p53-dependent chromatin relaxation is required for DNA double-strand break repair

The tumor suppressor p53, an indispensable nuclear transcription factor, plays a central role in orchestrating cellular responses when DNA damage occurs. In this study, we demonstrate that in the initial phases of DNA double-strand break (DSB) repair, p53 is rapidly recruited to sites of damage and...

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Main Authors: Chen Hongyu, Shan Jin, Qi Wenjing, Chen Lili, Zeng Xianlu
Format: Article
Language:English
Published: China Science Publishing & Media Ltd. 2025-02-01
Series:Acta Biochimica et Biophysica Sinica
Subjects:
Online Access:https://www.sciengine.com/doi/10.3724/abbs.2025008
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author Chen Hongyu
Shan Jin
Qi Wenjing
Chen Lili
Zeng Xianlu
author_facet Chen Hongyu
Shan Jin
Qi Wenjing
Chen Lili
Zeng Xianlu
author_sort Chen Hongyu
collection DOAJ
description The tumor suppressor p53, an indispensable nuclear transcription factor, plays a central role in orchestrating cellular responses when DNA damage occurs. In this study, we demonstrate that in the initial phases of DNA double-strand break (DSB) repair, p53 is rapidly recruited to sites of damage and the surrounding chromatin, where it enhances DSB repair efficiency. This enhancement occurs through the modulation of chromatin dynamics and the promotion of a more relaxed chromatin configuration, a process influenced by p53 in response to DSB-inducing factors such as etoposide, ultraviolet radiation, and nucleases. These results underscore the pivotal function of p53 <?A3B2 tlsb=-.015w?>as a rapid responder to DSBs, delineating a significant departure from its traditionally recognized role as a downstream <?A3B2 tlsb?> transcriptional regulator in DNA damage repair processes. This study emphasizes that the direct engagement of p53 in DNA repair through chromatin structure regulation extends beyond its established involvement in UV irradiation-induced nucleotide excision repair (NER), demonstrating analogous mechanistic attributes in the context of DSB repair. This newly illuminated perspective enhances our understanding of the multifaceted roles of p53 in genome stability and integrity.
format Article
id doaj-art-e38cc93569114da3ba41799a8610c053
institution OA Journals
issn 1672-9145
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publishDate 2025-02-01
publisher China Science Publishing & Media Ltd.
record_format Article
series Acta Biochimica et Biophysica Sinica
spelling doaj-art-e38cc93569114da3ba41799a8610c0532025-08-20T02:01:20ZengChina Science Publishing & Media Ltd.Acta Biochimica et Biophysica Sinica1672-91452025-02-015770171110.3724/abbs.202500820d259ccp53-dependent chromatin relaxation is required for DNA double-strand break repairChen Hongyu0Shan Jin1Qi Wenjing2Chen Lili3Zeng Xianlu4["The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China","Institute of Neuroscience, State Key Laboratory of Neuroscience, Center for Excellence in Brain Science & Intelligence Technology, Chinese Academy of Sciences, Shanghai 200031, China"]["The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China","Institute of Systems and Physical Biology, Shenzhen Bay Laboratory, Shenzhen 518107, China"]["The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China","Department of Bioscience, Changchun Normal University, Changchun 130032, China"]["The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China","College of Life Science, Liaoning University, Shenyang 110036, China"]["The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China"]The tumor suppressor p53, an indispensable nuclear transcription factor, plays a central role in orchestrating cellular responses when DNA damage occurs. In this study, we demonstrate that in the initial phases of DNA double-strand break (DSB) repair, p53 is rapidly recruited to sites of damage and the surrounding chromatin, where it enhances DSB repair efficiency. This enhancement occurs through the modulation of chromatin dynamics and the promotion of a more relaxed chromatin configuration, a process influenced by p53 in response to DSB-inducing factors such as etoposide, ultraviolet radiation, and nucleases. These results underscore the pivotal function of p53 <?A3B2 tlsb=-.015w?>as a rapid responder to DSBs, delineating a significant departure from its traditionally recognized role as a downstream <?A3B2 tlsb?> transcriptional regulator in DNA damage repair processes. This study emphasizes that the direct engagement of p53 in DNA repair through chromatin structure regulation extends beyond its established involvement in UV irradiation-induced nucleotide excision repair (NER), demonstrating analogous mechanistic attributes in the context of DSB repair. This newly illuminated perspective enhances our understanding of the multifaceted roles of p53 in genome stability and integrity.https://www.sciengine.com/doi/10.3724/abbs.2025008DNA damage repairDNA double-strand breaks (DSBs)p53chromatin relaxation
spellingShingle Chen Hongyu
Shan Jin
Qi Wenjing
Chen Lili
Zeng Xianlu
p53-dependent chromatin relaxation is required for DNA double-strand break repair
Acta Biochimica et Biophysica Sinica
DNA damage repair
DNA double-strand breaks (DSBs)
p53
chromatin relaxation
title p53-dependent chromatin relaxation is required for DNA double-strand break repair
title_full p53-dependent chromatin relaxation is required for DNA double-strand break repair
title_fullStr p53-dependent chromatin relaxation is required for DNA double-strand break repair
title_full_unstemmed p53-dependent chromatin relaxation is required for DNA double-strand break repair
title_short p53-dependent chromatin relaxation is required for DNA double-strand break repair
title_sort p53 dependent chromatin relaxation is required for dna double strand break repair
topic DNA damage repair
DNA double-strand breaks (DSBs)
p53
chromatin relaxation
url https://www.sciengine.com/doi/10.3724/abbs.2025008
work_keys_str_mv AT chenhongyu p53dependentchromatinrelaxationisrequiredfordnadoublestrandbreakrepair
AT shanjin p53dependentchromatinrelaxationisrequiredfordnadoublestrandbreakrepair
AT qiwenjing p53dependentchromatinrelaxationisrequiredfordnadoublestrandbreakrepair
AT chenlili p53dependentchromatinrelaxationisrequiredfordnadoublestrandbreakrepair
AT zengxianlu p53dependentchromatinrelaxationisrequiredfordnadoublestrandbreakrepair