Prophage induction and cell division in E. coli. III. Mutations sfiA and sfiB restore division in tif and lon strains and permit the expression of mutator properties of tif.

Abstract

In E. coli K12, cell filamentation promoted by tif is enhanced by the lon mutation; in contrast, prophage induction and repair of UV-irradiated phage lambda, also promoted by tif, are not affected by lon. From a tif lon double mutant, "revertants" having recovered the ability to divide at 41 degrees were isolated, among which most (95%) had also lost their Lon filamentous phenotype after ultraviolet (UV) irradiation. From these 95% of revertants: (1) 94% are suppressed for the whole Tif phenotype, by additional mutations that render them deficient in DNA repair, as judged from their high UV sensitivity; some have been characterized as recA mutants. (2) 1% have recovered a control on cell division at 41 degrees or after UV irradiation by means of secondary mutations altering neither the other phenotypic properties of tif and lon, nor the repair and recombination ability of the cells: in particular, this class of "revertants" remains thermoinducible upon lysogenisation; the mutations which specifically suppress filamentation have been mapped at two loci, sfiA and sfiB, cotransducible respectively with pyrD and leu. In the remaining 5% of revertants that still exhibit an UV-induced filamentous growth, 3% can be tentatively classified as true tif+ revertants; 2% behave as tif thermodependent revertants, showing suppression of the Tif (and Lon) phenotype only at 41 degrees: 2recAts have been identified in this class. Non-lysogenic tif lon sfi and tif sfi strains remain viable during prolonged growth at 41 degrees. Under these conditions, tif expresses mutator properties, which can be conveniently analyzed in this sfi background. The action of lif, lon and sfi mutations is tentatively interpreted on the basis of a negative control of cell division specifically associated with DNA repair.