In Escherichia coli, damage to DNA induces the expression of a set of genes known collectively as the SOS response. Part of the SOS response includes genes that repair DNA damage, but another part of the response coordinates DNA replication and septation to prevent untimely cell division. The classic SOS gene product that inhibits cell division is SfiA (or SulA), which binds to FtsZ and prevents septum formation until the DNA damage has been repaired. However, another pathway acts to coordinate DNA replication and cell division when sfiA, or the sfi-dependent pathway, is inoperative. Until recently, little was known of this alternative pathway, which is called the sfi-independent pathway. We report here that sfi-independent filamentation is suppressed by lexA(Ind-) mutations, suggesting that derepression of the LexA regulon is necessary for sfi-independent induction. However, expression of LexA-controlled genes is not sufficient; DNA damage is also required to induce this secondary pathway of cell division inhibition. Furthermore, we postulate that loss of the common regulatory circuitry of the sfi-dependent and sfi-independent pathways by recA or lexA mutants uncouples cell division and DNA replication.