Evidence map›Paper›PMID 38719994›Full record

ArticleThe EMBO journal2024

The GATAD2B-NuRD complex drives DNA:RNA hybrid-dependent chromatin boundary formation upon DNA damage.

Zhichao Liu, Kamal Ajit, Yupei Wu, Wei-Guo Zhu, Monika Gullerova

Abstract read
In one paragraph

Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

  1. Article
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  4. Review
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  11. Article
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  13. NEAT1 promotes genome stability via mGenes & development · 2024
    Article
  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Zhichao LiuSir William Dunn School of Pathology, South Parks Road, Oxford, OX1 3RE, United Kingdom.
Kamal AjitSir William Dunn School of Pathology, South Parks Road, Oxford, OX1 3RE, United Kingdom.
Yupei WuGuangdong Key Laboratory of Genome Instability and Human Disease Prevention, Shenzhen University International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Biochemistry and Molecular Biology, Shenzhen University School of Medicine, 518055, Shenzhen, China.
Wei-Guo ZhuGuangdong Key Laboratory of Genome Instability and Human Disease Prevention, Shenzhen University International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Biochemistry and Molecular Biology, Shenzhen University School of Medicine, 518055, Shenzhen, China.
Monika GullerovaSir William Dunn School of Pathology, South Parks Road, Oxford, OX1 3RE, United Kingdom. monika.gullerova@path.ox.ac.uk.ORCID http://orcid.org/0000-0002-4512-2779

Funding

Cancer Research UK (CRUK) BVR01170Edward Penley Abraham Trust Fund BVR01670| National Natural Science Foundation of China-Guangdong Joint Fund (-) 32090030 and 32090033Shenzhen Municipal Commission of Science and Technology Innovation JCYJ20200109114214463The Science and Technology Program of the Guangdong Province 2017B030301016
6 · The paper itself

Abstract

Double-strand breaks (DSBs) are the most lethal form of DNA damage. Transcriptional activity at DSBs, as well as transcriptional repression around DSBs, are both required for efficient DNA repair. The chromatin landscape defines and coordinates these two opposing events. However, how the open and condensed chromatin architecture is regulated remains unclear. Here, we show that the GATAD2B-NuRD complex associates with DSBs in a transcription- and DNA:RNA hybrid-dependent manner, to promote histone deacetylation and chromatin condensation. This activity establishes a spatio-temporal boundary between open and closed chromatin, which is necessary for the correct termination of DNA end resection. The lack of the GATAD2B-NuRD complex leads to chromatin hyperrelaxation and extended DNA end resection, resulting in homologous recombination (HR) repair failure. Our results suggest that the GATAD2B-NuRD complex is a key coordinator of the dynamic interplay between transcription and the chromatin landscape, underscoring its biological significance in the RNA-dependent DNA damage response.

Indexed as

ChromatinDNA Breaks, Double-StrandedMi-2 Nucleosome Remodeling and Deacetylase ComplexAnimalsDNADNA DamageDNA RepairHumansMiceRNATranscription, GeneticChromatinDNAMi-2 Nucleosome Remodeling and Deacetylase ComplexRNAChromatin BoundaryDNA DamageDNA:RNA HybridsGATAD2BNuRD Complex

Identifiers

PMID38719994
PMCPMC11183058

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.