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Regulation of DNA repair pathway choice in S and G2 phases by the NHEJ inhibitor CYREN.

作者信息

Arnoult Nausica, Correia Adriana, Ma Jiao, Merlo Anna, Garcia-Gomez Sara, Maric Marija, Tognetti Marco, Benner Christopher W, Boulton Simon J, Saghatelian Alan, Karlseder Jan

机构信息

The Salk Institute for Biological Studies, 10010 North Torrey Pines Rd., La Jolla, California 92037, USA.

Dsb Repair Metabolism Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.

出版信息

Nature. 2017 Sep 20;549(7673):548-552. doi: 10.1038/nature24023.


DOI:10.1038/nature24023
PMID:28959974
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5624508/
Abstract

Classical non-homologous end joining (cNHEJ) and homologous recombination compete for the repair of double-stranded DNA breaks during the cell cycle. Homologous recombination is inhibited during the G1 phase of the cell cycle, but both pathways are active in the S and G2 phases. However, it is unclear why cNHEJ does not always outcompete homologous recombination during the S and G2 phases. Here we show that CYREN (cell cycle regulator of NHEJ) is a cell-cycle-specific inhibitor of cNHEJ. Suppression of CYREN allows cNHEJ to occur at telomeres and intrachromosomal breaks during the S and G2 phases, and cells lacking CYREN accumulate chromosomal aberrations upon damage induction, specifically outside the G1 phase. CYREN acts by binding to the Ku70/80 heterodimer and preferentially inhibits cNHEJ at breaks with overhangs by protecting them. We therefore propose that CYREN is a direct cell-cycle-dependent inhibitor of cNHEJ that promotes error-free repair by homologous recombination during cell cycle phases when sister chromatids are present.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/250768a67009/emss-73757-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/539814c77525/emss-73757-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/d7d93e7d3f7f/emss-73757-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/0540daa99521/emss-73757-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/8ecb25d9776f/emss-73757-f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/7b9255e312d6/emss-73757-f009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/9df37cb2428f/emss-73757-f010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/0a4f7280a4ca/emss-73757-f011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/049aea01e4eb/emss-73757-f012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/fd9af80fbfaf/emss-73757-f013.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/999a855ccad4/emss-73757-f014.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/05a0cf75381a/emss-73757-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/98c3829f67c5/emss-73757-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/5141c5d96dad/emss-73757-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/250768a67009/emss-73757-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/539814c77525/emss-73757-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/d7d93e7d3f7f/emss-73757-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/0540daa99521/emss-73757-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/8ecb25d9776f/emss-73757-f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/7b9255e312d6/emss-73757-f009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/9df37cb2428f/emss-73757-f010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/0a4f7280a4ca/emss-73757-f011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/049aea01e4eb/emss-73757-f012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/fd9af80fbfaf/emss-73757-f013.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/999a855ccad4/emss-73757-f014.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/05a0cf75381a/emss-73757-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/98c3829f67c5/emss-73757-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/5141c5d96dad/emss-73757-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e60/5624508/250768a67009/emss-73757-f004.jpg

相似文献

[1]
Regulation of DNA repair pathway choice in S and G2 phases by the NHEJ inhibitor CYREN.

Nature. 2017-9-20

[2]
Analysis of chromatid-break-repair detects a homologous recombination to non-homologous end-joining switch with increasing load of DNA double-strand breaks.

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[3]
[Smart choice between two DNA double-strand break repair mechanisms].

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[4]
CDK-mediated Yku80 Phosphorylation Regulates the Balance Between Non-homologous End Joining (NHEJ) and Homologous Directed Recombination (HDR).

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[5]
A Stochastic Model of DNA Double-Strand Breaks Repair Throughout the Cell Cycle.

Bull Math Biol. 2020-1-14

[6]
The anaphase promoting complex promotes NHEJ repair through stabilizing Ku80 at DNA damage sites.

Cell Cycle. 2018-7-18

[7]
DNA end resection is needed for the repair of complex lesions in G1-phase human cells.

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[8]
Ku70 suppresses alternative end joining in G1-arrested progenitor B cells.

Proc Natl Acad Sci U S A. 2021-5-25

[9]
Cell cycle-dependent phosphorylation regulates RECQL4 pathway choice and ubiquitination in DNA double-strand break repair.

Nat Commun. 2017-12-11

[10]
MRI Is a DNA Damage Response Adaptor during Classical Non-homologous End Joining.

Mol Cell. 2018-7-12

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[3]
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[4]
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Mol Med. 2025-6-9

[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
The Ku-binding motif is a conserved module for recruitment and stimulation of non-homologous end-joining proteins.

Nat Commun. 2016-4-11

[2]
A human short open reading frame (sORF)-encoded polypeptide that stimulates DNA end joining.

J Biol Chem. 2014-3-7

[3]
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Nat Struct Mol Biol. 2014-1-12

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Double-strand break repair: 53BP1 comes into focus.

Nat Rev Mol Cell Biol. 2013-12-11

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Super-resolution fluorescence imaging of telomeres reveals TRF2-dependent T-loop formation.

Cell. 2013-10-10

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Nature. 2013-2-6

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A cell cycle-dependent regulatory circuit composed of 53BP1-RIF1 and BRCA1-CtIP controls DNA repair pathway choice.

Mol Cell. 2013-1-17

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53BP1 regulates DSB repair using Rif1 to control 5' end resection.

Science. 2013-1-10

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Science. 2013-1-3

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Playing the end game: DNA double-strand break repair pathway choice.

Mol Cell. 2012-8-24

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