Coupling of DNA replication and cell division: sulB is an allele of ftsZ.
Treatments that damage DNA in Escherichia coli result in the inhibition of cell division. This inhibition is controlled by the lexA- recA regulatory circuit and can be specifically uncoupled by the mutations sulA (sfiA) and sulB (sfiB), which map at 21 and 2 min, respectively. Presently it is thought that sulA codes for an inducible inhibitor of cell division, the expression of which is controlled directly by the lexA repressor. In this report, it is shown that sulB is an allele of ftsZ, an essential cell division gene. A sulB mutation leads to an altered ftsZ gene product which is slightly thermosensitive and has an altered mobility on polyacrylamide gels. It is suggested that the altered ftsZ gene product is resistant to the sulA inhibitor, thus permitting cell division after induction of the SOS response. It is also shown that an increase in the gene dosage of ftsZ delays the onset of filamentation after SOS induction.[1]References
- Coupling of DNA replication and cell division: sulB is an allele of ftsZ. Lutkenhaus, J.F. J. Bacteriol. (1983) [Pubmed]
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