Rothman R H, Clark A J
Mol Gen Genet. 1977 Oct 24;155(3):267-77. doi: 10.1007/BF00272805.
The mutation recL152 leads to a reduction of excision repair as measured by an increase in the time required to close uvrA uvrB dependent incision breaks, and by a reduction of host cell reactivation ability. Postreplication repair is also delayed when measured in a uvrB5 recL152 double mutant. Such a determination could not be made using the recL152 single mutant because the excision defect led to an accumulation of breaks in the unlabeled high molecular weight DNA to which the labeled DNA synthesized after irradiation must attach in order to achieve normal high molecular weight. Further, the recL gene product seems to be required to rejoin breaks in parental strand DNA which are generated during postreplication repair, since such gaps accumulate in a recL152 uvrB5 double mutant but not in a recL+ uvrB5 single mutant. We have noticed a striking phenotypic similarity between recL152 and polA1 and suggest that recL152 is required for full in vivo activity of DNA polymerase I.
突变recL152导致切除修复减少，这可通过uvrA uvrB依赖性切口断裂闭合所需时间增加以及宿主细胞再活化能力降低来衡量。当在uvrB5 recL152双突变体中进行测量时，复制后修复也会延迟。使用recL152单突变体无法做出这样的判定，因为切除缺陷导致未标记的高分子量DNA中出现断裂积累，辐照后合成的标记DNA必须附着于此才能形成正常的高分子量。此外，recL基因产物似乎是重新连接复制后修复过程中产生的亲代链DNA断裂所必需的，因为此类缺口在recL152 uvrB5双突变体中积累，而在recL+ uvrB5单突变体中则不会。我们注意到recL152和polA1之间存在显著的表型相似性，并表明recL152是DNA聚合酶I在体内充分发挥活性所必需的。
