Evidence map›Paper›PMID 29220657›Full record

ArticleMolecular cell2017

hnRNPK Recruits PCGF3/5-PRC1 to the Xist RNA B-Repeat to Establish Polycomb-Mediated Chromosomal Silencing.

Greta Pintacuda, Guifeng Wei, Chloë Roustan, Burcu Anil Kirmizitas, Nicolae Solcan, Andrea Cerase, Alfredo Castello, Shabaz Mohammed, Benoît Moindrot, Tatyana B Nesterova and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed
12.4field-weighted citation impact, top 1% 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

206 citing papers in PubMed, 391 citations in OpenAlex.

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146 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Greta PintacudaDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Guifeng WeiDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Chloë RoustanDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Burcu Anil KirmizitasDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Nicolae SolcanDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Andrea CeraseDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Alfredo CastelloPosttranscriptional Networks in Infection and Cell Cycle Progression, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Shabaz MohammedProteomics Technology Development and Application, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Benoît MoindrotDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Tatyana B NesterovaDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Neil BrockdorffDevelopmental Epigenetics, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK. Electronic address: neil.brockdorff@bioch.ox.ac.uk.
University of Oxford · GB

Funding

European Research Council 340081Medical Research Council MC_UU_12014/10Medical Research Council MR/L019434/1Wellcome Trust
6 · The paper itself

Abstract

The Polycomb-repressive complexes PRC1 and PRC2 play a key role in chromosome silencing induced by the non-coding RNA Xist. Polycomb recruitment is initiated by the PCGF3/5-PRC1 complex, which catalyzes chromosome-wide H2A lysine 119 ubiquitylation, signaling recruitment of other PRC1 complexes, and PRC2. However, the molecular mechanism for PCGF3/5-PRC1 recruitment by Xist RNA is not understood. Here we define the Xist RNA Polycomb Interaction Domain (XR-PID), a 600 nt sequence encompassing the Xist B-repeat element. Deletion of XR-PID abolishes Xist-dependent Polycomb recruitment, in turn abrogating Xist-mediated gene silencing and reversing Xist-induced chromatin inaccessibility. We identify the RNA-binding protein hnRNPK as the principal XR-PID binding factor required to recruit PCGF3/5-PRC1. Accordingly, synthetically tethering hnRNPK to Xist RNA lacking XR-PID is sufficient for Xist-dependent Polycomb recruitment. Our findings define a key pathway for Polycomb recruitment by Xist RNA, providing important insights into mechanisms of chromatin modification by non-coding RNA.

Indexed as

X Chromosome InactivationAnimalsBinding SitesCell LineEmbryonic Stem CellsHeterogeneous-Nuclear Ribonucleoprotein KHistonesLysineMicePolycomb-Group ProteinsPolycomb Repressive Complex 1Protein BindingProtein Interaction Domains and MotifsRibonucleoproteinsRNA InterferenceRNA, Long NoncodingHeterogeneous-Nuclear Ribonucleoprotein KHistonesHNRNPK protein, mouseLysinePcgf3 protein, mousePcgf5 protein, mousePolycomb-Group ProteinsPolycomb Repressive Complex 1RibonucleoproteinsRNA, Long NoncodingXIST non-coding RNA

Identifiers

PMID29220657
PMCPMC5735038
OpenAlexW2774477523

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.