Cranial placodes are ectodermal regions that contribute extensively to the vertebrate peripheral nervous system. The development of the ophthalmic trigeminal (opV) placode, which gives rise only to sensory neurons of the ophthalmic lobe of the trigeminal ganglion, is a well-studied model of sensory neuron development. While key differentiation processes have been characterized at the tissue and cellular levels, the molecules governing opV placode development have not been well described. This study identifies the canonical Wnt signaling pathway as a regulator of opV trigeminal placode development. Introducing dominant-negative TCF and dominant-active β-catenin expression constructs by in ovo electroporation, we have manipulated the canonical Wnt pathway within the opV placode domain and surrounding ectoderm of chick embryos. Inhibition of canonical Wnt signaling results in the failure of targeted cells to express or maintain Pax3 protein, the earliest known specific molecular marker of opV placode cells. Misexpression of dominant-active β-catenin as an activator of canonical Wnt signaling, however, is not sufficient to promote the opV placode cell fate. We conclude that canonical Wnt signaling is necessary for normal opV placode development, and propose that other molecular cues are required in addition to Wnt signaling to promote cells to an opV placode fate. Strategies for manipulating the Wnt pathway at the level of ligand and receptor are also reviewed. Because it is clear that Wnt signaling is not acting alone in early development of the opV placode, we have also begun to investigate additional signaling pathways, such as FGFs, that may be involved in these developmental processes.



College and Department

Life Sciences; Physiology and Developmental Biology



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Wnt, Pax3, ophthalmic, trigeminal, placode



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Physiology Commons