Barbé J, Vericat J A, Cairó J, Guerrero R
Mutat Res. 1985 Jul;146(1):23-32. doi: 10.1016/0167-8817(85)90051-3.
Expression of several SOS functions such as induction of lambda prophage, inhibition of cell division and induction of both umuC and recA genes after UV-irradiation, nalidixic acid or mitomycin C addition was studied in an RecBC- mutant. UV-irradiation and mitomycin C induced all SOS functions studied in the RecBC- cells but at a lower level and delayed with respect to the wild-type strain. On the contrary, nalidixic acid was unable to trigger any of these SOS functions. In the RecBC- mutant, adenine only had a stimulating effect on the amplification of RecA protein synthesis following UV-irradiation. Nevertheless, in the wild-type strain the stimulating effect occurred in all SOS functions studied following UV-irradiation as well as in the amplification of RecA protein synthesis by nalidixic acid but not in the other SOS functions triggered by this compound. Furthermore, adenine produced a decrease in the mitomycin C-mediated induction of all SOS functions studied in both RecBC- and wild-type strains.
在RecBC-突变体中研究了紫外线照射、添加萘啶酸或丝裂霉素C后几种SOS功能的表达情况,如λ原噬菌体的诱导、细胞分裂的抑制以及umuC和recA基因的诱导。紫外线照射和丝裂霉素C诱导了RecBC-细胞中研究的所有SOS功能,但水平较低且相对于野生型菌株有所延迟。相反,萘啶酸无法触发这些SOS功能中的任何一种。在RecBC-突变体中,腺嘌呤仅对紫外线照射后RecA蛋白合成的扩增有刺激作用。然而,在野生型菌株中,紫外线照射后研究的所有SOS功能以及萘啶酸对RecA蛋白合成的扩增均有刺激作用,但对该化合物触发的其他SOS功能则没有。此外,腺嘌呤使RecBC-和野生型菌株中研究的所有SOS功能的丝裂霉素C介导的诱导作用降低。