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InEscherichia coli , expression of thetif-1 mutation (in therecA gene) induces the “SOS response” at 40°C, including massive synthesis of therecA (tif ) protein, cell filamentation, appearance of new repair and mutagenic activities, and prophage induction. Expression of thetsl-1 mutation (in thelexA gene) induces massive synthesis of therecA protein and cell filamentation at 42°C, although other SOS functions are not induced. In this paper we show that the septation inhibition induced intif andtsl strains at 42°C is not due to the presence of a high concentration ofrecA protein since (i) norecA mutants (≤10−8 ) were isolated among thermoresistant nonfilamenting revertants of atif-1 tsl-1 strain, (ii) in atsl-1 zab-53 strain, only the low basal level ofrecA protein was synthesized at 42°C, yet cell division was inhibited, and (iii) in atsl-1 recA99 (amber) strain, norecA protein could be detected at 42°C, yet cell division was inhibited. Among suppressors oftsl-tif -induced lethality are mutations at a locus which we callinfB , located in the 66- to 83-min region. TheinfB1 mutation confers a highly pleiotropic phenotype, which is suggestive of a regulatory defect; it suppressedtsl-tif -induced filamentation but notrecA protein synthesis, it did not suppress ultraviolet-induced filamentation (in alon derivative), and it reduced but did not abolishtif -mediated induction of λ prophage and bacterial mutagenesis. The dissociation oftsl-tif -induced septation inhibition andrecA protein synthesis in thetif-1 tsl-1 infB1 strain suggests that the control of SOS filamentation may not be strictly identical to the control ofrecA protein synthesis.

Dissociation of tsl-tif -Induced Filamentation and recA Protein Synthesis in Escherichia coli K-12