ArticleNature communications2020
The Polycomb group protein Ring1 regulates dorsoventral patterning of the mouse telencephalon.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Disruption of PRC1 components RING1A and RING1B promotes angiogenesis via relieving BMP4 repression.Journal of advanced research · 2026Article
- The Zinc-Finger Protein POGZ Associates with Polycomb Repressive Complex 1 to Regulate Bone Morphogenetic Protein Signaling During Neuronal Differentiation.Stem cell reviews and reports · 2026Article
- Unbalanced chromatin binding of Polycomb complexes drives neurodevelopmental disorders.Molecular cell · 2026Article
- LPLAT11/MBOAT7-driven phosphatidylinositol remodeling ensures radial glial cell integrity in developing neocortex.iScience · 2026Article
- Pluripotent stem cells-based neural organoids for modelling human brain development and diseases.Cell & bioscience · 2025Review
- Widespread association of Polycomb complex-deposited histone H2A monoubiquitylation with enhancers and neuronal gene regulation.Science advances · 2025Article
- RING1 dictates GSDMD-mediated inflammatory response and host susceptibility to pathogen infection.Cell death and differentiation · 2025Article
- Polycomb repressive complexes 1 and 2 independently and dynamically regulate euchromatin during cerebellar neurodevelopment.PLoS genetics · 2025Article
- Article
- Structural insights into how DEK nucleosome binding facilitates H3K27 trimethylation in chromatin.Nature structural & molecular biology · 2025Article
- In vivo transition in chromatin accessibility during differentiation of deep-layer excitatory neurons in the neocortex.Development (Cambridge, England) · 2025Article
- Canonical and non-canonical PRC1 differentially contribute to regulation of neural stem cell fate.Life science alliance · 2025Article
- The microcephaly-associated transcriptional regulator AUTS2 cooperates with Polycomb complex PRC2 to produce upper-layer neurons in mice.The EMBO journal · 2025Article
- Cellular senescence in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2024Review
- Artificial Meshed Vessel-Induced Dimensional Breaking Growth of Human Brain Organoids and Multiregional Assembloids.ACS nano · 2024Article
- Acquisition of neural fate by combination of BMP blockade and chromatin modification.iScience · 2023Article
- KDM2B regulates hippocampal morphogenesis by transcriptionally silencing Wnt signaling in neural progenitors.Nature communications · 2023Article
- Age-associated reduction of nuclear shape dynamics in excitatory neurons of the visual cortex.Aging cell · 2023Article
- RINGs, DUBs and Abnormal Brain Growth-Histone H2A Ubiquitination in Brain Development and Disease.Epigenomes · 2022Review
- RYBP modulates embryonic neurogenesis involving the Notch signaling pathway in a PRC1-independent pattern.Stem cell reports · 2021Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dorsal-ventral patterning of the mammalian telencephalon is fundamental to the formation of distinct functional regions including the neocortex and ganglionic eminence. While Bone morphogenetic protein (BMP), Wnt, and Sonic hedgehog (Shh) signaling are known to determine regional identity along the dorsoventral axis, how the region-specific expression of these morphogens is established remains unclear. Here we show that the Polycomb group (PcG) protein Ring1 contributes to the ventralization of the mouse telencephalon. Deletion of Ring1b or both Ring1a and Ring1b in neuroepithelial cells induces ectopic expression of dorsal genes, including those for BMP and Wnt ligands, as well as attenuated expression of the gene for Shh, a key morphogen for ventralization, in the ventral telencephalon. We observe PcG protein-mediated trimethylation of histone 3 at lysine-27 and binding of Ring1B at BMP and Wnt ligand genes specifically in the ventral region. Furthermore, forced activation of BMP or Wnt signaling represses Shh expression. Our results thus indicate that PcG proteins suppress BMP and Wnt signaling in a region-specific manner and thereby allow proper Shh expression and development of the ventral telencephalon.
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