Abstract

Illegitimate recombination is a ubiquitous phenomenon and includes three types of events. In the first class, rearrangements occur by recombination between short homologous sequences. A second class is associated with site-specific elements. A last class groups all rearrangements in which the newly linked sequences share less than 3 bp of homology and have no homology with known specific sites. Oxidative lesions are known to induce rearrangements. Deletions by illegitimate recombination between short homologous sequences were reported in Escherichia coli fur mutants, in which a defect in iron metabolism regulation results in increased oxidative damage. In bacteria, transcription inhibits deletion between tandemly repeated sequences 10-fold. In contrast, transcription was shown to increase recombination between nonhomologous sequence. The stimulation of transposon excision by rolling-circle replication adds to the long list of indirect evidence that supports the occurrence of the replication slippage events in vivo. Most of the genetic studies of illegitimate recombination were performed in E. coli, either on the chromosome or with bacteriophages. Most of the recombination events between short homologous sequences occur independently from the action of RecA, since the length considered is far below the E. coli minimum efficient processing segment (MEPS). Topoisomerases are enzymes that modify the supercoiling of molecules through transient breakage and ligation of DNA strands. The first evidence that topoisomerases may promote rearrangements in bacteria came from the work of Ikeda and collaborators. Illegitimate recombination is a major issue in eukaryotes, because it is at the origin of numerous pathological disorders.

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