The Chromatin Architectural Protein CTCF Is Critical for Cell Survival upon Irradiation-Induced DNA Damage.
CTCF
DNA damage response
DNA repair
biophysical modeling
cancer
chromatin architecture
chromatin domain
clonogenic survival
ionizing radiation
radiosensitivity
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
31 Mar 2022
31 Mar 2022
Historique:
received:
27
02
2022
revised:
26
03
2022
accepted:
29
03
2022
entrez:
12
4
2022
pubmed:
13
4
2022
medline:
14
4
2022
Statut:
epublish
Résumé
CTCF is a nuclear protein initially discovered for its role in enhancer-promoter insulation. It has been shown to play a role in genome architecture and in fact, its DNA binding sites are enriched at the borders of chromatin domains. Recently, we showed that depletion of CTCF impairs the DNA damage response to ionizing radiation. To investigate the relationship between chromatin domains and DNA damage repair, we present here clonogenic survival assays in different cell lines upon CTCF knockdown and ionizing irradiation. The application of a wide range of ionizing irradiation doses (0-10 Gy) allowed us to investigate the survival response through a biophysical model that accounts for the double-strand breaks' probability distribution onto chromatin domains. We demonstrate that the radiosensitivity of different cell lines is increased upon lowering the amount of the architectural protein. Our model shows that the deficiency in the DNA repair ability is related to the changes in the size of chromatin domains that occur when different amounts of CTCF are present in the nucleus.
Identifiants
pubmed: 35409255
pii: ijms23073896
doi: 10.3390/ijms23073896
pmc: PMC8999573
pii:
doi:
Substances chimiques
CCCTC-Binding Factor
0
Chromatin
0
DNA
9007-49-2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : Project-ID 393547839 - SFB 1361
Organisme : Deutsche Forschungsgemeinschaft
ID : GRK1657/TP1C
Organisme : Deutsche Forschungsgemeinschaft
ID : CA 198/15-1
Organisme : Deutsche Forschungsgemeinschaft
ID : GRK1657/TP2C
Organisme : TU Darmstadt
ID : Open Access Publishing Fund
Organisme : Deutsche Forschungsgemeinschaft
ID : CA 198/9-2
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