Vericat J A, Guerrero R, Barbé J
Department of Genetics and Microbiology, Autonomous University of Barcelona, Bellaterra, Spain.
J Bacteriol. 1988 Mar;170(3):1354-9. doi: 10.1128/jb.170.3.1354-1359.1988.
Induction of the adaptive response by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) caused a decrease in the UV-mediated expression of both recA and sfiA genes but not of the umuDC gene. On the other hand, the adaptive response did not affect the temperature-promoted induction of SOS response in a RecA441 mutant. The inhibitory effect on the UV-triggered expression of the recA and sfiA genes was not dependent on either the alkA gene or the basal level of RecA protein, but rather required the ada gene. Furthermore, an increase in the level of the Ada protein, caused by the runaway plasmid pYN3059 in which the ada gene is regulated by the lac promoter, inhibited UV-mediated recA gene expression even in cells to which the MNNG-adaptive treatment had not been applied. This inhibitory effect of the adaptive pretreatment was not observed either in RecBC- strains or in RecBC mutants lacking exonuclease V-related nuclease activity. However, RecF- mutants showed an adaptive response-mediated decrease in UV-promoted induction of the recA gene.
N-甲基-N'-硝基-N-亚硝基胍（MNNG）诱导的适应性反应导致recA和sfiA基因的紫外线介导表达降低，但umuDC基因的表达未受影响。另一方面，适应性反应并不影响RecA441突变体中温度促进的SOS反应诱导。对recA和sfiA基因紫外线触发表达的抑制作用既不依赖于alkA基因，也不依赖于RecA蛋白的基础水平，而是需要ada基因。此外，由失控质粒pYN3059（其中ada基因由lac启动子调控）导致的Ada蛋白水平升高，即使在未进行MNNG适应性处理的细胞中也能抑制紫外线介导的recA基因表达。在RecBC-菌株或缺乏核酸外切酶V相关核酸酶活性的RecBC突变体中均未观察到适应性预处理的这种抑制作用。然而，RecF-突变体显示出适应性反应介导的recA基因紫外线促进诱导的降低。
