| Literature DB >> 33926096 |
Masayuki Murata1, Keiko Nakamura2, Tomoyuki Kosaka1,3, Natsuko Ota1, Ayumi Osawa1, Ryunosuke Muro2, Kazuya Fujiyama2, Taku Oshima4, Hirotada Mori5, Barry L Wanner6, Mamoru Yamada1,2,3.
Abstract
The SOS response is induced upon DNA damage and the inhibition of Z ring formation by the product of the sulA 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 sulA leads to cell lysis, suggesting SulA eliminates cells with unrepaired damaged DNA. Transcriptome analysis revealed that overexpression of sulA leads to up-regulation of numerous genes, including soxS. Deletion of soxS markedly reduced the extent of cell lysis by sulA overexpression and soxS 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 mazEF cell death pathways.Entities:
Keywords: DNA damage; LpxC; SoxS; SulA; cell lysis
Year: 2021 PMID: 33926096 DOI: 10.3390/ijms22094535
Source DB: PubMed Journal: Int J Mol Sci ISSN: 1422-0067 Impact factor: 5.923