Evidence map›Paper›PMID 33888563›Full record

ArticleGenes & development2021

BAP1 constrains pervasive H2AK119ub1 to control the transcriptional potential of the genome.

Nadezda A Fursova, Anne H Turberfield, Neil P Blackledge, Emma L Findlater, Anna Lastuvkova, Miles K Huseyin, Paula Dobrinić, Robert J Klose

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

49 citing papers in PubMed, 88 citations in OpenAlex.

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  20. Loss of histone deubiquitinase Bap1 triggers anti-tumor immunity.Cellular oncology (Dordrecht, Netherlands) · 2025
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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

8 authors at 1 institution in 1 country.

Nadezda A FursovaDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, United Kingdom.ORCID 0000-0001-9894-5958
Anne H TurberfieldDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, United Kingdom.ORCID 0000-0002-9541-4542
Neil P BlackledgeDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, United Kingdom.ORCID 0000-0002-7142-6477
Emma L FindlaterDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, United Kingdom.
Anna LastuvkovaDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, United Kingdom.
Miles K HuseyinDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, United Kingdom.ORCID 0000-0002-0258-2994
Paula DobrinićDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, United Kingdom.
Robert J KloseDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, United Kingdom.
University of Oxford · GB

Funding

Wellcome Trust 209400/Z/17/Z
6 · The paper itself

Abstract

Histone-modifying systems play fundamental roles in gene regulation and the development of multicellular organisms. Histone modifications that are enriched at gene regulatory elements have been heavily studied, but the function of modifications found more broadly throughout the genome remains poorly understood. This is exemplified by histone H2A monoubiquitylation (H2AK119ub1), which is enriched at Polycomb-repressed gene promoters but also covers the genome at lower levels. Here, using inducible genetic perturbations and quantitative genomics, we found that the BAP1 deubiquitylase plays an essential role in constraining H2AK119ub1 throughout the genome. Removal of BAP1 leads to pervasive genome-wide accumulation of H2AK119ub1, which causes widespread reductions in gene expression. We show that elevated H2AK119ub1 preferentially counteracts Ser5 phosphorylation on the C-terminal domain of RNA polymerase II at gene regulatory elements and causes reductions in transcription and transcription-associated histone modifications. Furthermore, failure to constrain pervasive H2AK119ub1 compromises Polycomb complex occupancy at a subset of Polycomb target genes, which leads to their derepression, providing a potential molecular rationale for why the BAP1 ortholog in

Indexed as

AnimalsCell LineGene Expression RegulationGenomeHEK293 CellsHistone CodeHistonesHumansMiceMouse Embryonic Stem CellsPhosphorylationPolycomb-Group ProteinsTumor Suppressor ProteinsUbiquitin ThiolesteraseBAP1 protein, humanBAP1 protein, mouseHistonesPolycomb-Group ProteinsTumor Suppressor ProteinsUbiquitin ThiolesteraseBAP1chromatindeubiquitylaseepigeneticsgene expressionH2AK119ub1histone modificationhistone monoubiquitylationPolycombtranscription

Identifiers

PMID33888563
PMCPMC8091973
OpenAlexW3154909682

What OpenQuestion holds

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LicenceCC BY
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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.