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Author Spotlight: Studying Clinical Characters and Epilepsy Outcomes After Frontal Disconnection in Patients with MOGHE

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Prickle1 regulates differentiation of frontal bone osteoblasts.

Yong Wan¹, Brandi Lantz¹, Brian J Cusack¹

¹Center for Craniofacial Regeneration, Department of Oral Biology, School of Dental Medicine, University of Pittsburgh, Pittsburgh, PA, USA.

Scientific Reports

|December 22, 2018

Summary

Prickle1 protein is crucial for skull development, regulating osteoblast migration and differentiation. Its dysfunction leads to skull defects like enlarged fontanelles and smaller frontal bones in mouse models.

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Area of Science:

Developmental biology
Craniofacial development
Molecular signaling

Background:

Skull bone development relies on osteoblast migration and differentiation.
The Wnt/Planar cell polarity (Wnt/PCP) pathway is vital for cell movement.
Prickle1 is a key regulator within the Wnt/PCP pathway.

Purpose of the Study:

To investigate the role of Prickle1 in skull development.
To analyze the impact of a specific Prickle1 mutation (Prickle1^Bj) on skull formation.

Main Methods:

Utilized the Prickle1^Beetlejuice (Prickle1^Bj/Bj) mouse model.
Observed craniofacial phenotypes and analyzed signaling pathways (Wnt/β-catenin, Hedgehog).
Examined osteoblast precursor proliferation, death, migration, and differentiation.

Main Results:

Prickle1^Bj/Bj mutants exhibit microcephaly, enlarged fontanelles, and smaller frontal bones.
Craniofacial defects include cleft lip, cleft palate, and reduced head growth.
Osteoblast precursors show delayed differentiation and reduced migratory marker expression, not altered proliferation or death.

Conclusions:

Prickle1 is essential for osteoblast precursor migration and differentiation during frontal bone development.
Prickle1 dysfunction contributes to specific skull and craniofacial malformations.