The mouse Wnt/PCP protein Vangl2 is necessary for migration of facial branchiomotor neurons, and functions independently of Dishevelled

Derrick M Glasco; Vinoth Sittaramane; Whitney Bryant; Bernd Fritzsch; Anagha Sawant; Anju Paudyal; Michelle Stewart; Philipp Andre; Gonçalo Cadete Vilhais-Neto; Yingzi Yang; Mi-Ryoung Song; Jennifer N Murdoch; Anand Chandrasekhar

doi:10.1016/j.ydbio.2012.06.021

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The mouse Wnt/PCP protein Vangl2 is necessary for migration of facial branchiomotor neurons, and functions independently of Dishevelled

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The mouse Wnt/PCP protein Vangl2 is necessary for migration of facial branchiomotor neurons, and functions independently of Dishevelled

Derrick M Glasco, Vinoth Sittaramane, Whitney Bryant, Bernd Fritzsch, Anagha Sawant, Anju Paudyal, Michelle Stewart, Philipp Andre, Gonçalo Cadete Vilhais-Neto, Yingzi Yang, …

Developmental biology, Vol.369(2), pp.211-222

09/15/2012

DOI: 10.1016/j.ydbio.2012.06.021

PMCID: PMC3484895

PMID: 22771245

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Abstract

During development, facial branchiomotor (FBM) neurons, which innervate muscles in the vertebrate head, migrate caudally and radially within the brainstem to form a motor nucleus at the pial surface. Several components of the Wnt/planar cell polarity (PCP) pathway, including the transmembrane protein Vangl2, regulate caudal migration of FBM neurons in zebrafish, but their roles in neuronal migration in mouse have not been investigated in detail. Therefore, we analyzed FBM neuron migration in mouse looptail (Lp) mutants, in which Vangl2 is inactivated. In Vangl2Lp/+ and Vangl2 Lp/Lp embryos, FBM neurons failed to migrate caudally from rhombomere (r) 4 into r6. Although caudal migration was largely blocked, many FBM neurons underwent normal radial migration to the pial surface of the neural tube. In addition, hindbrain patterning and FBM progenitor specification were intact, and FBM neurons did not transfate into other non-migratory neuron types, indicating a specific effect on caudal migration. Since loss-of-function in some zebrafish Wnt/PCP genes does not affect caudal migration of FBM neurons, we tested whether this was also the case in mouse. Embryos null for Ptk7, a regulator of PCP signaling, had severe defects in caudal migration of FBM neurons. However, FBM neurons migrated normally in Dishevelled (Dvl) 1/2 double mutants, and in zebrafish embryos with disrupted Dvl signaling, suggesting that Dvl function is essentially dispensable for FBM neuron caudal migration. Consistent with this, loss of Dvl2 function in Vangl2Lp/+ embryos did not exacerbate the Vangl2Lp/+ neuronal migration phenotype. These data indicate that caudal migration of FBM neurons is regulated by multiple components of the Wnt/PCP pathway, but, importantly, may not require Dishevelled function. Interestingly, genetic-interaction experiments suggest that rostral FBM neuron migration, which is normally suppressed, depends upon Dvl function. ► We examined facial branchiomotor (FBM) neuron migration in several Wnt/PCP mutants. ► Caudal migration lost in Vangl2 and Ptk7 mutants, but not in Dvl1/2 double mutants. ► Caudal migration of FBM neurons is independent of Dvl function. ► Rostral migration of FBM neurons, which is normally suppressed, is Dvl-dependent.

Facial branchiomotor neuron migration

Planar Cell Polarity signaling

Protein tyrosine kinase 7

Looptail

Disheveled

Van Gogh-like 2

Details

Title: Subtitle: The mouse Wnt/PCP protein Vangl2 is necessary for migration of facial branchiomotor neurons, and functions independently of Dishevelled
Creators: Derrick M Glasco - Division of Biological Sciences, Room 340D Bond Life Sciences Center, University of Missouri, 1201 Rollins Street, Columbia, MO 65211, USA
Vinoth Sittaramane - Division of Biological Sciences, Room 340D Bond Life Sciences Center, University of Missouri, 1201 Rollins Street, Columbia, MO 65211, USA
Whitney Bryant - Division of Biological Sciences, Room 340D Bond Life Sciences Center, University of Missouri, 1201 Rollins Street, Columbia, MO 65211, USA
Bernd Fritzsch - Department of Biological Sciences, University of Iowa, Iowa City, IA 52242, USA
Anagha Sawant - Division of Biological Sciences, Room 340D Bond Life Sciences Center, University of Missouri, 1201 Rollins Street, Columbia, MO 65211, USA
Anju Paudyal - Developmental Genetics Section, Medical Research Council Harwell, Oxfordshire, OX11 ORD, UK
Michelle Stewart - Developmental Genetics Section, Medical Research Council Harwell, Oxfordshire, OX11 ORD, UK
Philipp Andre - Developmental Genetics Section, National Human Genome Research Institute, NIH, Bethesda, MD 20892, USA
Gonçalo Cadete Vilhais-Neto - IGBMC, UMR 7104, Inserm U964, Université de Strasbourg, Illkirch, F-67400, France
Yingzi Yang - Developmental Genetics Section, National Human Genome Research Institute, NIH, Bethesda, MD 20892, USA
Mi-Ryoung Song - Bioimaging and Cell Dynamics Research Center, School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 500-712, South Korea
Jennifer N Murdoch - Developmental Genetics Section, Medical Research Council Harwell, Oxfordshire, OX11 ORD, UK
Anand Chandrasekhar - Division of Biological Sciences, Room 340D Bond Life Sciences Center, University of Missouri, 1201 Rollins Street, Columbia, MO 65211, USA
Resource Type: Journal article
Publication Details: Developmental biology, Vol.369(2), pp.211-222
DOI: 10.1016/j.ydbio.2012.06.021
PMID: 22771245
PMCID: PMC3484895
NLM abbreviation: Dev Biol
ISSN: 0012-1606
eISSN: 1095-564X
Publisher: Elsevier Inc
Language: English
Date published: 09/15/2012
Academic Unit: Iowa Neuroscience Institute; Biology; Craniofacial Anomalies Research Center
Record Identifier: 9984070956702771

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