Life Science, Graduate School of Science and Technology for Innovation, Yamaguchi University, Ube 755-8611, Japan.
Applied Molecular Bioscience, Graduate School of Medicine, Yamaguchi University, Ube 755-8505, Japan.
Int J Mol Sci. 2021 Apr 26;22(9):4535. doi: 10.3390/ijms22094535.
The SOS response is induced upon DNA damage and the inhibition of Z ring formation by the product of the 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 leads to cell lysis, suggesting SulA eliminates cells with unrepaired damaged DNA. Transcriptome analysis revealed that overexpression of leads to up-regulation of numerous genes, including Deletion of markedly reduced the extent of cell lysis by overexpression and 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 cell death pathways.
SOS 响应是在 DNA 损伤和 Z 环形成抑制的情况下诱导的,Z 环形成的抑制是基因产物的作用之一,该基因是 LexA 调控基因之一,它为修复受损的 DNA 提供了时间。另一方面,严重受损的 DNA 细胞会从细胞群体中被清除。的过度表达导致细胞裂解,表明 SulA 消除了未修复受损 DNA 的细胞。转录组分析显示,的过度表达导致许多基因的上调,包括。缺失显著降低了 过表达引起的细胞裂解程度,而过表达本身就导致了细胞裂解。对 SoxS 调控子的进一步实验表明,LpxC 是 SoxS 下游的主要参与者。这些发现表明,SulA 依赖性细胞裂解(SDCL)级联如下:SulA→SoxS→LpxC。其他测试表明,SDCL 级联途径与凋亡样和细胞死亡途径不重叠。