Cell Lysis Directed by SulA in Response to DNA Damage in Escherichia coli.
Masayuki MurataKeiko NakamuraTomoyuki KosakaNatsuko OtaAyumi OsawaRyunosuke MuroKazuya FujiyamaTaku OshimaHirotada MoriBarry L WannerMamoru YamadaPublished in: International journal of molecular sciences (2021)
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.
Keyphrases
- single cell
- dna damage
- cell therapy
- cell death
- escherichia coli
- oxidative stress
- cell proliferation
- cell cycle arrest
- transcription factor
- induced apoptosis
- stem cells
- single molecule
- gene expression
- endoplasmic reticulum stress
- staphylococcus aureus
- mesenchymal stem cells
- circulating tumor
- dna repair
- high glucose
- diabetic rats