Bagdasarian M, D'Ari R, Filipowicz W, George J
J Bacteriol. 1980 Feb;141(2):464-9. doi: 10.1128/jb.141.2.464-469.1980.
The tif-1 mutation in the recA gene of Escherichia coli caused, at 40 degrees C, lethal cell filamentation, induction of the recA protein, mutagenesis, and, in lambda lysogens, prophage induction. The presence of plasmid R100.1 in tif-1 strains suppressed tif-mediated cell filamentation and killing, recA protein induction, and prophage induction in lysogens. It also reduced mutagenesis in a tif-1 sfiA11(R100.1) strain. Plasmids F'lac, P1, and pMB9, in contrast, had little or no effect on tif-mediated induction of lambda. The presence of R100.1 did not inhibit the induction of the recA protein or of lambda by ultraviolet irradiation or mitomycin C treatment of tif-1(R100.1) or tif-1(lambda)(R100.1) strains.
大肠杆菌recA基因中的tif-1突变在40℃时会导致致死性细胞丝化、recA蛋白的诱导、诱变，并且在λ溶原菌中会导致原噬菌体诱导。tif-1菌株中质粒R100.1的存在抑制了tif介导的细胞丝化和杀伤、recA蛋白诱导以及溶原菌中的原噬菌体诱导。它还降低了tif-1 sfiA11（R100.1）菌株中的诱变作用。相比之下，质粒F'lac、P1和pMB9对tif介导的λ诱导几乎没有影响。R100.1的存在并不抑制通过紫外线照射或丝裂霉素C处理tif-1（R100.1）或tif-1（λ）（R100.1）菌株而诱导的recA蛋白或λ。
