GSK-3 signaling in developing cortical neurons is essential for radial migration and dendritic orientation
Open accessAbstract
GSK-3 is an essential mediator of several signaling pathways that regulate cortical development. We therefore created conditional mouse mutants lacking both GSK-3α and GSK-3β in newly born cortical excitatory neurons. Gsk3-deleted neurons expressing upper layer markers exhibited striking migration failure in all areas of the cortex. Radial migration in hippocampus was similarly affected. In contrast, tangential migration was not grossly impaired after Gsk3 deletion in interneuron precursors. Gsk3-deleted neurons extended axons and developed dendritic arbors. However, the apical dendrite was frequently branched while basal dendrites exhibited abnormal orientation. GSK-3 regulation of migration in neurons was independent of Wnt/β-catenin signaling. Importantly, phosphorylation of the migration mediator, DCX, at ser327, and phosphorylation of the semaphorin signaling mediator, CRMP-2, at Thr514 were markedly decreased. Our data demonstrate that GSK-3 signaling is essential for radial migration and dendritic orientation and suggest that GSK-3 mediates these effects by phosphorylating key microtubule regulatory proteins.
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Neurons fail to migrate to the cortical plate and accumulate within the intermediate zone when WNT and β-catenin signaling is upregulated.
“Thus, neurons fail to migrate to the cortical plate and accumulate within the intermediate zone [88, 104].”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [104]
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The ASD Living Biology: from cell proliferation to clinical phenotype
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- Authors
- Morgan-Smith, M., Wu, Y., Zhu, X., Pringle, J., & Snider, W. D.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Morgan-Smith, Meghan
- Snider, William D
- Venue
- eLife
- Publisher
- eLife Sciences Publications, Ltd
- Published
- 2014-07-29
- Volume
- 3
- Pages
- e02663-e02663
- ISSN
- 2050-084X (ISSN-L)
- PMC
- PMC4109311
- OpenAlex
- W1984598826
- Cited by
- 76
- References
- 78
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 7 · 2023: 11 · 2022: 7 · 2021: 6 · 2020: 12 · 2019: 4 · 2018: 5 · 2017: 7 · 2016: 5 · 2015: 7 · 2014: 2
- FWCI
- 2.43
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- eLife (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UNC Libraries
- Funders
- National Institutes of Health (NS050968, 5F31NS067838, NS045892)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- glycogen synthase kinase-3, GSK3α, GSK3β, radial migration, dendrite orientation, cortical development, excitatory neurons, microtubule regulation, Wnt/β-catenin signaling, hippocampus, conditional knockout mice
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Doublecortin Domain Proteins, Doublecortin Protein, Animals, Cell Movement, Cerebral Cortex, Dendrites, Hippocampus, Mice, Inbred C57BL, Microtubule-Associated Proteins, Mutation, Neuropeptides, Phosphorylation, Substrate Specificity, Signal Transduction, Gene Deletion, cdc42 GTP-Binding Protein, Glycogen Synthase Kinase 3, PTEN Phosphohydrolase, beta Catenin, Wnt Signaling Pathway
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