Migration of Cranial Motor Neurons is Eliminated in the Zebrafish Gastrulation Mutant trilobite

The zebrafish gastrulation mutant trilobite(tri) exhibits severe defects in the migration of hindbrain motor neurons. In the wild type hindbrain, facial (nVII) and glossopharyngeal (nIX) motor neurons are induced in rhombomeres 4 and 6, respectively, and subsequently migrate caudally into r6 and r7 (nVII), and r7 (niX). In all three trialleles examined, while normal numbers of motor neurons are induced, nVII motor neurons are found exclusively in r4, and niX-like motor neurons are found exclusively in r6, suggesting strongly that caudal migration of these neuronal populations is abolished. Migration of other cell populations such as neural crest cells, adaxial muscle cells, lateral line primordial cells, as well as axon guidance of several neuronal populations are all unaffected in trimutants, demonstrating the specificity of the neuron migration defect. Furthermore, the induction and patterning of other hindbrain neurons, and the expression of several rhombomere-specific genes are unaffected in trimutants, indicating that overall patterning of the hind-brain is normal. Interestingly, nVII and nIX neurons migrate normally in the gastrulation mutant knypek, suggesting that the trilobiteneuron migration defect does not arise non-specifically from aberrant gastrulation-associated cell movements. Current experiments include genetic mosaic analysis to determine whether trifunctions cell-autonomously during motor neuron migration, and time lapse microscopy to analyze defective migratory behavior in mutants. Our studies suggest that trilobiterepresents a genetic tool to analyze neuronal migration in the vertebrate hindbrain.