Review
Replication fork arrest and DNA recombination

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Abstract

Replication arrests are associated with genome rearrangements, which result from either homologous or non-homologous recombination. Interestingly, proteins involved in homologous recombination are able to convert an arrested replication fork into a recombination intermediate, which promotes replication restart and thus presumably prevents genome rearrangements.

Section snippets

Replication pause or arrest can cause DNA rearrangements

The replisome is composed of DNA polymerase III, which in Escherichia coli comprises two core polymerases and numerous accessory proteins, the DNA helicase DnaB, which progresses in front of the polymerase to unwind double-stranded DNA, and the primase DnaG, responsible for the synthesis of primers on the lagging strand. DnaB interacts with DnaG and with the τ subunit of the DNA polymerase III holoenzyme4. τ is the subunit that bridges the two polymerases that synthesize the leading and the

Concerted action of homologous recombination proteins can faithfully restore a replication fork following replication arrest

In addition to DnaB, the DNA helicase associated with the replication fork, a second DNA helicase, named Rep, participates in the replication of the E. coli chromosome. rep mutants have a reduced replication rate24, and because Rep can displace proteins from the DNA in vitro, it has been proposed to remove proteins from the path of the replication forks in vivo25, 26. In the absence of Rep, the encounter of obstacles causes frequent replication pausing, thus decreasing the apparent replication

Conclusion

On the one hand, replication defects have been shown to cause various kinds of DNA rearrangements that are either RecA-independent or RecA-dependent. On the other hand, homologous recombination proteins participate in the replication of the genome by promoting the restoration of a replication fork after arrest. This reaction presumably protects forks against breakage and limits the occurrence of rearrangements. How the recombination reaction at blocked replication forks facilitates replication

Acknowledgements

I thank V. Bidnenko, D. Canceill, D. Ehrlich, P. Noirot and M.A. Petit for helpful comments on the manuscript, and F. Haimet for help in figure drawing. B.M. is on the CNRS staff.

References (35)

  • D. Canceill et al.

    Copy-choice recombination mediated by DNA polymerase III holoenzyme from Escherichia coli

    Proc. Natl. Acad. Sci. U. S. A.

    (1996)
  • S.T. Lovett

    A sister-strand exchange mechanism for recA-independent deletion of repeated DNA sequences in Escherichia coli

    Genetics

    (1993)
  • S.C. Kowalczykowski

    Biochemistry of homologous recombination in Escherichia coli

    Microbiol. Rev.

    (1994)
  • H. Bierne

    Isolation of a dnaE mutation which enhances RecA-independent homologous recombination in the Escherichia coli chromosome

    Mol. Microbiol.

    (1997)
  • C.J. Saveson et al.

    Enhanced deletion formation by aberrant DNA replication in Escherichia coli

    Genetics

    (1997)
  • T.M. Hill

    Features of the chromosomal terminus region

  • H. Bierne

    The replication termination signal TerB of the Escherichia coli chromosome is a deletion hot spot

    EMBO J.

    (1991)
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