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Review
. 2014 Nov-Dec;49(6):463-72.
doi: 10.3109/10409238.2014.942450. Epub 2014 Jul 22.

The role of RecQ helicases in non-homologous end-joining

Affiliations
Review

The role of RecQ helicases in non-homologous end-joining

Guido Keijzers et al. Crit Rev Biochem Mol Biol. 2014 Nov-Dec.

Abstract

DNA double-strand breaks are highly toxic DNA lesions that cause genomic instability, if not efficiently repaired. RecQ helicases are a family of highly conserved proteins that maintain genomic stability through their important roles in several DNA repair pathways, including DNA double-strand break repair. Double-strand breaks can be repaired by homologous recombination (HR) using sister chromatids as templates to facilitate precise DNA repair, or by an HR-independent mechanism known as non-homologous end-joining (NHEJ) (error-prone). NHEJ is a non-templated DNA repair process, in which DNA termini are directly ligated. Canonical NHEJ requires DNA-PKcs and Ku70/80, while alternative NHEJ pathways are DNA-PKcs and Ku70/80 independent. This review discusses the role of RecQ helicases in NHEJ, alternative (or back-up) NHEJ (B-NHEJ) and microhomology-mediated end-joining (MMEJ) in V(D)J recombination, class switch recombination and telomere maintenance.

Keywords: Alternative end-joining; Ku70/80; RecQ helicases; microhomology-mediated end-joining; non-homologous end-joining; telomere.

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Conflict of interest statement

Declaration of interest

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic diagram of DNA end-joining pathways. C-NHEJ, canonical non-homologous end-joining; B-NHEJ, alternative non-homologous end-joining; MMEJ, micro-mediated end-joining; MRN, MRE11-RAD50-NBS1 complex. EXO1/BLM/MRN or BLM/DNA2/MRN carry out CtIP-stimulated end-resection during MMEJ. (see colour version of this figure at www.informahealthcare.com/bmg).
Figure 2
Figure 2
BLM, WRN, RECQL4, RECQL1 and RECQL5β in DNA end-joining, DNA homologous recombination and DNA replication. Only BLM is known to play a major role in MMEJ, SSA and CSR. (see colour version of this figure at www.informahealthcare.com/bmg).

References

    1. Ahnesorg P, Smith P, Jackson SP. XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining. Cell. 2006;124:301–13. - PubMed
    1. Aygün O, Svejstrup J, Liu Y. A RECQ5-RNA polymerase II association identified by targeted proteomic analysis of human chromatin. Proc Natl Acad Sci USA. 2008;105:8580–4. - PMC - PubMed
    1. Aygün O, Xu X, Liu Y, et al. Direct inhibition of RNA polymerase II transcription by RECQL5. J Biol Chem. 2009;284:23197–203. - PMC - PubMed
    1. Babbe H, McMenamin J, Hobeika E, et al. Genomic instability resulting from Blm deficiency compromises development, maintenance, and function of the B cell lineage. J Immunol. 2009;182:347–60. - PMC - PubMed
    1. Baynton K, Otterlei M, Bjørås M, et al. WRN interacts physically and functionally with the recombination mediator protein RAD52. J Biol Chem. 2003;278:36476–86. - PubMed

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