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DNA damage during S-phase mediates the proliferation-quiescence decision in the subsequent G1 via p21 expression

Abstract:
Following DNA damage caused by exogenous sources, such as ionizing radiation, the tumour suppressor p53 mediates cell cycle arrest via expression of the CDK inhibitor, p21. However, the role of p21 in maintaining genomic stability in the absence of exogenous DNA-damaging agents is unclear. Here, using live single-cell measurements of p21 protein in proliferating cultures, we show that naturally occurring DNA damage incurred over S-phase causes p53-dependent accumulation of p21 during mother G2- and daughter G1-phases. High p21 levels mediate G1 arrest via CDK inhibition, yet lower levels have no impact on G1 progression, and the ubiquitin ligases CRL4(Cdt2) and SCF(Skp2) couple to degrade p21 prior to the G1/S transition. Mathematical modelling reveals that a bistable switch, created by CRL4(Cdt2), promotes irreversible S-phase entry by keeping p21 levels low, preventing premature S-phase exit upon DNA damage. Thus, we characterize how p21 regulates the proliferation-quiescence decision to maintain genomic stability.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/ncomms14728

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Biochemistry
Role:
Author


More from this funder
Funding agency for:
Mansfeld, J
Grant:
MA 5831/1-1
More from this funder
Funding agency for:
Novák, B
Bakal, C
Grant:
BB/M00354X/1
BB/M00354X/1


Publisher:
Nature Publishing Group
Journal:
Nature Communications More from this journal
Volume:
8
Pages:
14728
Publication date:
2017-03-20
Acceptance date:
2017-01-26
DOI:
EISSN:
2041-1723


Language:
English
Keywords:
Pubs id:
pubs:686688
UUID:
uuid:4ec77933-5289-4c3e-9994-18344334f5c4
Local pid:
pubs:686688
Source identifiers:
686688
Deposit date:
2017-03-25

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