Evidence map›Paper›PMID 30304473›Full record

ArticleNucleic acids research2018

Bre1-dependent H2B ubiquitination promotes homologous recombination by stimulating histone eviction at DNA breaks.

Sihao Zheng, Dan Li, Zhen Lu, Guangxue Liu, Meng Wang, Poyuan Xing, Min Wang, Yang Dong, Xuejie Wang, Jingyao Li and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 13% of its field
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

25 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
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  8. DNA Repair in Nucleosomes: Insights from Histone Modifications and Mutants.International journal of molecular sciences · 2024
    Review
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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

15 authors at 4 institutions in 2 countries.

Sihao ZhengHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Dan LiHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Zhen LuHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Guangxue LiuHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Meng WangHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Poyuan XingHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Min WangNational Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Yang DongHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Xuejie WangHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Jingyao LiHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Simin ZhangHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Haoyang PengHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Grzegorz IraThe Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Guohong LiNational Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Xuefeng ChenHubei Key Laboratory of Cell Homeostasis, the Department of Genetics, College of Life Sciences and the Institute for Advanced Studies, Wuhan University, Wuhan, Hubei 430072, China.
Wuhan University · CNChinese Academy of Sciences · CNBaylor College of Medicine · USInstitute of Biophysics · CN

Funding

Regulation of Initial Steps of Chromosomal Breaks RepairR01GM125650 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI IRA, GRZEGORZ A · 2018 to 2025
$2.9M
6 · The paper itself

Abstract

Repair of DNA double-strand breaks (DSBs) requires eviction of the histones around DNA breaks to allow the loading of numerous repair and checkpoint proteins. However, the mechanism and regulation of this process remain poorly understood. Here, we show that histone H2B ubiquitination (uH2B) promotes histone eviction at DSBs independent of resection or ATP-dependent chromatin remodelers. Cells lacking uH2B or its E3 ubiquitin ligase Bre1 exhibit hyper-resection due to the loss of H3K79 methylation that recruits Rad9, a known negative regulator of resection. Unexpectedly, despite excessive single-strand DNA being produced, bre1Δ cells show defective RPA and Rad51 recruitment and impaired repair by homologous recombination and response to DNA damage. The HR defect in bre1Δ cells correlates with impaired histone loss at DSBs and can be largely rescued by depletion of CAF-1, a histone chaperone depositing histones H3-H4. Overexpression of Rad51 stimulates histone eviction and partially suppresses the recombination defects of bre1Δ mutant. Thus, we propose that Bre1 mediated-uH2B promotes DSB repair through facilitating histone eviction and subsequent loading of repair proteins.

Indexed as

DNA DamageUbiquitinationAdenosine TriphosphateChromatinDNA Breaks, Double-StrandedDNA RepairDNA, Single-StrandedHistonesHomologous RecombinationMicroscopy, FluorescenceMutationRecombination, GeneticSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSchizosaccharomycesSequence Analysis, RNAAdenosine TriphosphateBre1 protein, S cerevisiaeChromatinDNA, Single-StrandedHistonesSaccharomyces cerevisiae Proteins

Identifiers

PMID30304473
PMCPMC6265479
OpenAlexW2896605468

What OpenQuestion holds

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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.