SfiB and the control of cell division in E. coli.
thesisposted on 19.11.2015, 08:53 by Christopher Andrew. Jones
Mutations at two loci, sfiA and sfiB, suppress the filamentation seen on irradiation of lon mutants or expression of tsl (lexA (Ts)) or tif (recA441) mutations in Escherichia coli. The sfiA and sfiB genes have been assumed to be involved in the inhibition of cell division associated with the SOS response. The product of the sfiA gene has been shown to be a division inhibitor and the sfiB gene has been postulated to be the target for the action of such an inhibitor. The sfiB gene was mapped to the ftsQ-secA region of the E. coli chromosome using P1 transduction and specialised transducing phages. The sfiB+ and sfiB114 genes were cloned onto recombinant plasmids and sfiB114 found to be at least partially dominant in ts1 and lon strains. Using Tn1000 mutagenesis, it was found that the sfiB gene is allelic to the essential septation gene ftsZ and that an element within the preceeding and contiguous ftsA gene is required for full ftsZ (sfiB) expression. Maxi-cells containing plasmids encoding sfiA and either sfiB+ or sfiB114 were used to demonstrate an interaction between SfiA and FtsZ. The presence of an ftsZ(sfiB+) carrying plasmid in maxi-cells increased the half-life of the unstable SfiA protein to 10-14 min (compared to approximately 3 min in the presence of a sfiB114 encoding plasmid or where a sfiA plasmid was present in maxi-cells alone). Finally, maxi-cells containing sfiA and sfiB carrying plasmids were separated into subcellular fractions and it was found that both SfiA and SfiB(FtsZ) proteins bind to the E. coli inner membrane.