ArticleDevelopmental biology2018
Stage-specific roles of Ezh2 and Retinoic acid signaling ensure calvarial bone lineage commitment.
Article in Developmental biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Mouse scalp development requires Rac1 and SRF for the maintenance of mechanoresponsive mesenchyme.Development (Cambridge, England) · 2025Article
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- Mesenchymal Wnts are required for morphogenetic movements of calvarial osteoblasts during apical expansion.Development (Cambridge, England) · 2024Article
- Apical expansion of calvarial osteoblasts and suture patency is dependent on fibronectin cues.Development (Cambridge, England) · 2024Article
- The Roles of WNT Signaling Pathways in Skin Development and Mechanical-Stretch-Induced Skin Regeneration.Biomolecules · 2023Review
- RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis.Life science alliance · 2023Article
- Stuck on you: Meninges cellular crosstalk in development.Current opinion in neurobiology · 2023Review
- Epigenetic control of mesenchymal stem cells orchestrates bone regeneration.Frontiers in endocrinology · 2023Review
- EZH2 modulates retinoic acid signaling to ensure myotube formation during development.FEBS letters · 2022Article
- Dermal EZH2 orchestrates dermal differentiation and epidermal proliferation during murine skin development.Developmental biology · 2021Article
- Erf Affects Commitment and Differentiation of Osteoprogenitor Cells in Cranial Sutures via the Retinoic Acid Pathway.Molecular and cellular biology · 2021Article
- Polycomb Repressive Complex 2: a Dimmer Switch of Gene Regulation in Calvarial Bone Development.Current osteoporosis reports · 2020Review
- New Insights into the Control of Cell Fate Choices and Differentiation by Retinoic Acid in Cranial, Axial and Caudal Structures.Biomolecules · 2019Review
- Developmental biology of the meninges.Genesis (New York, N.Y. : 2000) · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Development of the skull bones requires the coordination of two stem progenitor populations, the cranial neural crest cells (CNCC) and head paraxial mesoderm (PM), to ensure cell fate selection and morphogenesis. The epigenetic methyltransferase, Ezh2, plays a role in skull bone formation, but the spatiotemporal function of Ezh2 between the CNCC- and PM-derived bone formation in vivo remains undefined. Here, using a temporally-inducible conditional deletion of Ezh2 in both the CNCC- and PM- derived cranial mesenchyme between E8.5 and E9.5, we find a reduction of the CNCC-derived calvarial bones and a near complete loss of the PM-derived calvarial bones due to an arrest in calvarial bone fate commitment. In contrast, deletion of Ezh2 after E9.5 permits PM-derived skull bone development, suggesting that Ezh2 is required early to guide calvarial bone progenitor commitment. Furthermore, exposure to all-trans Retinoic acid at E10.0 can mimic the Ezh2 mutant calvarial phenotype, and administration of the pan retinoic acid receptor (RAR) antagonist, BMS-453, to Ezh2 mutants partially restores the commitment to the calvarial bone lineage and PM-derived bone development in vivo. Exogenous RA signaling activation in the Ezh2 mutants leads to synergistic activation of the anti-osteogenic factors in the cranial mesenchyme in vivo. Thus, RA signaling and EZH2 can function in parallel to guide calvarial bone progenitor commitment by balancing the suppression of anti-osteogenic factors.
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