ArticleCerebral cortex (New York, N.Y. : 1991)2024
Polycomb repressive complex 2 is critical for mouse cortical glutamatergic neuron development.
Article in Cerebral cortex (New York, N.Y. : 1991), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Interactions of LINE-1 ORF1p with proteins and chromatin suggest a role in neuronal physiology.Life science alliance · 2026Article
- Systemic epigenetic dysregulation as a driver of ageing and a therapeutic target.Nature reviews. Molecular cell biology · 2026Review
- A multi-center cross-platform single-cell multimodal atlas of the mouse cerebral cortex.Scientific data · 2026Article
- Neurogenesis and the Epigenetic Landscape: Role of Histone Modifications and Chromatin Remodeling.Brain and behavior · 2026Review
- Single cell transcriptomics of the cerebral cortex of mice lacking the PRC2 gene eed.BMC research notes · 2024Article
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14 authors.
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Abstract
The Polycomb Repressive Complex 2 (PRC2) regulates corticogenesis, yet the consequences of mutations to this epigenetic modifier in the mature brain are poorly defined. Importantly, PRC2 core genes are haploinsufficient and causative of several human neurodevelopmental disorders. To address the role of PRC2 in mature cortical structure and function, we conditionally deleted the PRC2 gene Eed from the developing mouse dorsal telencephalon. Adult homozygotes displayed smaller forebrain structures. Single-nucleus transcriptomics revealed that glutamatergic neurons were particularly affected, exhibiting dysregulated gene expression profiles, accompanied by aberrations in neuronal morphology and connectivity. Remarkably, homozygous mice performed well on challenging cognitive tasks. In contrast, while heterozygous mice did not exhibit clear anatomical or behavioral differences, they displayed dysregulation of neuronal genes and altered neuronal morphology that was strikingly different from homozygous phenotypes. Collectively, these data reveal how alterations to PRC2 function shape the mature brain and reveal a dose-specific role for PRC2 in determining glutamatergic neuron identity.
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