Loss of Wdfy3 in mice alters cerebral cortical neurogenesis reflecting aspects of the autism pathology
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Autism spectrum disorders (ASDs) are complex and heterogeneous developmental disabilities affecting an ever-increasing number of children worldwide. The diverse manifestations and complex, largely genetic aetiology of ASDs pose a major challenge to the identification of unifying neuropathological features. Here we describe the neurodevelopmental defects in mice that carry deleterious alleles of the Wdfy3 gene, recently recognized as causative in ASDs. Loss of Wdfy3 leads to a regionally enlarged cerebral cortex resembling early brain overgrowth described in many children on the autism spectrum. In addition, affected mouse mutants display migration defects of cortical projection neurons, a recognized cause of epilepsy, which is significantly comorbid with autism. Our analysis of affected mouse mutants defines an important role for Wdfy3 in regulating neural progenitor divisions and neural migration in the developing brain. Furthermore, Wdfy3 is essential for cerebral expansion and functional organization while its loss-of-function results in pathological changes characteristic of ASDs.
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The Wdfy3 mutation mouse model of ASD displays heterogeneity of migration and focal patch defects across individual animals, as well as disrupted proliferation/differentiation and cortical overgrowth.
“The Wdfy3 mutation mouse model of ASD likewise displays heterogeneity of migration and focal patch defects across individual animals, as well as disrupted proliferation/differentiation and cortical overgrowth [177].”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [177]
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Additional file 1 of WDFY3 mutation alters laminar position and morphology of cortical neurons
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Self-citation
- Authors
- Orosco, L. A., Ross, A. P., Cates, S. L., Scott, S. E., Wu, D., Sohn, J., Pleasure, D., Pleasure, S. J., Adamopoulos, I. E., & Zarbalis, K. S.
- Affiliations
- Shriners Hospitals for Children - Northern California (US)
- University of California, San Francisco (US)
- Corresponding author
- Zarbalis, Konstantinos S
- ORCID
- Venue
- Nature Communications
- Published
- 2014-09-08
- Volume
- 5
- Issue
- 1
- Pages
- 4692-4692
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4159772
- OpenAlex
- W2059543801
- Cited by
- 90
- References
- 72
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 3 · 2023: 6 · 2022: 9 · 2021: 9 · 2020: 7 · 2019: 6 · 2018: 11 · 2017: 8 · 2016: 14 · 2015: 5
- FWCI
- 5.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Simons Foundation (286567)
- Nancy Lurie Marks Family Foundation
- Regeneron Pharmaceuticals
- Shriners Hospitals for Children
- Simons Foundation Autism Research Initiative
- National Institutes of Health
- U.S. Public Health Service (NICHD R21HD67855)
- University of California, Davis (U42RR024244)
- National Institute of Mental Health (R01MH105360)
- National Human Genome Research Institute (U01HG004085, U01HG004080)
- National Center for Research Resources (U42RR024244)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R21HD067855)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- WDFY3, autism spectrum disorder, neuronal migration, cortical expansion, brain overgrowth, epilepsy comorbidity, mouse mutants, gene dosage
- MeSH terms
- Autophagy-Related Proteins, Animals, Cell Movement, Cerebral Cortex, Child Development Disorders, Pervasive, Mice, Transgenic, Vesicular Transport Proteins, Adaptor Proteins, Signal Transducing, Mice, Neurogenesis
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