Bacteria carrying mutations in the recA gene are defective in general recombination and DNA repair. Bacteria deficient in RecA protein have a complex phenotype, including defective DNA repair. Two important properties of RecA are as follows:

1. RecA catalyzes strand pairing, or strand assimilation-the joining of two different DNAs by homologous base pairing with each other.

2. RecA is a genetic regulator, activating the synthesis of many proteins (including DNA repair proteins) that help a bacterium adapt to a variety of metabolic stresses. This adaptation is called the SOS response. The transcriptional activations and a fuller description of the SOS response are presented here

The bacterial SOS response helps the cell to save itself in the presence of potentially lethal stresses, such as ultraviolet irradiation, thymine starvation, DNA-modifying reagents, and inactivation of genes essential to DNA replication.

The effects of the SOS response are confusing. They include mutagenesis, filamentation (in which cells elongate by growth but don't divide), and activated excision repair. Mutagenesis occurs because, under SOS conditions, the gaps that are formed opposite thymine dimers can be filled by replication rather than by recombination (see here), and this replication is extremely inaccurate. In fact, error prone replication is the principal pathway by which ultraviolet light stimulates mutagenesis in bacteria.

A pair of bacterial genes, called umuC and umuD have been implicated in error prone repair. After expression of the two genes, the umuD gene product undergoes proteolytic cleavage to give the UmuD' protein. Two of these combine with UmuC (the protein product of umuC) to yield trimeric UmuD'2C. This trimeric complex may be the error prone polymerase.

Why do cells have such a mechanism for accumulating mutations? It is not known for sure, but it probably represents a last gasp chance for the cell to survive a harsh treatment.

It is not known whether eukaryotic cells have a comparable SOS process.