ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
N-cadherin sustains motility and polarity of future cortical interneurons during tangential migration.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 57 citations in OpenAlex.
- Somatic variants in SLC35A2 leading to defects in N-glycosylation in mild malformation of cortical development with oligodendroglial hyperplasia in epilepsy (MOGHE).Acta neuropathologica · 2025Article
- PAK3 activation promotes the tangential to radial migration switch of cortical interneurons by increasing leading process dynamics and disrupting cell polarity.Molecular psychiatry · 2024Article
- Mispatterning and interneuron deficit in Tourette Syndrome basal ganglia organoids.Molecular psychiatry · 2022Article
- Modifying PCDH19 levels affects cortical interneuron migration.Frontiers in neuroscience · 2022Article
- Flying under the radar: CDH2 (N-cadherin), an important hub molecule in neurodevelopmental and neurodegenerative diseases.Frontiers in neuroscience · 2022Review
- Directional Persistence of Cell Migration in Schizophrenia Patient-Derived Olfactory Cells.International journal of molecular sciences · 2021Article
- Glypican 4 regulates planar cell polarity of endoderm cells by controlling the localization of Cadherin 2.Development (Cambridge, England) · 2021Article
- Review
- N-cadherin (Cdh2) Maintains Migration and Postmitotic Survival of Cortical Interneuron Precursors in a Cell-Type-Specific Manner.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Molecular Mechanisms of Cadherin Function During Cortical Migration.Frontiers in cell and developmental biology · 2020Review
- Article
- Cadherin 8 regulates proliferation of cortical interneuron progenitors.Brain structure & function · 2019Article
- Detachment of Chain-Forming Neuroblasts by Fyn-Mediated Control of cell-cell Adhesion in the Postnatal Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- In Vitro Models to Analyze the Migration of MGE-Derived Interneurons.Methods in molecular biology (Clifton, N.J.) · 2018Article
- Auditory cortex interneuron development requires cadherins operating hair-cell mechanoelectrical transduction.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Morphological and Molecular Basis of Cytoplasmic Dilation and Swelling in Cortical Migrating Neurons.Brain sciences · 2017Review
- Article
- Drebrin-mediated microtubule-actomyosin coupling steers cerebellar granule neuron nucleokinesis and migration pathway selection.Nature communications · 2017Article
- Cell migration in the developing rodent olfactory system.Cellular and molecular life sciences : CMLS · 2016Review
- Cadherin-2 Is Required Cell Autonomously for Collective Migration of Facial Branchiomotor Neurons.PloS one · 2016Article
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Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
Abstract
In the developing brain, cortical GABAergic interneurons migrate long distances from the medial ganglionic eminence (MGE) in which they are generated, to the cortex in which they settle. MGE cells express the cell adhesion molecule N-cadherin, a homophilic cell-cell adhesion molecule that regulates numerous steps of brain development, from neuroepithelium morphogenesis to synapse formation. N-cadherin is also expressed in embryonic territories crossed by MGE cells during their migration. In this study, we demonstrate that N-cadherin is a key player in the long-distance migration of future cortical interneurons. Using N-cadherin-coated substrate, we show that N-cadherin-dependent adhesion promotes the migration of mouse MGE cells in vitro. Conversely, mouse MGE cells electroporated with a construct interfering with cadherin function show reduced cell motility, leading process instability, and impaired polarization associated with abnormal myosin IIB dynamics. In vivo, the capability of electroporated MGE cells to invade the developing cortical plate is altered. Using genetic ablation of N-cadherin in mouse embryos, we show that N-cadherin-depleted MGEs are severely disorganized. MGE cells hardly exit the disorganized proliferative area. N-cadherin ablation at the postmitotic stage, which does not affect MGE morphogenesis, alters MGE cell motility and directionality. The tangential migration to the cortex of N-cadherin ablated MGE cells is delayed, and their radial migration within the cortical plate is perturbed. Altogether, these results identify N-cadherin as a pivotal adhesion substrate that activates cell motility in future cortical interneurons and maintains cell polarity over their long-distance migration to the developing cortex.
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