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The SOS response is induced upon DNA damage and the inhibition of Z ring formation by the product of the <i>sulA</i> gene, which is one of the LexA-regulated genes, allows time for repair of damaged DNA. On the other hand, severely DNA-damaged cells are eliminated from cell populations. Overexpression of <i>sulA</i> leads to cell lysis, suggesting SulA eliminates cells with unrepaired damaged DNA. Transcriptome analysis revealed that overexpression of <i>sulA</i> leads to up-regulation of numerous genes, including <i>soxS.</i> Deletion of <i>soxS</i> markedly reduced the extent of cell lysis by <i>sulA</i> overexpression and <i>soxS</i> overexpression alone led to cell lysis. Further experiments on the SoxS regulon suggested that LpxC is a main player downstream from SoxS. These findings suggested the SulA-dependent cell lysis (SDCL) cascade as follows: SulA→SoxS→LpxC. Other tests showed that the SDCL cascade pathway does not overlap with the apoptosis-like and <i>mazEF</i> cell death pathways.