Whitby M C, Lloyd R G
Department of Genetics, University of Nottingham, Queens Medical Centre, UK.
Mol Gen Genet. 1995 Jan 20;246(2):174-9. doi: 10.1007/BF00294680.
The SOS system of Escherichia coli aids survival following damage to DNA by promoting DNA repair while cell division is delayed. Induction of the SOS response is dependent on RecA and also on the product of recF. We show that normal induction also requires the products of recO and recR. SOS induction was monitored using a sfiA-lacZ fusion strain. Induction was delayed to a similar degree by mutation in recF, recO or recR. A similar effect was observed following overexpression of RecR from a recombinant recR+ plasmid. We show that the overexpression of RecR also reduces the UV resistance of a recBC sbcBC strain and of a sfiA strain, but not of a rec+sfiA+ strain. The implications of these data for the kinetics of DNA repair are discussed.
大肠杆菌的SOS系统通过促进DNA修复来帮助细胞在DNA受损后存活，同时细胞分裂会延迟。SOS反应的诱导依赖于RecA以及recF的产物。我们发现正常诱导还需要recO和recR的产物。使用sfiA-lacZ融合菌株监测SOS诱导。recF、recO或recR的突变会使诱导延迟到相似程度。从重组recR⁺质粒过表达RecR后也观察到类似效果。我们发现RecR的过表达还会降低recBC sbcBC菌株和sfiA菌株的紫外线抗性，但不会降低rec⁺sfiA⁺菌株的紫外线抗性。本文讨论了这些数据对DNA修复动力学的影响。
