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First published online 16 April 2008
doi: 10.1242/dev.017954

Development 135, 1863-1874 (2008)
Published by The Company of Biologists 2008
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Essential role for PDGF signaling in ophthalmic trigeminal placode induction

Kathryn L. McCabe and Marianne Bronner-Fraser*

Division of Biology 139-74, California Institute of Technology, Pasadena, CA 91125, USA.

* Author for correspondence (e-mail: mbronner{at}caltech.edu)

Accepted 20 March 2008

Much of the peripheral nervous system of the head is derived from ectodermal thickenings, called placodes, that delaminate or invaginate to form cranial ganglia and sense organs. The trigeminal ganglion, which arises lateral to the midbrain, forms via interactions between the neural tube and adjacent ectoderm. This induction triggers expression of Pax3, ingression of placode cells and their differentiation into neurons. However, the molecular nature of the underlying signals remains unknown. Here, we investigate the role of PDGF signaling in ophthalmic trigeminal placode induction. By in situ hybridization, PDGF receptor β is expressed in the cranial ectoderm at the time of trigeminal placode formation, with the ligand PDGFD expressed in the midbrain neural folds. Blocking PDGF signaling in vitro results in a dose-dependent abrogation of Pax3 expression in recombinants of quail ectoderm with chick neural tube that recapitulate placode induction. In ovo microinjection of PDGF inhibitor causes a similar loss of Pax3 as well as the later placodal marker, CD151, and failure of neuronal differentiation. Conversely, microinjection of exogenous PDGFD increases the number of Pax3+ cells in the trigeminal placode and neurons in the condensing ganglia. Our results provide the first evidence for a signaling pathway involved in ophthalmic (opV) trigeminal placode induction.

Key words: PDGF, Induction, Neurogenesis, Trigeminal placode, Chicken


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