Mild replication stress causes premature centriole disengagement via a sub-critical Plk1 activity under the control of ATR-Chk1.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
29 09 2023
29 09 2023
Historique:
received:
07
11
2022
accepted:
18
09
2023
medline:
2
10
2023
pubmed:
29
9
2023
entrez:
29
9
2023
Statut:
epublish
Résumé
A tight synchrony between the DNA and centrosome cycle is essential for genomic integrity. Centriole disengagement, which licenses centrosomes for duplication, occurs normally during mitotic exit. We recently demonstrated that mild DNA replication stress typically seen in cancer cells causes premature centriole disengagement in untransformed mitotic human cells, leading to transient multipolar spindles that favour chromosome missegregation. How mild replication stress accelerates the centrosome cycle at the molecular level remained, however, unclear. Using ultrastructure expansion microscopy, we show that mild replication stress induces premature centriole disengagement already in G2 via the ATR-Chk1 axis of the DNA damage repair pathway. This results in a sub-critical Plk1 kinase activity that primes the pericentriolar matrix for Separase-dependent disassembly but is insufficient for rapid mitotic entry, causing premature centriole disengagement in G2. We postulate that the differential requirement of Plk1 activity for the DNA and centrosome cycles explains how mild replication stress disrupts the synchrony between both processes and contributes to genomic instability.
Identifiants
pubmed: 37773176
doi: 10.1038/s41467-023-41753-1
pii: 10.1038/s41467-023-41753-1
pmc: PMC10541884
doi:
Substances chimiques
Cell Cycle Proteins
0
Separase
EC 3.4.22.49
ATR protein, human
EC 2.7.11.1
Ataxia Telangiectasia Mutated Proteins
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
6088Subventions
Organisme : Swiss National Science Foundation
ID : 31003A_179413
Pays : Switzerland
Informations de copyright
© 2023. Springer Nature Limited.
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