Further characterization of sfiA and sfiB mutations in Escherichia coli

Abstract

The sfiA and sfiB mutations, originally isolated in thermoresistant ultraviolet-resistant revertants of a tif lon strain, also suppressed filamentation in tsl strains (mutated at the lexA locus). When deoxyribonucleic acid synthesis was arrested, however, sfi-independent filamentation occurred. Other SOS functions were not affected by sfiA and sfiB mutations; in particular, ultraviolet-induced repair and mutagenesis of bacterial deoxyribonucleic acid were normal, as was tsl-tif-induced synthesis of recA protein. Genetic studies (i) established the identity of map location of the sfiA and sulA loci, (ii) showed that the two sfiB mutations are recessive, and (iii) showed that of six independent sfiA mutations, three are recessive and three are dominant. One sfiB strain was shown to have a 6% growth disadvantage relative to a sfi+ or sfiA strain. It is proposed that the sfiA locus may define the structural gene of a hypothetical inducible SOS-associated division inhibitor.

Inactivation of essential division genes, ftsA, ftsZ, suppresses mutations at sfiB, a locus mediating division inhibition during the SOS response in E. coli.

“…Finally, some comment is required on the previously reported recessivity of sjiBl 14 and other sfj1B alleles. In the case of sf11B1 14, the presence of a recessive allele in partial diploids appeared to be demonstrated unequivocally by subsequent P1 transduction analysis (Huisman et al, 1980c). Nevertheless, both in this study and that recently reported by Lutkenhaus (1983), sf1B (suiB) alleles were clearly shown to be dominant.…”

“…Similar results are obtained with mutations, (tij), in recA which lead to activation of the protease form of the recA protein at 42°C, and consequent cleavage of the lexA repressor (Little et al, 1980). Mutations in sflA and a second locus sfiB suppress filament formation in both tsl and tif mutants at 42°C (Witkin, 1976;Huisman et al, 1980bHuisman et al, , 1980c. Similarly, mutations in another gene, Ion, which block or delay recovery from u.v.induced division inhibition are also suppressed by sflA (sulA) and sJfB (suiB) mutations (George et al, 1975;Johnson, 1977;Gottesman et al, 1981).…”

“…Mapping by X transducing phages The two minute region is well covered by specialised X transducing phages (Fletcher et al, 1978; and some of these were tested for the presence of sflB + in lysogens of a host strain carrying sfiB1 14. This sfiB allele was previously reported to be recessive in partial diploids (Huisman et al, 1980c). Phages of interest were used to lysogenise strain GC2490 (tsl, sfiB1 14) by selection for leu+, and the lysogens tested for the restoration of temperaturesensitive filamentation.…”

Bacterial cell division protein FtsZ is stable against degradation by AAA family protease FtsH in Escherichia coli cells

“…It is known that cell division arrest induced during DNA damage is mediated by the binding of FtsZ by SulA protein in order to prevent FtsZ-ring assembly (Huang et al 1996, Higashitani et al 1997, Mukherjee et al 1998, Trusca et al 1998, Justice et al 2000, Cordell et al 2003, Kawai et al 2003, thereby leaving FtsZ unutilized. In a similar manner, it is possible that FtsH might degrade unutilized FtsZ if septation arrest is induced by DNA replication inhibition (Huisman et al 1980, 1984, Huisman and D'Ari, 1981. AR5090/pSTD113 cultures were induced for FtsH expression for 60 min, and then treated with the DNA replication inhibitors, hydroxyurea, nalidixic acid, phenethylalcohol or mitomycin C at the final concentrations of 66 mM (Sinha and Snustad 1972) or 20 µg/ml (Goss et al 1965) or 0.4% (Kaneko et al 1977) or 3 µg/ml (Khil and Camerini-Otero 2002), respectively, for further 60 min.…”

Role of sulA and sulB in filamentation by lon mutants of Escherichia coli K-12

“…These tif Ion strains filament extensively at a high temperature; the sfi survivors show less filamentation. We will assume in our discussion that the sulA and sfiA mutations are allelic and that sulB and sfiB are allelic, since their phenotypes are indistinguishable and they map in the same regions of the chromosome (6,12,13,14).…”