Bailone A, Sommer S, Devoret R
Proc Natl Acad Sci U S A. 1985 Sep;82(17):5973-7. doi: 10.1073/pnas.82.17.5973.
Dispensable replicons such as F plasmid [95 kilobases (kb)] or its mini-derivatives such as mini-F (9.3 kb) or lambda mini-F efficiently induced cellular SOS genes such as sfiA (sulA) when they were damaged by UV irradiation and then introduced into a recipient bacterium. To generate an SOS signal, UV light-damaged mini-F or mini-F conditional mutants deficient in replication required that the bacterial RecBC enzyme retained some activity different from the nuclease activity that was dispensable. In contrast, UV light-damaged F plasmid produced an SOS signal independently of the activity of the RecBC enzyme and of the expression of the mini-F, -H, and -G proteins. Our findings are consistent with a picture in which the SOS signal is constituted by stretches of single-stranded DNA on a replicon. Moreover, our present data combined with other data previously published lead to the hypothesis that the SOS signal induced by mini-F plasmid is located in trans on the host chromosome, whereas the one generated by UV light-damaged F plasmid is in cis on the transferred DNA.
诸如F质粒[95千碱基(kb)]之类的可自主复制子或其微型衍生物,如微型F(9.3 kb)或λ微型F,在受到紫外线照射损伤后再导入受体细菌时,能有效诱导细胞SOS基因,如sfiA(sulA)。为了产生SOS信号,紫外线损伤的微型F或复制缺陷的微型F条件突变体要求细菌RecBC酶保留一些不同于可缺失的核酸酶活性的活性。相比之下,紫外线损伤的F质粒独立于RecBC酶的活性以及微型F、-H和-G蛋白的表达产生SOS信号。我们的发现与这样一种情况相符,即SOS信号由复制子上的单链DNA片段构成。此外,我们目前的数据与先前发表的其他数据相结合,得出一个假说:微型F质粒诱导的SOS信号位于宿主染色体的反式位置,而紫外线损伤的F质粒产生的SOS信号位于转移DNA的顺式位置。