In bacteria, the major function of homologous genetic recombination is recombinational DNA repair. This is not a process reserved only for rare double-strand breaks caused by ionizing radiation, nor is it limited to situations in which the SOS response has been induced. Recombinational DNA repair in bacteria is closely tied to the cellular replication systems, and it functions to repair damage at stalled replication forks, Studies with a variety of rec mutants, carried out under normal aerobic growth conditions, consistently suggest that at least 10-30% of all replication forks originating at the bacterial origin of replication are halted by DNA damage and must undergo recombinational DNA repair. The actual frequency may be much higher. Recombinational DNA repair is both the most complex and the least understood of bacterial DNA repair processes. When replication forks encounter a DNA lesion or strand break, repair is mediated by an adaptable set of pathways encompassing most of the enzymes involved in DNA metabolism. There are five separate enzymatic processes involved in these repair events: (1) The replication fork assembled at OriC stalls and/or collapses when encountering DNA damage. (2) Recombination enzymes provide a complementary strand for a lesion isolated in a single-strand gap, or reconstruct a branched DNA at the site of a double-strand break. (3) The phi X174-type primosome (or repair primosome) functions in the origin-independent reassembly of the replication fork. (4) The XerCD site-specific recombination system resolves the dimeric chromosomes that are the inevitable by-product of frequent recombination associated with recombinational DNA repair. (5) DNA excision repair and other repair systems eliminate lesions left behind in double-stranded DNA. The RecA protein plays a central role in the recombination phase of the process. Among its many activities, RecA protein is a motor protein, coupling the hydrolysis of ATP to the movement of DNA branches.