SOS response

It is an error-prone repair system that contributes significantly to DNA changes observed in a wide range of species.

[3][4] Later, by characterizing the phenotypes of mutagenised E. coli, she and post doctoral student Miroslav Radman detailed the SOS response to UV radiation in bacteria.

Under normal conditions, LexA binds to a 20-bp consensus sequence (the SOS box) in the operator region for those genes.

The SOS dependent tisB-istR toxin-antitoxin system has, for example, been linked to DNA damage-dependent persister cell induction.

A lactose analog is added to the bacteria, which is then degraded by beta-galactosidase, thereby producing a colored compound which can be measured quantitatively through spectrophotometry.

The degree of color development is an indirect measure of the beta-galactosidase produced, which itself is directly related to the amount of DNA damage.

[13] Commercial kits which measures the primary response of the E. coli cell to genetic damage are available and may be highly correlated with the Ames Test for certain materials.

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 ]
Overview of the use of the SOS response for genotoxicity testing.