Journal article
The atypical cadherin Celsr1 functions non-cell autonomously to block rostral migration of facial branchiomotor neurons in mice
Developmental biology, Vol.417(1), pp.40-49
09/01/2016
DOI: 10.1016/j.ydbio.2016.07.004
PMCID: PMC5007083
PMID: 27395006
Abstract
The caudal migration of facial branchiomotor (FBM) neurons from rhombomere (r) 4 to r6 in the hindbrain is an excellent model to study neuronal migration mechanisms. Although several Wnt/Planar Cell Polarity (PCP) components are required for FBM neuron migration, only Celsr1, an atypical cadherin, regulates the direction of migration in mice. In Celsr1 mutants, a subset of FBM neurons migrates rostrally instead of caudally. Interestingly, Celsr1 is not expressed in the migrating FBM neurons, but rather in the adjacent floor plate and adjoining ventricular zone. To evaluate the contribution of different expression domains to neuronal migration, we conditionally inactivated Celsr1 in specific cell types. Intriguingly, inactivation of Celsr1 in the ventricular zone of r3–r5, but not in the floor plate, leads to rostral migration of FBM neurons, greatly resembling the migration defect of Celsr1 mutants. Dye fill experiments indicate that the rostrally-migrated FBM neurons in Celsr1 mutants originate from the anterior margin of r4. These data suggest strongly that Celsr1 ensures that FBM neurons migrate caudally by suppressing molecular cues in the rostral hindbrain that can attract FBM neurons.
•Celsr1 regulates the directionality of mouse facial branchiomotor neuron migration.•Celsr1 functions specifically in the ventricular zone of rhombomeres 3–5.•In Celsr1 mutants, rostrally-migrated neurons originate from anterior rhombomere 4.•Celsr1 may suppress attractive cues to prevent inappropriate rostral migration.
Details
- Title: Subtitle
- The atypical cadherin Celsr1 functions non-cell autonomously to block rostral migration of facial branchiomotor neurons in mice
- Creators
- Derrick M Glasco - Division of Biological Sciences, and Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USAWhitney Pike - Division of Biological Sciences, and Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USAYibo Qu - Institute of Neuroscience, Developmental Neurobiology, Université Catholique de Louvain, Brussels, BelgiumLindsay Reustle - Division of Biological Sciences, and Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USAKamana Misra - Center for Advanced Biotechnology and Medicine, UMDNJ-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USAMaria Di Bonito - INSERM UMR 1091, University of Nice-Sophia Antipolis, F-06108 Nice, FranceMichele Studer - INSERM UMR 1091, University of Nice-Sophia Antipolis, F-06108 Nice, FranceBernd Fritzsch - Department of Biology, The University of Iowa, Iowa City, IA 52242, USAAndré M Goffinet - Institute of Neuroscience, Developmental Neurobiology, Université Catholique de Louvain, Brussels, BelgiumFadel Tissir - Institute of Neuroscience, Developmental Neurobiology, Université Catholique de Louvain, Brussels, BelgiumAnand Chandrasekhar - Division of Biological Sciences, and Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USA
- Resource Type
- Journal article
- Publication Details
- Developmental biology, Vol.417(1), pp.40-49
- DOI
- 10.1016/j.ydbio.2016.07.004
- PMID
- 27395006
- PMCID
- PMC5007083
- NLM abbreviation
- Dev Biol
- ISSN
- 0012-1606
- eISSN
- 1095-564X
- Publisher
- Elsevier Inc
- Grant note
- DOI: 10.13039/501100002582, name: Gwangju Institute of Science and Technology
- Language
- English
- Date published
- 09/01/2016
- Academic Unit
- Iowa Neuroscience Institute; Biology; Craniofacial Anomalies Research Center
- Record Identifier
- 9984070137902771
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