The autism-related gene SNRPN regulates cortical and spine development via controlling nuclear receptor Nr4a1
Open accessAbstract
The small nuclear ribonucleoprotein polypeptide N (SNRPN) gene, encoding the RNA-associated SmN protein, duplications or deletions of which are strongly associated with neurodevelopmental disabilities. SNRPN-coding protein is highly expressed in the brain. However, the role of SNRPN protein in neural development remains largely unknown. Here we showed that the expression of SNRPN increased markedly during postnatal brain development. Overexpression or knockdown of SNRPN in cortical neurons impaired neurite outgrowth, neuron migration and the distribution of dendritic spines. We found that SNRPN regulated the expression level of Nr4a1, a critical nuclear receptor during neural development, in cultured primary cortical neurons. The abnormal spine development caused by SNRPN overexpression could be fully rescued by Nr4a1 co-expression. Importantly, we found that either knockdown of Nr4a1 or 3, 3′- Diindolylmethane (DIM), an Nr4a1 antagonist, were able to rescue the effects of SNRPN knockdown on neurite outgrowth of embryonic cortical neurons, providing the potential therapeutic methods for SNRPN deletion disorders. We thus concluded that maintaining the proper level of SNRPN is critical in cortical neurodevelopment. Finally, Nr4a1 may serve as a potential drug target for SNRPN-related neurodevelopmental disabilities, including Prader-Willi syndrome (PWS) and autism spectrum disorders (ASDs).
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In vitro overexpression of Snrpn reduces dendrite length, increases spine density, and alters spine distribution on cortical neurons.
“In vitro studies using overexpression of Snrpn show that the gene reduces dendrite length, increases spine density and alters spine distribution on cortical neurons [215].”
From Autism spectrum disorder: neuropathology and animal models (2017) · cites this paper as [215]
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Buck, J. M., Melnick, M., & Stitzel, J. A. (2026) · Genes · doi:10.3390/genes17020128
Intramembrane protease SPPL2b deficiency linked to synaptic proteostasis remodeling with brain agingPreprint
Contini, C., Schirru, A., Lai, G., Zodio, G., Badman, J., Bakker, B. R. V., Lai, Y., Nilsson, P., Diaz, G., Cabras, T., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.07.27.740894
- Authors
- Li, H., Zhao, P., Xu, Q., Shan, S., Hu, C., Qiu, Z., & Xu, X.
- Affiliations
- Fudan University (CN)
- Chinese Academy of Sciences (CN)
- Corresponding author
- Qiu, Zilong
- Xu, Xiu
- Venue
- Scientific Reports
- Published
- 2016-07-19
- Volume
- 6
- Issue
- 1
- Pages
- 29878-29878
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC4949425
- OpenAlex
- W2489724827
- Cited by
- 56
- References
- 39
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 18 · 2023: 5 · 2022: 4 · 2021: 7 · 2020: 6 · 2019: 2 · 2018: 2 · 2017: 2
- FWCI
- 1.60
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (91432111, 81371270)
- 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
- SNRPN, Nur77, nuclear receptors, cortical development, dendritic spine development, neurite outgrowth, neuronal migration, SMN protein, 3,3'-diindolylmethane, Prader-Willi syndrome, autism spectrum disorder, neurodevelopmental disorders, postnatal brain development
- MeSH terms
- Autistic Disorder, Autoantigens, Brain, Cell Line, Humans, Genomic Imprinting, Gene Expression Regulation, Developmental, snRNP Core Proteins, Nuclear Receptor Subfamily 4, Group A, Member 1
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