Recombinational DNA Repair in Bacteria: Postreplication


Recombinational DNA repair represents the primary function for homologous DNA recombination in bacteria. Most of this repair occurs at replication forks that are stalled at sites of DNA damage.

Keywords: RecA protein; DNA damage; SOS response; reactivation of stalled replication forks

Figure 1.

Pathways for the reactivation of stalled replication forks in bacteria. The pathways diverge depending on what type of damage is encountered. If an unrepaired lesion is encountered (left path), the lesion is left in a DNA gap. A complementary strand is recruited from the other side of the replication fork, with the aid of the RecA, RecFOR, and probably other proteins. Once recombination intermediates are processed (using the RuvABC and/or RecG activities), replication is reinitiated by a specialized set of replication restart enzymes. If the fork instead encounters a DNA strand break, a double‐strand break results (right path). The major repair pathway in this case utilizes the RecBCD enzyme. Processing of recombination intermediates and replication restart ensues, as described above. Some of the recombination intermediates generated in the gap (left) repair path may be cleaved and thus funnelled into the double‐strand break repair path, as indicated by the broken red arrow.

Figure 2.

The bacterial RecA protein and DNA strand exchange. (a) A portion of a RecA filament is shown, containing 24 RecA monomers. There are approximately six monomers per turn in the helical filament, and a single monomer is highlighted in red. The DNA is bound in the filament groove. The image is based on the structural work of Randy Story and Thomas Steitz, using PDB file 1REB. (b) Typical DNA strand exchange reactions ulitized to study RecA protein function in vitro. RecA filaments will form on the single‐stranded or gapped DNA circles. DNA pairing and strand exchange will then ensue with the double‐stranded linear DNA molecule. The four‐strand exchange exhibits an absolute requirement for ATP hydrolysis. The DNA substrates are usually derived from bacteriophage or plasmid DNAs, and the reactions shown were originally chosen for ease of assay.

Figure 3.

The activity of the RuvAB complex at a Holliday junction. A tetramer of octamer of RuvA protein binds at the junction, and two RuvB hexamers then bind to it as shown. The RuvB hexamers act as DNA pumps, forcing the DNA outward and promoting migration of the branch. The drawing is based on the work of Stephen West and colleagues.

Figure 4.

If a Holliday intermediate is formed behind the replication fork via recombinational repair reactions, resolution of the crossover by RuvC or related enzymes can have two different consequences. Resolution via path A will result ultimately in a dimeric chromosome, and will later require conversion to monomers by the site‐specific recombination system XerCD.



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Further Reading

Cox MM (1998) A broadening view of recombinational DNA repair in bacteria. Genes to Cells 3: 65–78.

Cox MM, Goodman MF, Kreuzer KN et al. (2000) The importance of repairing stalled replication forks. Nature 404: 37–41.

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Kogoma T (1997) Stable DNA replication: interplay between DNA replication, homologous recombination, and transcription. Microbiology and Molecular Biology Reviews 61: 212–238.

Kuzminov A (1996) Recombinational Repair of DNA Damage. Georgetown, TX: Landes.

Kuzminov A (1999) Recombinational repair of DNA damage in Escherichia coli and bacteriophage λ. Microbiology and Molecular Biology Reviews 63: 751–813.

Marians KJ (1999) PriA: at the crossroads of DNA replication and recombination. Progress in Nucleic Acid Research and Molecular Biology 63: 39–67.

Mosig G (1998) Recombination and recombination‐dependent DNA replication in bacteriophage T4. Annual Review of Genetics 32: 379–413.

Roca AI and Cox MM (1997) RecA protein: structure, function, and role in recombinational DNA repair. Progress in Nucleic Acid Research and Molecular Biology 56: 129–223.

Sandler SJ and Marians KJ (2000) Role of PriA in replication fork reactivation in Escherichia coli. Journal of Bacteriology 182: 9–13.

Seigneur M, Bidnenko V, Ehrlich SD and Michel B (1998) RuvAB acts at arrested replication forks. Cell 95: 419–430.

Shinagawa H (1996) SOS response as an adaptive response to DNA damage in prokaryotes. EXS 77: 221–235.

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Rice, Kevin P, and Cox, Michael M(Apr 2001) Recombinational DNA Repair in Bacteria: Postreplication. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1038/npg.els.0000689]