Abstract
This chapter reviews the current knowledge about the mechanism of the LexA/RecA regulated response and its output in Escherichia coli, stressing newly emerging areas such as regulation of RecA filament formation and management of specialized DNA repair polymerases. It also talks about the SOS response in other bacterial species and its implications for the evolution and treatment of bacterial pathogens, and further discusses the more poorly understood LexA/ RecA‐independent damage response in several model organisms and a potentially larger network of the response to DNA damage. ATP binding, but not hydrolysis, is required for DNA binding; DNA binding greatly stimulates ATP hydrolysis, which in turn promotes RecA's release from DNA. The current widespread use of fluoroquinolone antibiotics, which, as topoisomerase II poisons, are potent SOS inducers, has potentially serious clinical consequences and influence on evolution of pathogens. In E. coli, Bacillus subtilis, and Mycobacterium tuberculosis there is increasing evidence of LexA/RecA independent modes of DNA damage response, including genes involved in DNA replication and repair. The majority of DNA damage inducible genes are not controlled by LexA or RecA. The DNA damage response has important implications for the evolution and treatment of bacterial pathogens because of its ability to promote genetic change through mutation and induction of mobile genetic elements, potentially induced by the very agents used to treat bacterial infections.