A cellular response to extensive DNA damage in which certain genes, called SOS genes, are sequentially activated in order to repair the damaged DNA. In E. coli about 20 such genes have been identified, including lexA, whose product normally represses the SOS genes. The remainder include genes such as uvrA, uvrB, recA, sulA, and umuC. Among the functions assigned to these genes are recombinational repair, nucleotide excision repair, inhibition of cell division, and error-prone repair. Normally, SOS genes are repressed by the LexA protein, which binds to operator sequences, called SOS boxes (q.v.), upstream of each of these genes. When DNA is damaged, single-stranded regions become exposed, and these interact with the RecA protein (q.v.) to form a complex (RecA*), which acquires protease activity and facilitates the cleavage of the LexA repressor (q.v.). The cleaved LexA protein is unable to bind DNA, thus allowing the SOS genes to be de-repressed. When the DNA has been repaired, RecA becomes inactivated, LexA is no longer cleaved and accumulates in the cell, and the SOS genes are shut down. In addition to accurate, error-free repair, the SOS response also induces DNA repair that leads to mutagenesis, i.e., error-prone or mutagenic repair, in which the DNA template is read with reduced fidelity. Thus, in the presence of extensive DNA damage the cells survive, albeit at the cost of introducing some errors in their DNA. The acronym, SOS, is derived from “Save Our Souls,” the Morse code signal given by ships in danger and conveys that this is an emergency response in cells that are in danger of dying. See Chronology, 1967, Witkins.
Subjects: Genetics and Genomics.