Evidence map›Paper›PMID 28903048›Full record

ArticleCell reports2017

Set2 Methyltransferase Facilitates DNA Replication and Promotes Genotoxic Stress Responses through MBF-Dependent Transcription.

Chen-Chun Pai, Anastasiya Kishkevich, Rachel S Deegan, Andrea Keszthelyi, Lisa Folkes, Stephen E Kearsey, Nagore De León, Ignacio Soriano, Robertus Antonius Maria de Bruin, Antony M Carr and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Chen-Chun PaiCRUK-MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, ORCRB, Roosevelt Drive, Oxford OX3 7DQ, UK. Electronic address: chen-chun.pai@oncology.ox.ac.uk.
Anastasiya KishkevichMRC Laboratory for Molecular Cell Biology, University College London, Gower Street, London WC1E 6B, UK.
Rachel S DeeganCRUK-MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, ORCRB, Roosevelt Drive, Oxford OX3 7DQ, UK.
Andrea KeszthelyiGenome Damage and Stability Centre, School of Life Sciences, University of Sussex, Falmer, Brighton, Sussex BN1 9RQ, UK.
Lisa FolkesCRUK-MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, ORCRB, Roosevelt Drive, Oxford OX3 7DQ, UK.
Stephen E KearseyDepartment of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK.
Nagore De LeónDepartment of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK.
Ignacio SorianoDepartment of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK.
Robertus Antonius Maria de BruinMRC Laboratory for Molecular Cell Biology, University College London, Gower Street, London WC1E 6B, UK.
Antony M CarrGenome Damage and Stability Centre, School of Life Sciences, University of Sussex, Falmer, Brighton, Sussex BN1 9RQ, UK.
Timothy C HumphreyCRUK-MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, ORCRB, Roosevelt Drive, Oxford OX3 7DQ, UK. Electronic address: timothy.humphrey@oncology.ox.ac.uk.
University of Oxford · GBCRUK/MRC Oxford Institute for Radiation Oncology · GBMRC Laboratory for Molecular Cell Biology · GBUniversity of Sussex · GB

Funding

Cancer Research UK 20147European Research Council 268788Medical Research Council MC_PC_12003Medical Research Council MC_U142784382Medical Research Council MC_UU_00001/4Medical Research Council MR/L016591/1
6 · The paper itself

Abstract

Chromatin modification through histone H3 lysine 36 methylation by the SETD2 tumor suppressor plays a key role in maintaining genome stability. Here, we describe a role for Set2-dependent H3K36 methylation in facilitating DNA replication and the transcriptional responses to both replication stress and DNA damage through promoting MluI cell-cycle box (MCB) binding factor (MBF)-complex-dependent transcription in fission yeast. Set2 loss leads to reduced MBF-dependent ribonucleotide reductase (RNR) expression, reduced deoxyribonucleoside triphosphate (dNTP) synthesis, altered replication origin firing, and a checkpoint-dependent S-phase delay. Accordingly, prolonged S phase in the absence of Set2 is suppressed by increasing dNTP synthesis. Furthermore, H3K36 is di- and tri-methylated at these MBF gene promoters, and Set2 loss leads to reduced MBF binding and transcription in response to genotoxic stress. Together, these findings provide new insights into how H3K36 methylation facilitates DNA replication and promotes genotoxic stress responses in fission yeast.

Indexed as

DNA DamageDNA ReplicationTranscription, GeneticCell Cycle CheckpointsCell Cycle ProteinsDNA, FungalDown-RegulationGene Expression Regulation, FungalGenes, FungalHistone-Lysine N-MethyltransferaseMutationNucleotidesReplication OriginSchizosaccharomycesSchizosaccharomyces pombe ProteinsS PhaseCell Cycle ProteinsDNA, FungalDSC1 protein, S pombeHistone-Lysine N-MethyltransferaseNucleotidesSchizosaccharomyces pombe ProteinsSet2 protein, S pombeTranscription FactorsDNA replicationdNTPhistone H3K36 methylationhistone methylationMBFribonucleotide reductaseSchizosaccharomyces pombeSet2

Identifiers

PMID28903048
PMCPMC5608972
OpenAlexW2755608496

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.