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Updated: Mar 12, 2026

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
Published on: April 1, 2022
PDGFRβ regulates craniofacial development through homodimers and functional heterodimers with PDGFRα
Katherine A Fantauzzo1, Philippe Soriano1
1Department of Cell Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.
Insights
Platelet-derived growth factor receptor beta (PDGFRβ) plays a crucial role in craniofacial development. Its interaction with PDGFRα influences facial structure, and disruptions lead to birth defects.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- Craniofacial development is vital, with disruptions causing common birth defects.
- Platelet-derived growth factor receptor alpha (PDGFRα) is known to be involved.
- The function of PDGFRβ in murine craniofacial development is not well understood.
Purpose of the Study:
- To investigate the role of PDGFRβ in murine craniofacial development.
- To explore the interaction between PDGFRα and PDGFRβ in neural crest cells.
- To elucidate the signaling mechanisms of PDGF receptors in craniofacial morphogenesis.
Main Methods:
- Analyzing Pdgfrb knockout mouse models in neural crest lineage.
- Examining craniofacial phenotypes including nasal septum width and palatal shelf development.
- Investigating genetic interactions and physical associations between PDGFRα and PDGFRβ.
Main Results:
- PDGFRα and PDGFRβ are coexpressed in craniofacial mesenchyme.
- PDGFRβ ablation in neural crest cells causes nasal septum defects and delayed palatal development.
- Double mutants exhibit more severe facial clefting, indicating genetic interaction.
- PDGFRα and PDGFRβ form functional heterodimers with unique signaling properties.
Conclusions:
- PDGFRβ is essential for normal craniofacial development.
- PDGFRα and PDGFRβ form functional heterodimers, revealing a novel PDGF signaling pathway.
- This study uncovers a new mode of PDGF family signaling in vertebrate development.
Abstract:
Craniofacial development is a complex morphogenetic process, disruptions in which result in highly prevalent human birth defects. While platelet-derived growth factor (PDGF) receptor α (PDGFRα) has well-documented functions in this process, the role of PDGFRβ in murine craniofacial development is not well established. We demonstrate that PDGFRα and PDGFRβ are coexpressed in the craniofacial mesenchyme of mid-gestation mouse embryos and that ablation of Pdgfrb in the neural crest lineage results in increased nasal septum width, delayed palatal shelf development, and subepidermal blebbing. Furthermore, we show that the two receptors genetically interact in this lineage, as double-homozygous mutant embryos exhibit an overt facial clefting phenotype more severe than that observed in either single-mutant embryo. We reveal a physical interaction between PDGFRα and PDGFRβ in the craniofacial mesenchyme and demonstrate that the receptors form functional heterodimers with distinct signaling properties. Our studies thus uncover a novel mode of signaling for the PDGF family during vertebrate development.
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