Yamamoto K, Hiramoto T, Shinagawa H, Fujiwara Y
Chem Biol Interact. 1984 Feb;48(2):145-52. doi: 10.1016/0009-2797(84)90116-9.
The induction of umuC gene expression, cell lethality, induction of W-reactivation of UV-irradiated lambda-phage and the induction of mutagenesis caused by bleomycin (Blm) were studied in Escherichia coli K-12 strains with special references to the effects of SOS repair deficiencies. (1) The umuC gene is inducible by Blm and the induction is regulated by the lexA and recA genes. (2) The lexA and recA mutants are slightly more sensitive to Blm-killing than wild-type strain. (3) The plating efficiency of UV-irradiated lambda-phage increased by Blm treatment of the host cell. This increase was not observed in the umuC mutant. The plating efficiency of UV-irradiated lambda-phage was drastically reduced in the lexA and recA strains treated with Blm. (4) No significant increase of the reversion of nonsense mutation (his-4 to His+) in AB1157 by the treatment of Blm was observed. Possible implications of these results are discussed.
以特别关注SOS修复缺陷的影响为目的，在大肠杆菌K-12菌株中研究了博来霉素（Blm）诱导umuC基因表达、细胞致死性、诱导紫外线照射的λ噬菌体W-复活以及诱变作用。（1）Blm可诱导umuC基因表达，且该诱导作用受lexA和recA基因调控。（2）lexA和recA突变体对Blm杀伤的敏感性略高于野生型菌株。（3）宿主细胞经Blm处理后，紫外线照射的λ噬菌体的平板效率提高。在umuC突变体中未观察到这种提高。在用Blm处理的lexA和recA菌株中，紫外线照射的λ噬菌体的平板效率大幅降低。（4）未观察到用Blm处理AB1157导致无义突变（his-4突变为His+）的回复率显著增加。讨论了这些结果可能的意义。
