ArticleScientific reports2020
Arid1b haploinsufficiency in parvalbumin- or somatostatin-expressing interneurons leads to distinct ASD-like and ID-like behavior.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Autism-like behavior Increases with age and is predated by molecular changes in Arid1b haploinsufficient mice.Neuroscience · 2026Article
- Key Risk Genes Identified From the Postmortem Brain of Patients With Major Depressive Disorder and Their Potential Clinical Applications.The international journal of neuropsychopharmacology · 2023Article
- Critical periods and Autism Spectrum Disorders, a role for sleep.Neurobiology of sleep and circadian rhythms · 2023Article
- Relating enhancer genetic variation across mammals to complex phenotypes using machine learning.Science (New York, N.Y.) · 2023Article
- Review
- Genetic background determines synaptic phenotypes inFrontiers in psychiatry · 2023Article
- Interneuron odyssey: molecular mechanisms of tangential migration.Frontiers in neural circuits · 2023Review
- Autism spectrum disorder and Coffin-Siris syndrome-Case report.Frontiers in psychiatry · 2023Article
- MACF1, Involved in the 1p34.2p34.3 Microdeletion Syndrome, is Essential in Cortical Progenitor Polarity and Brain Integrity.Cellular and molecular neurobiology · 2022Article
- A novel heterozygous missense variant of the ARID4A gene identified in Han Chinese families with schizophrenia-diagnosed siblings that interferes with DNA-binding activity.Molecular psychiatry · 2022Article
- Cell-type specific transcriptomic signatures of neocortical circuit organization and their relevance to autism.Frontiers in neural circuits · 2022Article
- Neurobiology of ARID1B haploinsufficiency related to neurodevelopmental and psychiatric disorders.Molecular psychiatry · 2022Review
- Inability to switch from ARID1A-BAF to ARID1B-BAF impairs exit from pluripotency and commitment towards neural crest formation in ARID1B-related neurodevelopmental disorders.Nature communications · 2021Article
- The emerging role of chromatin remodelers in neurodevelopmental disorders: a developmental perspective.Cellular and molecular life sciences : CMLS · 2021Review
- Differential roles of ARID1B in excitatory and inhibitory neural progenitors in the developing cortex.Scientific reports · 2021Article
- The Evolutionary Conserved SWI/SNF Subunits ARID1A and ARID1B Are Key Modulators of Pluripotency and Cell-Fate Determination.Frontiers in cell and developmental biology · 2021Review
- Review
- The phenomenal epigenome in neurodevelopmental disorders.Human molecular genetics · 2020Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Inhibitory interneurons are essential for proper brain development and function. Dysfunction of interneurons is implicated in several neurodevelopmental disorders, including autism spectrum disorder (ASD) and intellectual disability (ID). We have previously shown that Arid1b haploinsufficiency interferes with interneuron development and leads to social, cognitive, and emotional impairments consistent with ASD and ID. It is unclear, however, whether interneurons play a major role for the behavioral deficits in Arid1b haploinsufficiency. Furthermore, it is critical to determine which interneuron subtypes contribute to distinct behavioral phenotypes. In the present study, we generated Arid1b haploinsufficient mice in which a copy of the Arid1b gene is deleted in either parvalbumin (PV) or somatostatin (SST) interneurons, and examined their ASD- and ID-like behaviors. We found that Arid1b haploinsufficiency in PV or SST interneurons resulted in distinct features that do not overlap with one another. Arid1b haploinsufficiency in PV neurons contributed to social and emotional impairments, while the gene deletion in the SST population caused stereotypies as well as learning and memory dysfunction. These findings demonstrate a critical role of interneurons in Arid1b haploinsufficient pathology and suggest that PV and SST interneurons may have distinct roles in modulating neurological phenotypes in Arid1b haploinsufficiency-induced ASD and ID.
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