Expression of PAX-3 and FREK in placodal cells contributing to the trigeminal ganglion

6th International Congress on Cell Biology & 36th American Society for Cell Biology Annual Meeting December 7-11, 1996, San Francisco, California.-- Monday: Poster Sessions, Pt.IV.During embryonic development, most cranial sensory ganglia form with a dual contribution from the neural crest and ectodermally-derived placodal cells. Cranial ganglia develop abnormally in Pax-3 deficient Splotch mutant mice. To evaluate the origin of these defects, we have examined the development of the trigeminal ganglion in avian embryos using in stu hybridization with RNA probes for the FGF receptor FREK (which was previously shown to be expressed in the trigeminal placode) and for Pax-3. Transient, low level Pax-3 expression can be detected in midbrain and hindbrain neural crest cells as they leave the neural tube. In 10-13 somite avian embryos, cells in the presumptive trigeminal placode ectoderm express Pax-3 at significantly higher levels than do neural crest cells. As development proceeds, presumptive ganglion cells expressing high levels of Pax-3 are observed in the mesenchyme adjacent to and in continuity with Pax-3 expressing ectoderm cells, and eventually in the ophthalmic lobe of the forming trigeminal ganglion. Surface Dil labeling confirms the placodal origin of Pax-3 expressing cells in the head mesenchyme and later in the condensed trigeminal ganglion. FREK expression in the developing trigeminal ganglion is restricted to placode cells and is similar to Pax-3 expression. We conclude that FREK and high levels of Pax-3 are expressed in pre-migratory and migratory placode cells contributing to the ophthalmic lobe of the trigeminal ganglia. We hypothesize that dysfunction of Pax-3 in trigeminal placode cells of Splotch mice might lead to their failure to differentiate and/or migrate in the trigeminal ganglion, contributing to some cranial ganglia deficiencies observed in these mutants.N