Overview of Homologous Recombination and Repair Machines

Abstract

The study of homologous recombination between plasmids, or between a plasmid and the chromosome, revealed that the RecFOR pathway is less of a poor cousin than first thought. When the exquisite sensitivity to DNA damage of the first recombination-deficient mutants was found, it became clear that homologous recombination might be the only way to repair certain DNA lesions. Generally, the stronger the defect in homologous recombination, the higher the sensitivity to DNA damage. In Escherichia coli, chromosomal lesions are repaired by homology-guided strand exchange between sister chromatids. The evidence in support of this notion comes in three forms. First, physical connections between parental and daughter strands, associated with lesion repair, can be detected. Second, repair of chromosomal lesions is not observed in recA mutants. Third, DNA damage stimulates homologous recombination although the structure of chromosomal lesions in this case is unspecified. Single-stranded DNA-binding protein (SSB) complexes single-stranded DNA (ssDNA), facilitating its subsequent use in replication and in degradation and repair pathways of DNA metabolism. Chromosomal dimerization in E. coli creates a chromosomal lesion, because it prevents segregation of the replicated chromosomes into daughter cells. The understanding of the formation of replication-dependent chromosomal lesions is still primitive. There is one in vivo study on the structure of stalled replication forks, a report documenting replication fork reversal in vivo, as well as a few reports of replication fork reversal in vitro, likely to be an artifact of DNA isolation.