Evidence map›Paper›PMID 42267784›Full record

ArticleInvestigative ophthalmology & visual science2026

Ezh2 Control of Bivalent Genes Fine-Tunes Developmental Competence During Retinogenesis.

Emily Davis, Abdullah Khan, Issam Aldiri

Abstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Emily DavisDepartments of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States.
Abdullah KhanDepartments of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States.
Issam AldiriDepartments of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States.

Funding

Virus Production and Manipulation of Protein/Gene Expression ModuleP30EY008098 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Yuanyuan Chen · 1989 to 2026
$17.8M
Epigenetic basis of retinal cell fate determinationR01EY030861 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AL DIRI, ISSAM · 2020 to 2024
$1.9M
Wiring and rewiring of the chromatin landscape during retinogenesisR01EY035619 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Issam Al Diri · 2024 to 2026
$1.2M
NEI NIH HHS P30 EY008098NEI NIH HHS R01 EY030861NEI NIH HHS R01 EY035619
6 · The paper itself

Abstract

Purpose: Chromatin-based repression is essential for retinal development, yet the genome-wide binding landscape of Polycomb repressive complex 2 (PRC2) in the developing retina has not been defined. In particular, how the PRC2 catalytic subunit EZH2 associates with chromatin and relates to transcriptional control in retinal progenitor cells (RPCs) remains incompletely characterized. Methods: Genome-wide EZH2 binding and H3K27me3 deposition were profiled in the developing mouse retina and integrated with transcriptomic analyses following conditional Ezh2 deletion in RPCs. Chromatin state annotations and enhancer-promoter interaction data were used to examine regulatory features associated with EZH2-bound loci. Results: EZH2 binding was enriched at promoter regions and strongly associated with H3K27me3-marked chromatin. Integration with transcriptomic data revealed that genes upregulated following Ezh2 loss were frequently EZH2-bound and enriched for loci exhibiting overlapping H3K27me3 and H3K4me3 signals at the population level. Among upregulated genes, those bound by EZH2 showed greater fold-change magnitude than unbound genes, whereas H3K27me3 occupancy alone did not differentiate fold-change within the upregulated set. Analysis of transcription factor-occupied loci indicated partial overlap between retinal progenitor transcriptional networks and Polycomb-marked regions. At the Pitx2 locus, EZH2 and H3K27me3 occupancy coincided with a distal enhancer that is accessible and transcriptionally competent in the developing retina. Conclusions: These findings provide a genome-wide characterization of EZH2 occupancy in the developing mouse retina and support a model in which EZH2-mediated repression is associated with reduced transcription from chromatin that otherwise displays features of transcriptional competence. This work offers a framework for understanding how Polycomb-associated chromatin states intersect with retinal transcriptional programs to maintain lineage-appropriate gene expression.

Indexed as

Enhancer of Zeste Homolog 2 ProteinGene Expression Regulation, DevelopmentalRetinaAnimalsChromatinHistonesMicePromoter Regions, GeneticStem CellsChromatinEnhancer of Zeste Homolog 2 ProteinEzh2 protein, mouseHistones

Identifiers

PMID42267784
PMCPMC13263970

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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 Socratic graph.