ArticleCell reports2019
Trio Haploinsufficiency Causes Neurodevelopmental Disease-Associated Deficits.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 60 citations in OpenAlex.
- The Molecular Machinery of Synaptic Plasticity and Its Potential Role in the Aetiology of Schizophrenia.Molecular neurobiology · 2026Review
- Sh3rf3 Deficiency drives autism-like behaviors via presynaptic dysfunction in mice.Molecular psychiatry · 2026Article
- E2f1 transcription factor is required for neurodevelopment through regulation of conserved miR-33 and RhoGEF trio.Cell communication and signaling : CCS · 2026Article
- Elevated synaptic PKA activity and abnormal striatal dopamine signaling in Akap11 mutant mice, a genetic model of schizophrenia and bipolar disorder.Nature communications · 2025Article
- Elevated synaptic PKA activity and abnormal striatal dopamine signaling inbioRxiv : the preprint server for biology · 2025Article
- Oligodendrocyte myelin glycoprotein impairs dendritic arbors via schizophrenia risk gene Trio.Neurobiology of disease · 2025Article
- Article
- Both GEF domains of the autism and developmental epileptic encephalopathy-associated Trio protein are required for proper tangential migration of GABAergic interneurons.Molecular psychiatry · 2025Article
- Integrated neurobehavioral and organ-specific safety profiling of baicalin: acute/subacute toxicity studies.Frontiers in pharmacology · 2025Article
- Dentate Gyrus Morphogenesis is Regulated by an Autism Risk Gene Trio Function in Granule Cells.Neuroscience bulletin · 2025Article
- Genetic Diversity in Schizophrenia: Developmental Implications of Ultra-Rare, Protein-Truncating Mutations.Genes · 2024Review
- The RNA-binding protein Nab2 regulates levels of the RhoGEF Trio to govern axon and dendrite morphology.Molecular biology of the cell · 2024Article
- Post-translational modification-centric base editor screens to assess phosphorylation site functionality in high throughput.Nature methods · 2024Article
- A de novo missense mutation in synaptotagmin-1 associated with neurodevelopmental disorder desynchronizes neurotransmitter release.Molecular psychiatry · 2024Article
- Connectivity and molecular profiles of Foxp2- and Dbx1-lineage neurons in the accessory olfactory bulb and medial amygdala.The Journal of comparative neurology · 2024Article
- A regulatory circuit controlled by extranuclear and nuclear retinoic acid receptor α determines T cell activation and function.Immunity · 2023Article
- Critical periods and Autism Spectrum Disorders, a role for sleep.Neurobiology of sleep and circadian rhythms · 2023Article
- Pathogenic TRIO variants associated with neurodevelopmental disorders perturb the molecular regulation of TRIO and axon pathfinding in vivo.Molecular psychiatry · 2023Article
- Neonatal exposures to sevoflurane in rhesus monkeys alter synaptic ultrastructure in later life.iScience · 2022Article
- Comparative chromatin accessibility upon BDNF stimulation delineates neuronal regulatory elements.Molecular systems biology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Heterozygous coding mutations in TRIO are associated with neurodevelopmental disorders, including autism, schizophrenia, bipolar disorder, and epilepsy, and impair TRIO's biochemical activities. To model mutant alleles, we ablated one or both Trio alleles from excitatory neurons in the cortex and hippocampus of mice. Trio haploinsufficiency increases anxiety and impairs social preference and motor coordination. Trio loss reduces forebrain size and dendritic arborization but increases dendritic spine densities. Cortical synapses in Trio haploinsufficient mice are small, exhibit pre- and postsynaptic deficits, and cannot undergo long-term potentiation. Similar phenotypes are observed in Trio knockout mice. Overall, Trio haploinsufficiency causes severe disease-relevant deficits in behavior and neuronal structure and function. Interestingly, phosphodiesterase 4A5 (PDE4A5) levels are reduced and protein kinase A (PKA) signaling is increased when TRIO levels are reduced. Elevation of PDE4A5 and drug-based attenuation of PKA signaling rescue Trio haploinsufficiency-related dendritic spine defects, suggesting an avenue for therapeutic intervention for TRIO-related neurodevelopmental disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.