Caillet-Fauquet P, Maenhaut-Michel G, Radman M
EMBO J. 1984 Apr;3(4):707-12. doi: 10.1002/j.1460-2075.1984.tb01873.x.
We have used bacteriophage lambda to characterize the mutator effect of the SOS response induced by u.v. irradiation of Escherichia coli. Mutagenesis of unirradiated phages grown in irradiated or unirradiated bacteria was detected by measuring forward mutagenesis in the immunity genes or reversion mutagenesis of an amber codon in the R gene. Relative to the wild-type, the SOS mutator effect was higher in E. coli mismatch correction-deficient mutants (mutH, mutL and mutS) and lower in an adenine methylation-deficient mutant ( dam3 ). We conclude that a large proportion of SOS-induced 'untargeted' mutations are removed by the methyl-directed mismatch correction system, which acts on newly synthesized DNA strands. The lower SOS mutator effect observed in E. coli dam mutants may be due to a selective killing of mismatch-bearing chromosomes resulting from undirected mismatch repair. The SOS mutator effect on undamaged lambda DNA, induced by u.v. irradiation of the host, appears to result from decreased fidelity of DNA synthesis.
我们利用噬菌体λ来表征紫外线照射大肠杆菌所诱导的SOS应答的诱变效应。通过检测免疫基因中的正向诱变或R基因中琥珀密码子的回复诱变，来检测在经照射或未经照射的细菌中生长的未照射噬菌体的诱变情况。相对于野生型，SOS诱变效应在大肠杆菌错配修复缺陷型突变体（mutH、mutL和mutS）中较高，而在腺嘌呤甲基化缺陷型突变体（dam3）中较低。我们得出结论，很大一部分SOS诱导的“非靶向”突变被甲基导向的错配修复系统去除，该系统作用于新合成的DNA链。在大肠杆菌dam突变体中观察到的较低的SOS诱变效应可能是由于未定向错配修复导致的携带错配的染色体被选择性杀伤。宿主经紫外线照射诱导的对未受损λDNA的SOS诱变效应似乎是由于DNA合成保真度降低所致。
