Pre-rRNA Facilitates TopBP1-Mediated DNA Double-Strand Break Response.
ATR activation
DNA damage response
TopBP1
pre-ribosomal RNA
Journal
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
ISSN: 2198-3844
Titre abrégé: Adv Sci (Weinh)
Pays: Germany
ID NLM: 101664569
Informations de publication
Date de publication:
10 2023
10 2023
Historique:
revised:
28
06
2023
received:
24
11
2022
medline:
3
11
2023
pubmed:
16
8
2023
entrez:
15
8
2023
Statut:
ppublish
Résumé
In response to genotoxic stress-induced DNA damage, TopBP1 mediates ATR activation for signaling transduction and DNA damage repair. However, the detailed molecular mechanism remains elusive. Here, using unbiased protein affinity purification and RNA sequencing, it is found that TopBP1 is associated with pre-ribosomal RNA (pre-rRNA). Pre-rRNA co-localized with TopBP1 at DNA double-strand breaks (DSBs). Similar to pre-rRNA, ribosomal proteins also colocalize with TopBP1 at DSBs. The recruitment of TopBP1 to DSBs is suppressed when cells are transiently treated with RNA polymerase I inhibitor (Pol I-i) to suppress pre-rRNA biogenesis but not protein translation. Moreover, the BRCT4-5 of TopBP1 recognizes pre-rRNA and forms liquid-liquid phase separation (LLPS) with pre-rRNA, which may be the molecular basis of DSB-induced foci of TopBP1. Finally, Pol I-i treatment impairs TopBP1-associated cell cycle checkpoint activation and homologous recombination repair. Collectively, this study reveals that pre-rRNA plays a key role in the TopBP1-dependent DNA damage response.
Identifiants
pubmed: 37582658
doi: 10.1002/advs.202206931
pmc: PMC10558638
doi:
Substances chimiques
RNA Precursors
0
DNA-Binding Proteins
0
Cell Cycle Proteins
0
Nuclear Proteins
0
Carrier Proteins
0
Ataxia Telangiectasia Mutated Proteins
EC 2.7.11.1
DNA
9007-49-2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2206931Subventions
Organisme : National Natural Science Foundation of China
ID : 32090034
Organisme : National Natural Science Foundation of China
ID : 81874160
Informations de copyright
© 2023 The Authors. Advanced Science published by Wiley-VCH GmbH.
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