombinational DNA repair.
recF、recO和recR基因构成用于DNA修复的recFOR上位性组。recF突变体对紫外线照射敏感，且无法正确诱导SOS反应。利用过表达recO⁺和recR⁺基因组合的质粒衍生物，我们测试了如下假设：体内recO⁺和recR⁺（recOR）的高水平表达将间接抑制上述recF突变体表型。我们发现，仅从质粒上过表达recR⁺将部分抑制这两种表型。染色体recO⁺基因的表达对于recR⁺的抑制作用至关重要。因此，我们将此称为recF突变体表型的RecOR抑制。对于SOS诱导的RecOR抑制，来自质粒的recO⁺表达比来自染色体的recO⁺表达更有效。对于紫外线敏感性的RecOR抑制则并非如此（二者效果相同）。RecOR抑制与recA801和recA803引起的抑制作用的比较表明，RecOR对紫外线敏感性的抑制比recA803抑制更有效，并且RecOR对紫外线敏感性的抑制与recA801抑制一样，需要recJ⁺。我们提出了一个模型来解释这些数据，并提出了recFOR上位性组在SOS反应诱导和重组DNA修复中的功能。
