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Updated: Mar 23, 2026

Spatial and Temporal Analysis of Active ERK in the C. elegans Germline

Spatial and Temporal Analysis of Active ERK in the C. elegans Germline

Published on: November 29, 2016

FGFR2c-mediated ERK-MAPK activity regulates coronal suture development.

Miles J Pfaff¹, Ke Xue², Li Li¹

¹Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, New Haven, CT, United States.

Developmental Biology

|April 2, 2016

Summary

This summary is machine-generated.

Fibroblast growth factor receptor 2 (FGFR2) signaling impacts craniofacial development. This study reveals FGFR2c-mediated ERK-MAPK signaling is key to coronal suture development, resolving paradoxes in related genetic mutations.

Keywords:

Coronal suture Craniosynostosis Crouzon syndrome ERK–MAPK FGF FGFR2

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Area of Science:

Craniofacial development and genetics.
Molecular mechanisms of skeletal development.

Background:

Fibroblast growth factor receptor 2 (FGFR2) signaling is crucial for craniofacial development.
Gain-of-function mutations in FGFR2 are linked to Crouzon syndrome, causing craniosynostosis (premature suture fusion).
The ERK-MAPK pathway is implicated in regulating cranial suture patency.

Purpose of the Study:

To investigate the role of FGFR2c-mediated ERK-MAPK signaling in coronal suture development.
To understand the distinct pathogenic mechanisms in loss-of-function versus gain-of-function FGFR2c mutants.

Main Methods:

Utilized loss-of-function and gain-of-function Fgfr2c mutant mouse models.
Performed in vivo analysis of coronal sutures.
Analyzed calvarial osteoblast function and ERK-MAPK activation in vitro.
Inhibited ERK signaling using U0126.

Main Results:

Both loss-of-function and gain-of-function mutants exhibited coronal synostosis and craniofacial dysmorphia.
Distinct pathogenic mechanisms were identified for coronal suture synostosis in the two mutant types.
Gain-of-function osteoblasts showed enhanced function and maturation with increased ERK-MAPK activation.
U0126 inhibition reduced ERK activation and alkaline phosphatase activity in vitro.

Conclusions:

FGFR2c-mediated ERK-MAPK signaling is a key regulator of craniofacial growth and coronal suture development.
This signaling pathway explains the observed phenotypes in FGFR2c mutants.
The study resolves the apparent paradox between loss-of-function and gain-of-function FGFR2c mutant phenotypes regarding coronal suture synostosis.