Sandler S J
Department of Molecular and Cell Biology, University of California, Berkeley, 94720.
Mol Gen Genet. 1994 Dec 15;245(6):741-9. doi: 10.1007/BF00297281.
UV-inducible sulAp expression, an indicator of the SOS response, is reduced by recF+ overexpression in vivo. Different DNA-damaging agents and amounts of RecO and RecR were tested for their effects on this phenotype. It was found that recF+ overexpression reduced sulAp expression after DNA damage by mitomycin C or nalidixic acid, recO+ and recR+ overexpression partially suppressed the reduction of UV-induced sulAp expression caused by recF+ overexpression. The requirement for ATP binding to RecF to produce the phenotype was tested by genetically altering the putative phosphate binding cleft of recF in a way that should prevent the mutant recF protein from binding ATP. It was found that a change of lysine to glutamine at codon 36 results in a mutant recF protein (RecF4115) that is unable to reduce UV-inducible sulAp expression when overproduced. It is inferred from these results that recF overexpression may reduce UV-inducible sulAp expression by a mechanism that is sensitive to the ability of RecF to bind ATP and to the levels of RecO and RecR (RecOR) in the cell, but not to the type of DNA damage per se. Models are explored that can explain how recF+ overexpression reduces UV induction of sulAp and how RecOR overproduction might suppress this phenotype.
紫外线诱导的sulAp表达是SOS反应的一个指标，在体内recF+过表达会使其降低。测试了不同的DNA损伤剂以及不同量的RecO和RecR对该表型的影响。发现recF+过表达会降低丝裂霉素C或萘啶酸造成DNA损伤后的sulAp表达，recO+和recR+过表达部分抑制了recF+过表达所导致的紫外线诱导的sulAp表达的降低。通过以一种应能阻止突变recF蛋白结合ATP的方式对recF假定的磷酸结合裂隙进行基因改造，测试了RecF结合ATP产生该表型的必要性。发现第36位密码子的赖氨酸突变为谷氨酰胺会产生一种突变recF蛋白（RecF4115），该蛋白过量表达时无法降低紫外线诱导的sulAp表达。从这些结果推断，recF过表达可能通过一种对RecF结合ATP的能力以及细胞中RecO和RecR（RecOR）水平敏感，但对DNA损伤本身类型不敏感的机制来降低紫外线诱导的sulAp表达。探讨了能够解释recF+过表达如何降低sulAp的紫外线诱导以及RecOR过量产生如何抑制该表型的模型。
