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Isolation and Time-Lapse Imaging of Primary Mouse Embryonic Palatal Mesenchyme Cells to Analyze Collective Movement Attributes

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EphB2 and EphB3 forward signalling are required for palate development.

Michael Risley¹, David Garrod, Mark Henkemeyer

¹Faculty of Life Sciences, Michael Smith Building, Oxford Road, University of Manchester, Manchester M13 9PT, UK. michael.risley@manchester.ac.uk

Mechanisms of Development

|November 27, 2008

Summary

This summary is machine-generated.

Forward signaling through Eph receptors is crucial for proper palate development. Disrupting this pathway in mice leads to cleft palate due to smaller palatal shelves.

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Area of Science:

Cell biology
Developmental biology
Genetics

Background:

Eph and ephrin proteins mediate bidirectional cell signaling.
Loss of ephrinB1 or EphB2/EphB3 causes cleft palate.
The specific signaling pathway (forward or reverse) responsible for cleft palate was unclear.

Purpose of the Study:

To determine whether Eph forward or ephrin reverse signaling is essential for palatogenesis.
To elucidate the role of EphB2 and EphB3 in palate development.

Main Methods:

Utilized mouse models with specific genetic alterations in EphB2 and EphB3.
Analyzed palatal shelf development, proliferation, and vascularization.
Assessed in vivo and in vitro palatal shelf elevation, adhesion, and fusion.

Main Results:

Mice with impaired Eph forward signaling (cytoplasmically truncated EphB2) and EphB3 null exhibited cleft palate.
Palatal shelves were too small to contact due to reduced mesenchymal proliferation.
Reduced proliferation was independent of abnormal vascular development.

Conclusions:

Forward signaling mediated by Eph receptors is essential for palatogenesis.
EphB2 and EphB3 play specific and cooperative roles in palate development.
Disruption of Eph forward signaling leads to cleft palate via impaired mesenchymal proliferation.