Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Blocking endogenous FGF-2 activity prevents cranial osteogenesis.

Rachel Moore1, Patrizia Ferretti, Andrew Copp

  • 1Developmental Biology Unit, University College London, London, WC1N 1EH, United Kingdom.

Developmental Biology
|February 16, 2002
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

GNAQ Induces Melanomagenesis in Mitfa-Independent Melanocyte Progenitors in a Zebrafish Model of Uveal Melanoma.

Cancer research·2026
Same author

A Health Beliefs Model of Long-Term Prescription Opioid Use for Chronic Pain.

Pain practice : the official journal of World Institute of Pain·2026
Same author

The rise and fall of SARM1 base-exchange inhibitors.

Communications chemistry·2026
Same author

Captopril-induced Cough: Does it Matter in Children? A Retrospective Cohort Study.

Current pediatric reviews·2026
Same author

Communication and Psychosocial Outcomes of a Six-Month Group Intervention for Older Transgender Women.

Journal of voice : official journal of the Voice Foundation·2025
Same author

Measuring dietary intake among participants with a urea cycle disorder using standard diet records or a novel food photography app.

Molecular genetics and metabolism·2025

Fibroblast growth factor-2 (FGF-2) signaling intensity dictates cranial bone development. High FGF-2 levels promote differentiation, while low levels enhance proliferation, crucial for normal cranial vault morphogenesis.

Area of Science:

  • Developmental biology
  • Craniofacial development
  • Skeletal biology

Background:

  • Normal cranial vault growth relies on balanced cell proliferation and osteogenesis.
  • Craniosynostosis involves premature suture fusion and craniofacial malformations, often linked to fibroblast growth factor receptor (FGFR) gene mutations.

Purpose of the Study:

  • To investigate the role of endogenous FGF-2 ligand levels in embryonic chick cranial vault morphogenesis.
  • To determine how FGF-2 signaling intensity influences skeletogenic cell fate in cranial development.

Main Methods:

  • Utilized a grafting technique to manipulate FGF-2 ligand levels in embryonic chick cranial vaults.
  • Implanted beads loaded with FGF-2 or a neutralizing antibody to FGF-2.
  • Observed effects on cell proliferation, differentiation, and overall cranial bone development.

Related Experiment Videos

Main Results:

  • FGF-2 beads did not affect cranial development but impacted limb morphogenesis.
  • Neutralizing FGF-2 antibody caused concentration-dependent effects: increased growth with low inactivation, blocked differentiation and proliferation with higher inactivation.
  • Demonstrated that FGF-2 signaling intensity correlates with skeletogenic cell fate: high levels promote differentiation, low levels promote proliferation.

Conclusions:

  • The intensity of FGF-mediated signaling critically determines the developmental fate of cranial vault skeletogenic cells.
  • A balance between FGF-2-induced differentiation and proliferation is essential for normal cranial vault morphogenesis.
  • Findings support the link between dysregulated FGFR signaling and craniosynostosis.