Persistent repair intermediates induce senescence

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F18%3A00495503" target="_blank" >RIV/68378050:_____/18:00495503 - isvavai.cz</a>

Result on the web

<a href="http://dx.doi.org/10.1038/s41467-018-06308-9" target="_blank" >http://dx.doi.org/10.1038/s41467-018-06308-9</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/s41467-018-06308-9" target="_blank" >10.1038/s41467-018-06308-9</a>

Result language

angličtina

Original language name

Persistent repair intermediates induce senescence

Original language description

Double-stranded DNA breaks activate a DNA damage checkpoint in G2 phase to trigger a cell cycle arrest, which can be reversed to allow for recovery. However, damaged G2 cells can also permanently exit the cell cycle, going into senescence or apoptosis, raising the question how an individual cell decides whether to recover or withdraw from the cell cycle. Here we find that the decision to withdraw from the cell cycle in G2 is critically dependent on the progression of DNA repair. We show that delayed processing of double strand breaks through HR-mediated repair results in high levels of resected DNA and enhanced ATR-dependent signalling, allowing p21 to rise to levels at which it drives cell cycle exit. These data imply that cells have the capacity to discriminate breaks that can be repaired from breaks that are difficult to repair at a time when repair is still ongoing.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

10608 - Biochemistry and molecular biology

Project

<a href="/en/project/GA16-19437S" target="_blank" >GA16-19437S: Role of deficient checkpoint barrier in cancerogenesis</a><br>

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year

2018

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Nature Communications

ISSN

2041-1723

e-ISSN

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Volume of the periodical

9

Issue of the periodical within the volume

September

Country of publishing house

GB - UNITED KINGDOM

Number of pages

10

Pages from-to

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UT code for WoS article

000445562800002

EID of the result in the Scopus database

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