Lutkenhaus J F
J Bacteriol. 1983 Jun;154(3):1339-46. doi: 10.1128/jb.154.3.1339-1346.1983.
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.
能损伤大肠杆菌DNA的处理会导致细胞分裂受到抑制。这种抑制由lexA-recA调控回路控制,并且可以通过分别位于21分钟和2分钟处的sulA(sfiA)和sulB(sfiB)突变特异性地解除耦合。目前认为sulA编码一种细胞分裂的诱导性抑制剂,其表达直接受lexA阻遏物控制。在本报告中,表明sulB是ftsZ(一个必需的细胞分裂基因)的一个等位基因。sulB突变导致ftsZ基因产物发生改变,该产物对温度稍有敏感性,并且在聚丙烯酰胺凝胶上迁移率发生改变。有人提出,改变后的ftsZ基因产物对sulA抑制剂具有抗性,因此在SOS应答诱导后允许细胞分裂。还表明,ftsZ基因剂量的增加会延迟SOS诱导后丝状化的开始。