Prenatal β-catenin/Brn2/Tbr2 transcriptional cascade regulates adult social and stereotypic behaviors
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Social interaction is a fundamental behavior in all animal species, but the developmental timing of the social neural circuit formation and the cellular and molecular mechanisms governing its formation are poorly understood. We generated a mouse model with mutations in two Disheveled genes, Dvl1 and Dvl3, that displays adult social and repetitive behavioral abnormalities associated with transient embryonic brain enlargement during deep layer cortical neuron formation. These phenotypes were mediated by the embryonic expansion of basal neural progenitor cells (NPCs) via deregulation of a β-catenin/Brn2/Tbr2 transcriptional cascade. Transient pharmacological activation of the canonical Wnt pathway during this period of early corticogenesis rescued the β-catenin/Brn2/Tbr2 transcriptional cascade and the embryonic brain phenotypes. Remarkably, this embryonic treatment prevented adult behavioral deficits and partially rescued abnormal brain structure in Dvl mutant mice. Our findings define a mechanism that links fetal brain development and adult behavior, demonstrating a fetal origin for social and repetitive behavior deficits seen in disorders such as autism.
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Dvl1−/−3+/− mutant mice display reduced social interaction and transient embryonic brain overgrowth, the result of reduced β-catenin transcriptional activity and reduced levels of the transcription factor Brn2 or Pou3f2.
“Dvl1−/−3+/− mutant mice display reduced social interaction and transient embryonic brain overgrowth, the result of reduced β-catenin transcriptional activity and reduced levels of the transcription factor Brn2 or Pou3f235.”
From Altered proliferation and networks in neural cells derived from idiopathic autistic individuals (2017) · cites this paper as [35]
LiCl treatment does not affect neuronal function significantly, suggesting that there are multiple pathways involved in the ASD phenotypical deficit or that stabilization of the Wnt-β-catenin pathway is also required at the early stages of differentiation.
“Hence, contrary to IGF1 treatment, LiCl treatment (and consequent stabilization Wnt-β-catenin pathway and rescue of NPC proliferation) does not affect neuronal function significantly, suggesting that there are multiple pathways involved in the ASD phenotypical deficit or that stabilization of the Wnt-β-catenin pathway is also required at the early stages of differentiation35.”
From Altered proliferation and networks in neural cells derived from idiopathic autistic individuals (2017) · cites this paper as [35]
Transient activation of the canonical Wnt pathway in utero normalized the adult social behavior deficits in Dvl mutant mice.
“Transient activation of the canonical Wnt pathway in utero normalized the adult social behavior deficits in Dvl mutant mice.”
From Altered proliferation and networks in neural cells derived from idiopathic autistic individuals (2017) · cites this paper as [35]
Dvl mutants displayed adult social behavior abnormalities and transient brain overgrowth during embryonic deep layer cortical neuron formation mediated by a similar β-catenin/Brn2/Tbr2 transcriptional cascade.
“we found that Dvl mutants displayed adult social behavior abnormalities and transient brain overgrowth during embryonic deep layer cortical neuron formation mediated by a similar β-catenin/Brn2/Tbr2 transcriptional cascade35.”
From Altered proliferation and networks in neural cells derived from idiopathic autistic individuals (2017) · cites this paper as [35]
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- Authors
- Belinson, H., Nakatani, J., Babineau, B. A., Birnbaum, R. Y., Ellegood, J., Bershteyn, M., McEvilly, R. J., Long, J. M., Willert, K., Klein, O. D., Ahituv, N., Lerch, J. P., Rosenfeld, M. G., & Wynshaw-Boris, A.
- Affiliations
- University of California, San Francisco (US)
- Ben-Gurion University of the Negev (IL)
- Hospital for Sick Children (CA)
- Howard Hughes Medical Institute (US)
- National Institute on Aging (US)
- University of California San Diego (US)
- University of Toronto (CA)
- Corresponding author
- Wynshaw-Boris, A
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2016-02-02
- Volume
- 21
- Issue
- 10
- Pages
- 1417-1433
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC5685528
- OpenAlex
- W2462659332
- Cited by
- 79
- References
- 73
- Citations by year
- 2026: 8 · 2025: 5 · 2024: 5 · 2023: 4 · 2022: 4 · 2021: 9 · 2020: 9 · 2019: 10 · 2018: 9 · 2017: 8 · 2016: 8
- FWCI
- 9.42
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Autism Speaks
- Simons Foundation Autism Research Initiative
- National Institutes of Health
- Japan Society for the Promotion of Science (16K10250)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK039949)
- National Institute of Neurological Disorders and Stroke (P30NS065780, R01NS073159, R01NS048243, R01NS034934, R01NS079231)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Keywords
- DVL1, DVL3, Wnt signaling, cortical development, social behavior, stereotypy, autism spectrum disorder
- MeSH terms
- Dishevelled Proteins, Animals, Behavior, Animal, Brain, Humans, Nerve Tissue Proteins, Neurons, Phosphoproteins, Stereotyped Behavior, Signal Transduction, Stereotypic Movement Disorder, T-Box Domain Proteins, Adaptor Proteins, Signal Transducing, POU Domain Factors, Wnt Proteins, beta Catenin, Mice, Neural Stem Cells, Wnt Signaling Pathway
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