Jeggo P, Defais T M, Samson L, Schendel P
Mol Gen Genet. 1977 Nov 29;157(1):1-9. doi: 10.1007/BF00268680.
We have described previously an inducible response in Escherichia coli which occurs during growth on low levels of the methylating agent, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and which enables cells both to survive better and to be less mutated by a subsequent challenge dose of MNNG than control cultures (Samson and Cairns, 1977). We show here that this response is distinct from previously characterised pathways of DNA repair, and particularly from the SOS response, which is another inducible effect resulting from DNA damage. An examination of the cross-reactivity of this response with other mutagens has shown that it is a generalised mechanism affecting alkylation damage to DNA. It cannot, however, be induced by UV or the UV-mimetic mutagen, 4-nitroquinoline 1-oxide, nor act on lesions put into DNA by those mutagens.
我们之前曾描述过大肠杆菌中的一种诱导性反应,这种反应发生在低水平甲基化剂N-甲基-N'-硝基-N-亚硝基胍(MNNG)存在下的生长过程中,与对照培养物相比,它能使细胞更好地存活,并且在后续接受MNNG挑战剂量时发生的突变更少(Samson和Cairns,1977)。我们在此表明,这种反应不同于先前已表征的DNA修复途径,特别是不同于SOS反应,SOS反应是由DNA损伤引起的另一种诱导效应。对该反应与其他诱变剂的交叉反应性进行的研究表明,它是一种影响DNA烷基化损伤的普遍机制。然而,它不能被紫外线或紫外线模拟诱变剂4-硝基喹啉1-氧化物诱导,也不能作用于由这些诱变剂引入DNA的损伤。