Pten Mutations Alter Brain Growth Trajectory and Allocation of Cell Types through Elevated -Catenin Signaling
Open accessAbstract
Abnormal patterns of head and brain growth are a replicated finding in a subset of individuals with autism spectrum disorder (ASD). It is not known whether risk factors associated with ASD and abnormal brain growth (both overgrowth and undergrowth) converge on common biological pathways and cellular mechanisms in the developing brain. Heterozygous mutations in PTEN (PTEN(+/-)), which encodes a negative regulator of the PI3K-Akt-mTOR pathway, are a risk factor for ASD and macrocephaly. Here we use the developing cerebral cortex of Pten(+/-) mice to investigate the trajectory of brain overgrowth and underlying cellular mechanisms. We find that overgrowth is detectable from birth to adulthood, is driven by hyperplasia, and coincides with excess neurons at birth and excess glia in adulthood. β-Catenin signaling is elevated in the developing Pten(+/-) cortex, and a heterozygous mutation in Ctnnb1 (encoding β-catenin), itself a candidate gene for ASD and microcephaly, can suppress Pten(+/-) cortical overgrowth. Thus, a balance of Pten and β-catenin signaling regulates normal brain growth trajectory by controlling cell number, and imbalance in this relationship can result in abnormal brain growth. SIGNIFICANCE STATEMENT: We report that Pten haploinsufficiency leads to a dynamic trajectory of brain overgrowth during development and altered scaling of neuronal and glial cell populations. β-catenin signaling is elevated in the developing cerebral cortex of Pten haploinsufficient mice, and a heterozygous mutation in β-catenin, itself a candidate gene for ASD and microcephaly, suppresses Pten(+/-) cortical overgrowth. This leads to the new insight that Pten and β-catenin signaling act in a common pathway to regulate normal brain growth trajectory by controlling cell number, and disruption of this pathway can result in abnormal brain growth.
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One mutation in PTEN was found, previously implicated in ASD brain growth trajectory.
“including one mutation found in PTEN (rs181113165), previously implicated in ASD brain growth trajectory33.”
From Altered proliferation and networks in neural cells derived from idiopathic autistic individuals (2017) · cites this paper as [33]
This PTEN mutation is consistent with a role for this gene in ASD brain growth trajectory and Wnt signaling.
“consistent with a role for this gene in ASD brain growth trajectory and Wnt signaling33.”
From Altered proliferation and networks in neural cells derived from idiopathic autistic individuals (2017) · cites this paper as [33]
Mutations in PTEN alter the brain growth trajectory and allocation of cell types through elevated Beta-Catenin signaling.
“It has been claimed that mutations in PTEN alter the brain growth trajectory and allocation of cell types through elevated Beta-Catenin signaling77.”
From A catalog of single nucleotide changes distinguishing modern humans from archaic hominins (2019) · cites this paper as [77]
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Spinella, A., Weston, M. C., & Barry, J. M. (2018) · ScholarWorks -A service of University of Vermont Libraries (University of Vermont)
- Authors
- Chen, Y., Huang, W.-C., Sejourne, J., Clipperton-Allen, A. E., & Page, D. T.
- Affiliations
- Scripps Research Institute (US)
- Venue
- Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2015-07-15
- Volume
- 35
- Issue
- 28
- Pages
- 10252-10267
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6605343
- OpenAlex
- W1511752676
- Cited by
- 117
- References
- 75
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 9 · 2023: 8 · 2022: 10 · 2021: 12 · 2020: 14 · 2019: 13 · 2018: 13 · 2017: 4 · 2016: 18 · 2015: 1
- FWCI
- 8.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Fraternal Order of Eagles
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- PTEN, β-catenin signaling, autism spectrum disorder, brain overgrowth, macrocephaly, cortical development, glial cell proliferation, PI3K/AKT/mTOR pathway, CTNNB1, haploinsufficiency, cell number regulation, microcephaly
- MeSH terms
- Empty Spiracles Homeobox Proteins, Animals, Animals, Newborn, Brain, Carrier Proteins, Cell Cycle, Embryo, Mammalian, Female, Gene Expression Regulation, Male, Mice, Inbred C57BL, Mice, Transgenic, Nerve Tissue Proteins, Neuroglia, Neurons, Transcription Factors, Signal Transduction, Homeodomain Proteins, Cell Cycle Proteins, PTEN Phosphohydrolase, beta Catenin, Mice, Haploinsufficiency, TOR Serine-Threonine Kinases
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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