Homologous recombination promotes the pairing between identical — or nearly identical – DNA sequences and the subsequent exchange of genetic material between them. It is an important and widely conserved function in living organisms, from bacteria to humans, that serves to repair double-stranded breaks or single-stranded gaps in the DNA, arising as a consequence of ionizing radiations, ultraviolet (UV) light, or chemical treatments creating replication-blocking adducts (Kuzminov, 1999). More recently, homologous recombination functions were also found in bacteria to rescue replication forks that have stalled for various reasons, such as a missing factor (e.g., the helicase), or a particular difficulty upstream of the fork, such as supercoiling or intense traffic of proteins (Michel et al., 2001).

Besides its molecular role, homologous recombination has played a major role in genome dynamics, by changing gene copy numbers through deletions, duplications, and amplifications: Intrachromosomal recombination between ribosomal operons or between mobile elements scattered into the genome leads to deletion or tandem duplications of large regions within the genome, up to several hundred kilobases (Roth et al., 1996). The duplications are unstable. Mostly they recombine back to the parental organization, and, therefore, remain undetected, except when appropriate selection, by gene dosage mostly, is exerted (Petes and Hill, 1988). In contrast, such duplications are ideal substrate for the diversification of genes: One gene is kept intact whereas the other is mutagenized, which leads to the birth of gene families.