Sargentini N J, Smith K C
Carcinogenesis. 1981;2(9):863-72. doi: 10.1093/carcin/2.9.863.
The role of DNA repair genes (uvrA, uvrB, uvrD, recA, recB, lexA, and umuC) in spontaneous mutation rate per bacterium per cell division (micro) was determined for the reversion of UAA (his-4 and trpE65), UAG (lacZ53), and frameshift (trpE9777) mutations, and for the occurrence of forward mutations to valine resistance. Rich growth medium enhanced micro in a wildtype strain but not in a uvrB5 strain. In minimal growth medium, the uvrA and uvrB strains had the largest micro (1.9-6.2-fold greater than that for isogenic wild-type strains, depending on the mutation assay). The uvrB strains carrying lexA, recA, umuC, or both the uvrD and rec B mutations (in combination), i.e., mutations that inhibit error-prone DNA repair, had the lowest micro values (approximately 10-fold less than the uvrB strain). Teh recA and lexA mutations also reduced micro (by approximately 2-fold) in uvr+ strains. The genetic control of the error prone repair-dependent sector of spontaneous mutagenesis was shown to be qualitatively similar to the genetic control for u.v. radiation mutagenesis. The umuC mutation, which drastically reduced spontaneous mutagensis, had no effect on genetic recombination. It is proposed that the low level of spontaneous mutagenesis observed in the recA, lexA, umuC, and the uvrD recB strains is due to errors made during DNA replication, while the enhanced level of spontaneous mutagenesis observed in the wild type, and especially in the uvrA and uvrB strains, is due to excisable lesions that are produced in the DNA by normal metabolic reactions, and that such unexcised lesions induce mutations via error-prone DNA repair. These results are discussed in terms of their relevance to spontaneous carcinogenesis.
测定了DNA修复基因（uvrA、uvrB、uvrD、recA、recB、lexA和umuC）在每个细菌每次细胞分裂的自发突变率（微）中的作用，该作用针对UAA（his-4和trpE65）、UAG（lacZ53）和移码（trpE9777）突变的回复，以及缬氨酸抗性正向突变的发生情况。丰富的生长培养基可提高野生型菌株的微，但uvrB5菌株则不然。在基本生长培养基中，uvrA和uvrB菌株的微最大（比同基因野生型菌株大1.9至6.2倍，具体取决于突变检测方法）。携带lexA、recA、umuC或uvrD和rec B突变（组合）的uvrB菌株，即抑制易错DNA修复的突变，其微值最低（比uvrB菌株低约10倍）。recA和lexA突变也使uvr+菌株的微降低（约2倍）。自发诱变中易错修复依赖部分的遗传控制在性质上与紫外线辐射诱变的遗传控制相似。显著降低自发诱变的umuC突变对基因重组没有影响。有人提出，在recA、lexA、umuC和uvrD recB菌株中观察到的低水平自发诱变是由于DNA复制过程中产生的错误，而在野生型，尤其是uvrA和uvrB菌株中观察到的自发诱变水平升高是由于正常代谢反应在DNA中产生的可切除损伤，并且这种未切除的损伤通过易错DNA修复诱导突变。根据这些结果与自发致癌作用的相关性进行了讨论。
