SOS response

E. coli SOS System: DNA can be damaged by cross-linking agents, UV irradiation, alkylating agents, etc. Once damaged, RecA, a LexA protease, senses that damaged DNA and becomes activated by removing its repressor. Once the LexA dimer repressor is removed, the expression of LexA operon is autoregulatory. In addition to being a LexA protease, the RecA protein also catalyzes a few novel DNA reactions such as annealing of single-stranded DNA and transfer of strands. The SOS system has enhanced DNA-repair capacity, including excision and post-replication repair, enhanced mutagenesis and prophage induction. The system can also inhibit cell division and cell respiration.[1]
The SOS response has been proposed as a model for bacterial evolution of certain types of antibiotic resistance.[2]

The SOS response is a global response to DNA damage in which the cell cycle is arrested and DNA repair and mutagenesis are induced. The system involves the RecA protein (Rad51 in eukaryotes). The RecA protein, stimulated by single-stranded DNA, is involved in the inactivation of the repressor (LexA) of SOS response genes thereby inducing the response. It is an error-prone repair system that contributes significantly to DNA changes observed in a wide range of species.

  1. ^ Little, John W.; Mount, David W. (May 1982). "The SOS regulatory system of Escherichia coli". Cell. 29 (1): 11–22. doi:10.1016/0092-8674(82)90085-X. PMID 7049397. S2CID 12476812.
  2. ^ Michel, Bénédicte (12 July 2005). "After 30 Years of Study, the Bacterial SOS Response Still Surprises Us". PLoS Biology. 3 (7): e255. doi:10.1371/journal.pbio.0030255. PMC 1174825. PMID 16000023.