Basal CHK1 activity safeguards its stability to maintain intrinsic S-phase checkpoint functions.


Journal

The Journal of cell biology
ISSN: 1540-8140
Titre abrégé: J Cell Biol
Pays: United States
ID NLM: 0375356

Informations de publication

Date de publication:
02 09 2019
Historique:
received: 14 02 2019
revised: 12 06 2019
accepted: 08 07 2019
pubmed: 2 8 2019
medline: 19 5 2020
entrez: 2 8 2019
Statut: ppublish

Résumé

The DNA replication machinery frequently encounters impediments that slow replication fork progression and threaten timely and error-free replication. The CHK1 protein kinase is essential to deal with replication stress (RS) and ensure genome integrity and cell survival, yet how basal levels and activity of CHK1 are maintained under physiological, unstressed conditions is not well understood. Here, we reveal that CHK1 stability is controlled by its steady-state activity during unchallenged cell proliferation. This autoactivatory mechanism, which depends on ATR and its coactivator ETAA1 and is tightly associated with CHK1 autophosphorylation at S296, counters CHK1 ubiquitylation and proteasomal degradation, thereby preventing attenuation of S-phase checkpoint functions and a compromised capacity to respond to RS. Based on these findings, we propose that steady-state CHK1 activity safeguards its stability to maintain intrinsic checkpoint functions and ensure genome integrity and cell survival.

Identifiants

pubmed: 31366665
pii: jcb.201902085
doi: 10.1083/jcb.201902085
pmc: PMC6719454
doi:

Substances chimiques

Antigens, Surface 0
ETAA1 protein, human 0
ATR protein, human EC 2.7.11.1
Ataxia Telangiectasia Mutated Proteins EC 2.7.11.1
CHEK1 protein, human EC 2.7.11.1
Checkpoint Kinase 1 EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2865-2875

Informations de copyright

© 2019 Michelena et al.

Références

Cell. 2000 Mar 17;100(6):681-92
pubmed: 10761933
Genes Dev. 2000 Jun 15;14(12):1439-47
pubmed: 10859163
Genes Dev. 2000 Jun 15;14(12):1448-59
pubmed: 10859164
EMBO J. 2004 Feb 25;23(4):908-18
pubmed: 14765108
Cancer Cell. 2004 Jul;6(1):45-59
pubmed: 15261141
Mol Cell Biol. 2005 May;25(9):3553-62
pubmed: 15831461
Mol Cell. 2005 Sep 2;19(5):607-18
pubmed: 16137618
Mol Cell. 2006 Aug 4;23(3):307-18
pubmed: 16885021
Mol Cell. 2006 Aug 4;23(3):319-29
pubmed: 16885022
Curr Biol. 2006 Oct 10;16(19):1950-5
pubmed: 16934469
J Cell Sci. 2006 Oct 15;119(Pt 20):4269-75
pubmed: 17003105
Nat Cell Biol. 2007 Apr;9(4):391-401
pubmed: 17384638
EMBO J. 2007 Jun 6;26(11):2719-31
pubmed: 17491592
Cancer Res. 2009 Mar 15;69(6):2630-7
pubmed: 19276361
Mol Cell. 2009 Aug 28;35(4):442-53
pubmed: 19716789
PLoS One. 2010 Jan 05;5(1):e8581
pubmed: 20052416
EMBO J. 2010 Aug 18;29(16):2802-12
pubmed: 20639859
J Cell Biol. 2010 Dec 27;191(7):1285-97
pubmed: 21173116
Nucleic Acids Res. 2012 Jan;40(2):477-86
pubmed: 21937510
Mol Cell. 2011 Nov 4;44(3):397-409
pubmed: 22055186
FEBS Lett. 2012 Nov 16;586(22):3974-9
pubmed: 23068608
Mol Cell Biol. 2013 Jan;33(2):213-26
pubmed: 23109433
Mol Cell. 2013 Oct 24;52(2):206-20
pubmed: 24055346
Cell. 2013 Nov 21;155(5):1088-103
pubmed: 24267891
Cell Rep. 2013 Nov 27;5(4):1095-107
pubmed: 24268773
Nat Cell Biol. 2014 Jan;16(1):2-9
pubmed: 24366029
Nucleic Acids Res. 2014 Apr;42(7):4463-73
pubmed: 24500207
Cell Cycle. 2014;13(24):3921-6
pubmed: 25483066
Mutat Res Rev Mutat Res. 2015 Jan-Mar;763:168-80
pubmed: 25795119
Nat Commun. 2015 Apr 16;6:6823
pubmed: 25880015
Nat Rev Cancer. 2015 May;15(5):276-89
pubmed: 25907220
Nat Rev Drug Discov. 2015 Jun;14(6):405-23
pubmed: 25953507
FEBS J. 2015 Oct;282(19):3681-92
pubmed: 26216057
Oncotarget. 2015 Nov 3;6(34):35755-69
pubmed: 26437225
Science. 2016 Jun 3;352(6290):1178-9
pubmed: 27257245
Annu Rev Genet. 2016 Nov 23;50:155-173
pubmed: 27617969
Nat Cell Biol. 2016 Nov;18(11):1196-1207
pubmed: 27723717
Nat Cell Biol. 2016 Nov;18(11):1185-1195
pubmed: 27723720
Curr Biol. 2016 Dec 19;26(24):3257-3268
pubmed: 27818175
Mol Cell. 2017 Jan 19;65(2):272-284
pubmed: 28107649
Nucleic Acids Res. 2017 May 5;45(8):4532-4549
pubmed: 28180282
Oncogene. 2017 Jun 29;36(26):3740-3748
pubmed: 28192407
Mol Cell. 2017 Mar 2;65(5):832-847.e4
pubmed: 28257700
Mol Cell. 2017 Jun 15;66(6):735-749
pubmed: 28622519
Mol Cell. 2017 Jun 15;66(6):801-817
pubmed: 28622525
Nat Rev Genet. 2017 Sep;18(9):535-550
pubmed: 28714480
Nat Rev Mol Cell Biol. 2017 Oct;18(10):622-636
pubmed: 28811666
Oncotarget. 2018 Apr 3;9(25):17512-17522
pubmed: 29707125
Proc Natl Acad Sci U S A. 2018 May 22;115(21):5546-5551
pubmed: 29735693
Science. 2018 Aug 24;361(6404):806-810
pubmed: 30139873
Mol Oncol. 2019 Feb;13(2):307-321
pubmed: 30428154
Nucleic Acids Res. 2019 Jan 25;47(2):762-778
pubmed: 30445466

Auteurs

Jone Michelena (J)

Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.

Marco Gatti (M)

Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.

Federico Teloni (F)

Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.
Molecular Life Sciences Program, Life Science Zurich Graduate School, Zurich, Switzerland.

Ralph Imhof (R)

Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.

Matthias Altmeyer (M)

Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland matthias.altmeyer@uzh.ch.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH