Between sisters: Watching replication-associated recombinational DNA repair

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Abstract

Lovett previews work from Amarh et al. describing the dynamics of RecA-mediated repair at replication-dependent breaks.

Abstract

Amarh et al. (2018. J. Cell Biol. https://doi.org/10.1083/jcb.201803020) visualize for the first time the repair of double-strand breaks during DNA replication. As viewed by live-cell fluorescent imaging of Escherichia coli, repair of replication-dependent breaks is extraordinarily rapid and localized within the cell.

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Endogenous DNA double-strand breaks: production, fidelity of repair, and induction of cancer.

Michael Vilenchik, Alfred Knudson (2003)

This article extends our previous quantitative analysis of the relationship between the dynamics of the primary structure of DNA and mutagenesis associated with single-strand lesions to an analysis of the production and processing of endogenous double-strand breaks (EDSBs) and to their implications for oncogenesis. We estimate that in normal human cells approximately 1% of single-strand lesions are converted to approximately 50 EDSBs per cell per cell cycle. This number is similar to that for EDSBs produced by 1.5-2.0 Gy of sparsely ionizing radiation. Although EDSBs are usually repaired with high fidelity, errors in their repair contribute significantly to the rate of cancer in humans. The doubling dose for induced DSBs is similar to doubling doses for mutation and for the induction of carcinomas by ionizing radiation. We conclude that rates of production of EDSBs and of ensuing spontaneous mitotic recombination events can account for a substantial fraction of the earliest oncogenic events in human carcinomas.

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Regulation of bacterial RecA protein function.

Michael Cox (2015)

The RecA protein is a recombinase functioning in recombinational DNA repair in bacteria. RecA is regulated at many levels. The expression of the recA gene is regulated within the SOS response. The activity of the RecA protein itself is autoregulated by its own C-terminus. RecA is also regulated by the action of other proteins. To date, these include the RecF, RecO, RecR, DinI, RecX, RdgC, PsiB, and UvrD proteins. The SSB protein also indirectly affects RecA function by competing for ssDNA binding sites. The RecO and RecR, and possibly the RecF proteins, all facilitate RecA loading onto SSB-coated ssDNA. The RecX protein blocks RecA filament extension, and may have other effects on RecA activity. The DinI protein stabilizes RecA filaments. The RdgC protein binds to dsDNA and blocks RecA access to dsDNA. The PsiB protein, encoded by F plasmids, is uncharacterized, but may inhibit RecA in some manner. The UvrD helicase removes RecA filaments from RecA. All of these proteins function in a network that determines where and how RecA functions. Additional regulatory proteins may remain to be discovered. The elaborate regulatory pattern is likely to be reprised for RecA homologues in archaeans and eukaryotes.

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RecA bundles mediate homology pairing between distant sisters during DNA break repair

Christian Lesterlin, Graeme Ball, Lothar Schermelleh … (2013)

DNA double-strand break (DSB) repair by homologous recombination (HR) has evolved to maintain genetic integrity in all organisms 1 . Although many reactions that occur during HR are known 1-3 , it is unclear where, when and how they occur in cells is lacking. Here, by using conventional and super-resolution microscopy we describe the progression of DSB repair in live Escherichia coli. Specifically, we investigate whether HR can occur efficiently between distant sister loci that have segregated to opposite halves of an E. coli cell. We show that a site-specific DSB in one sister can be repaired efficiently using distant sister homology. After RecBCD processing of the DSB, RecA is recruited to the cut locus, where it nucleates into a bundle that contains many more RecA molecules than can associate with the two ssDNA regions that form at the DSB. Mature bundles extend along the cell long axis in the space between the bulk nucleoid and the inner membrane. Bundle formation is followed by pairing in which the two ends of the cut locus relocate at the periphery of the nucleoid and together move rapidly towards the homology of the uncut sister. After sister locus pairing, RecA bundles disassemble and proteins that act late in HR are recruited to give viable recombinants 1-2 generation time equivalents after formation of the initial DSB. Mutated RecA proteins that do not form bundles are defective in sister pairing and in DSB-induced repair. The work reveals an unanticipated role of RecA bundles in channeling the movement of the DNA DSB ends, thereby facilitating the long-range homology search that occurs before the strand invasion and transfer reactions.

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Journal

Journal ID (nlm-ta): J Cell Biol

Journal ID (iso-abbrev): J. Cell Biol

Journal ID (publisher-id): jcb

Journal ID (hwp): jcb

Title: The Journal of Cell Biology

Publisher: Rockefeller University Press

ISSN (Print): 0021-9525

ISSN (Electronic): 1540-8140

Publication date (Print): 02 July 2018

Volume: 217

Issue: 7

Pages: 2225-2227

Affiliations

[1]Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, MA

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Correspondence to Susan T. Lovett: lovett@ 123456brandeis.edu

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Susan T. Lovett http://orcid.org/0000-0003-2792-1857

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Publisher ID: 201805091

DOI: 10.1083/jcb.201805091

PMC ID: 6028551

PubMed ID: 29895696

SO-VID: e2bdf1be-046a-4df2-9d29-a92d8dd143ce

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This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Funded by: National Institute for General Medical Sciences, DOI 10.13039/100000057;

Between sisters: Watching replication-associated recombinational DNA repair

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Most cited references 10

Endogenous DNA double-strand breaks: production, fidelity of repair, and induction of cancer.

Regulation of bacterial RecA protein function.

RecA bundles mediate homology pairing between distant sisters during DNA break repair

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