ArticleMolecular psychiatry2018
Neural progenitor fate decision defects, cortical hypoplasia and behavioral impairment in Celsr1-deficient mice.
Article in Molecular psychiatry, 2018. 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, 38 citations in OpenAlex.
- Interpretable spatial multi-omics data integration and dimensionality reduction with SpaMV.Nature communications · 2026Article
- Biallelic variants in CELSR1 cause brain malformations, neurodevelopmental disorders and epilepsy in humans.Nature communications · 2026Article
- Adhesion G-Protein Coupled Receptors in Neurological and Psychiatric Disorders.Journal of psychiatry and brain science · 2025Article
- Autism Spectrum Disorder: The Cerebellum, Genes, and Pathways.Neurology international · 2025Review
- Interpretable spatial multi-omics data integration and dimension reduction with SpaMV.Research square · 2025Article
- Article
- The Function and Regulation of celsr1a in Skeletal Age-associated Homeostasis and Repair in Zebrafish.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- Auts2 enhances neurogenesis and promotes expansion of the cerebral cortex.Journal of advanced research · 2025Article
- Genotype-Phenotype Associations in Phelan-McDermid Syndrome: Insights into Novel Genes BeyondInternational journal of molecular sciences · 2025Article
- Review
- Functional analysis and transcriptome profile of meninges and skin fibroblasts from human-aged donors.Cell proliferation · 2024Article
- Review
- Conditional deletion of KCC2 impairs synaptic plasticity and both spatial and nonspatial memory.Frontiers in molecular neuroscience · 2023Article
- Serial Gene Expression Profiling of Neural Stem Cells Shows Transcriptome Switch by Long-Term Physioxia from Metabolic Adaption to Cell Signaling Profile.Stem cells international · 2022Article
- WNT signaling at the intersection between neurogenesis and brain tumorigenesis.Frontiers in molecular neuroscience · 2022Review
- Overexpression of wild-type human amyloid precursor protein alters GABAergic transmission.Scientific reports · 2021Article
- Genotype-phenotype correlation in Phelan-McDermid syndrome: A comprehensive review of chromosome 22q13 deleted genes.American journal of medical genetics. Part A · 2021Review
- DIAPH3 deficiency links microtubules to mitotic errors, defective neurogenesis, and brain dysfunction.eLife · 2021Article
- Progenitor cell diversity in the developing mouse neocortex.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Gpr125 Marks Distinct Cochlear Cell Types and Is Dispensable for Cochlear Development and Hearing.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The development of the cerebral cortex is a tightly regulated process that relies on exquisitely coordinated actions of intrinsic and extrinsic cues. Here, we show that the communication between forebrain meninges and apical neural progenitor cells (aNPC) is essential to cortical development, and that the basal compartment of aNPC is key to this communication process. We found that Celsr1, a cadherin of the adhesion G protein coupled receptor family, controls branching of aNPC basal processes abutting the meninges and thereby regulates retinoic acid (RA)-dependent neurogenesis. Loss-of-function of Celsr1 results in a decreased number of endfeet, modifies RA-dependent transcriptional activity and biases aNPC commitment toward self-renewal at the expense of basal progenitor and neuron production. The mutant cortex has a reduced number of neurons, and Celsr1 mutant mice exhibit microcephaly and behavioral abnormalities. Our results uncover an important role for Celsr1 protein and for the basal compartment of neural progenitor cells in fate decision during the development of the cerebral cortex.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.