Journal article

Ryk-deficient mice exhibit craniofacial defects associated with perturbed Eph receptor crosstalk

MM Halford, J Armes, M Buchert, V Meskenaite, D Grail, ML Hibbs, AF Wilks, PG Farlie, DF Newgreen, CM Hovens, SA Stacker

Nature Genetics | NATURE AMERICA INC | Published : 2000

Abstract

Secondary palate formation is a complex process that is frequently disturbed in mammals, resulting in the birth defect cleft palate. Gene targeting has identified components of cytokine/growth factor signalling systems such as Tgf-alpha/Egfr, Eph receptors B2 and B3 (Ephb2 and Ephb3, respectively), Tgf-beta2, Tgf-beta3 and activin-betaA (ref. 3) as regulators of secondary palate development. Here we demonstrate that the mouse orphan receptor 'related to tyrosine kinases' (Ryk) is essential for normal development and morphogenesis of craniofacial structures including the secondary palate. Ryk belongs to a subclass of catalytically inactive, but otherwise distantly related, receptor protein ty..

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