Related Experiment Video
Updated: Jun 25, 2026
09:16
Analyzing Craniofacial Morphogenesis in Zebrafish Using 4D Confocal Microscopy
Published on: January 30, 2014
Convergent signalling through Fgfr2 regulates divergent craniofacial morphogenesis.
Lotta Veistinen1, Thomas Aberg, David P C Rice
1Department of Orthodontics, Institute of Dentistry, University of Helsinki, Helsinki, Finland.
Summary
Fibroblast growth factor receptor 2 (Fgfr2) signaling is crucial for tooth and palate development. Aberrant Fgfr2IIIb/Fgf10 signaling in the mesenchyme causes abnormal calvarial bone development.
Area of Science:
- Developmental biology
- Molecular biology
- Genetics
Background:
- Fibroblast growth factor receptor 2 (Fgfr2) has two key splice variants: Fgfr2IIIb and Fgfr2IIIc.
- Fgfr2IIIb signaling regulates epithelial-mesenchymal interactions essential for organogenesis, including palate and tooth development.
Purpose of the Study:
- To investigate the roles of Fgfr2IIIb and Fgf10 in molar tooth and palate morphogenesis.
- To examine the expression patterns of Fgfr2IIIb, Fgfr2IIIc, Fgf3, Fgf7, and Fgf10 in developing murine tooth, palate, and calvaria.
- To understand the impact of Fgfr2IIIb/Fgf10 signaling on calvarial development.
Main Methods:
- Analysis of Fgfr2IIIb(-/-) and Fgf10(-/-) mouse models to assess molar tooth development.
- Quantitative analysis of cell proliferation in epithelial and mesenchymal compartments.
- mRNA expression analysis of Fgfr2 and Fgf ligands in developing tissues.
Main Results:
- Molar tooth development is arrested in Fgfr2IIIb(-/-) mice due to reduced cell proliferation.
- Fgf10(-/-) mice exhibit reduced molar tooth cell proliferation, but morphogenesis proceeds normally.
- Fgf7 and Fgf10 are expressed in the developing calvaria, with Fgf10 localized to osteoprogenitors.
- Elevated Fgfr2IIIb/Fgf10 signaling in the mesenchyme leads to abnormal calvarial morphogenesis.
Conclusions:
- Fgfr2IIIb and Fgf10 signaling pathways play overlapping roles in normal palate and tooth morphogenesis.
- Dysregulation of Fgfr2IIIb/Fgf10 signaling, particularly in the mesenchyme, can cause craniosynostosis and abnormal calvarial development.
More Related Videos
Related Concept Videos
01:51Determination
During embryogenesis, cells become progressively committed to different fates through a two-step process: specification followed by determination. Specification is demonstrated by removing a segment of an early embryo, “neutrally” culturing the tissue in vitro—for example, in a petri dish with simple medium—and then observing the derivatives. If the cultured region gives rise to cell types that it would normally generate in the embryo, this means that it is specified. In contrast, determination...
01:16TGF - β Signaling Pathway
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
03:14Notch Signaling Pathway
The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
03:14Notch Signaling Pathway
The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
01:41Non-Canonical Wnt Signaling Pathways
Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
02:33Hedgehog Signaling Pathway
The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...