Evidence map›Paper›PMID 24986859›Full record

ArticleeLife2014

Interactions with RNA direct the Polycomb group protein SCML2 to chromatin where it represses target genes.

Roberto Bonasio, Emilio Lecona, Varun Narendra, Philipp Voigt, Fabio Parisi, Yuval Kluger, Danny Reinberg

Open access · goldAbstract read
In one paragraph

Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  3. Polycomb-mediated genome architecture enables long-range spreading of H3K27 methylation.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  18. Samd7 is a cell type-specific PRC1 component essential for establishing retinal rod photoreceptor identity.Proceedings of the National Academy of Sciences of the United States of America · 2017
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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

7 authors at 2 institutions in 1 country.

Roberto BonasioDepartment of Biochemistry and Molecular Pharmacology, Howard Hughes Medical Institute, New York University School of Medicine, New York, United States.
Emilio LeconaDepartment of Biochemistry and Molecular Pharmacology, Howard Hughes Medical Institute, New York University School of Medicine, New York, United States.
Varun NarendraDepartment of Biochemistry and Molecular Pharmacology, Howard Hughes Medical Institute, New York University School of Medicine, New York, United States.
Philipp VoigtDepartment of Biochemistry and Molecular Pharmacology, Howard Hughes Medical Institute, New York University School of Medicine, New York, United States.
Fabio ParisiDepartment of Pathology, Yale University School of Medicine, New Haven, United States Yale Cancer Center, Yale University School of Medicine, New Haven, United States.
Yuval KlugerDepartment of Pathology, Yale University School of Medicine, New Haven, United States Yale Cancer Center, Yale University School of Medicine, New Haven, United States.
Danny ReinbergDepartment of Biochemistry and Molecular Pharmacology, Howard Hughes Medical Institute, New York University School of Medicine, New York, United States danny.reinberg@nyumc.org.
New York University · USYale University · US

Funding

Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI DAVID L RIMM · 1985 to 2026
$85.0M
Transcription Regulation by NC2R01GM064844 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI REINBERG, DANNY · 2002 to 2014
$3.3M
NCI NIH HHS CA-16359NCI NIH HHS P30 CA016359NIGMS NIH HHS GM-64844NIGMS NIH HHS R01 GM064844PHS HHS R37-37120
6 · The paper itself

Abstract

Polycomb repressive complex-1 (PRC1) is essential for the epigenetic regulation of gene expression. SCML2 is a mammalian homolog of Drosophila SCM, a Polycomb-group protein that associates with PRC1. In this study, we show that SCML2A, an SCML2 isoform tightly associated to chromatin, contributes to PRC1 localization and also directly enforces repression of certain Polycomb target genes. SCML2A binds to PRC1 via its SPM domain and interacts with ncRNAs through a novel RNA-binding region (RBR). Targeting of SCML2A to chromatin involves the coordinated action of the MBT domains, RNA binding, and interaction with PRC1 through the SPM domain. Deletion of the RBR reduces the occupancy of SCML2A at target genes and overexpression of a mutant SCML2A lacking the RBR causes defects in PRC1 recruitment. These observations point to a role for ncRNAs in regulating SCML2 function and suggest that SCML2 participates in the epigenetic control of transcription directly and in cooperation with PRC1.DOI: http://dx.doi.org/10.7554/eLife.02637.001.

Indexed as

Cell NucleusChromatinGenome, HumanHeLa CellsHumansPolycomb-Group ProteinsPolycomb Repressive Complex 1Protein BindingProtein Structure, TertiaryProtein TransportRepressor ProteinsRNARNA-Binding ProteinsRNA, UntranslatedSequence Analysis, RNATranscription, GeneticBMI1 protein, humanChromatinPolycomb-Group ProteinsPolycomb Repressive Complex 1Repressor ProteinsRNARNA-Binding ProteinsRNA, UntranslatedSCML2 protein, humanchromatinMBTnoncoding RNAsPolycombPRC1SCML2

Identifiers

PMID24986859
PMCPMC4074974
OpenAlexW2124574849

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.