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The PCP protein Vangl2 regulates migration of hindbrain motor neurons by acting in floor plate cells,and independently of cilia function
Authors:Vinoth Sittaramane  Xiufang Pan  Derrick M. Glasco  Peng Huang  Suman Gurung  Anagha Bock  Shike Li  Hui Wang  Koichi Kawakami  Michael P. Matise  Anand Chandrasekhar
Affiliation:1. Division of Biological Sciences, and Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USA;2. Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA;3. Departments of Neuroscience and Cell Biology, UMDNJ/Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA;4. Division of Molecular and Developmental Biology, National Institute of Genetics, Shizuoka, 411-8540, JAPAN
Abstract:Vangl2, a core component of the Planar Cell Polarity pathway, is necessary for the caudal migration of Facial Branchiomotor (FBM) neurons in the vertebrate hindbrain. Studies in zebrafish suggest that vangl2 functions largely non-cell autonomously to regulate FBM neuron migration out of rhombomere 4 (r4), but the cell-type within which it acts is not known. Here, we demonstrate that vangl2 functions largely in floor plate cells to regulate caudal neuronal migration. Furthermore, FBM neurons fail to migrate caudally in the mouse Gli2 mutant that lacks the floor plate, suggesting an evolutionarily conserved role for this cell type in neuronal migration. Although hindbrain floor plate cilia are disorganized in vangl2 mutant embryos, cilia appear to be dispensable for neuronal migration. Notably, Vangl2 is enriched in the basolateral, but not apical, membranes of floor plate cells. Taken together, our data suggest strongly that Vangl2 regulates FBM neuron migration by acting in floor plate cells, independently of cilia function.
Keywords:Hindbrain   Facial Branchiomotor Neuron   Floor plate cells   Van gogh-like 2   Neuronal migration   Cilia
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