Volkert M R, Hartke M A
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester 01605.
Mutat Res. 1987 Nov;184(3):181-6. doi: 10.1016/0167-8817(87)90015-0.
In recb recC sbcB mutants genetic recombination is dependent upon the recF gene. recA801, recA802 and recA803 (formerly called srfA mutations) were originally isolated as mutations that suppress recombination deficiency caused by a recF mutation in a recB recC sbcB genetic background. Since the recA801 mutation also suppressed some of the UV sensitivity due to recF143, we sought to determine what DNA-repair pathways were actually being restored by the recA801 mutation in this genetic background. In this paper we show that the suppression of recF143 by recA801 does not extend to the recF143-mediated defects in induced repair of UV-damaged phages. In addition, we show that recA801 suppresses only slightly the recF143-associated defect in induced expression of the SOS-regulated muc genes of pKM101. These results suggest that recA801 suppresses primarily the RecF pathway of recombinational repair.
在recB recC sbcB突变体中,基因重组依赖于recF基因。recA801、recA802和recA803(以前称为srfA突变)最初是作为抑制recB recC sbcB遗传背景中recF突变引起的重组缺陷的突变而分离出来的。由于recA801突变也抑制了部分由recF143导致的紫外线敏感性,我们试图确定在这种遗传背景下,recA801突变实际恢复了哪些DNA修复途径。在本文中,我们表明recA801对recF143的抑制并不延伸至recF143介导的紫外线损伤噬菌体诱导修复缺陷。此外,我们表明recA801仅轻微抑制recF143相关的pKM101 SOS调控粘基因诱导表达缺陷。这些结果表明,recA801主要抑制重组修复的RecF途径。