ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Gene dosage in the dysbindin schizophrenia susceptibility network differentially affect synaptic function and plasticity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
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- Pre-Pulse Inhibition of an escape response in adult fruit fly, Drosophila melanogaster.Translational psychiatry · 2026Article
- Genetic dissection of theMolecular biology of the cell · 2025Article
- BLOC-1 and BORC: Complex regulators of endolysosomal dynamics.Cell chemical biology · 2025Review
- Peering into the mind: unraveling schizophrenia's secrets using models.Molecular psychiatry · 2025Review
- Beyond vertebrates:Frontiers in psychiatry · 2025Review
- Sex dimorphism controls dysbindin-related cognitive dysfunctions in mice and humans with the contribution of COMT.Molecular psychiatry · 2024Article
- Advantages and Limitations of Animal Schizophrenia Models.International journal of molecular sciences · 2022Review
- Dysbindin-1, BDNF, and GABAergic Transmission in Schizophrenia.Frontiers in psychiatry · 2022Review
- Dysbindin-1 regulates mitochondrial fission and gamma oscillations.Molecular psychiatry · 2021Article
- Assessing olfactory, memory, social and circadian phenotypes associated with schizophrenia in a genetic model based on Rim.Translational psychiatry · 2021Article
- Abnormalities in the copper transporter CTR1 in postmortem hippocampus in schizophrenia: A subregion and laminar analysis.Schizophrenia research · 2021Article
- Schizophrenia-associated dysbindin modulates axonal mitochondrial movement in cooperation with p150Molecular brain · 2021Article
- Golgi-Dependent Copper Homeostasis Sustains Synaptic Development and Mitochondrial Content.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Loss of dysbindin-1 affects GABAergic transmission in the PFC.Psychopharmacology · 2019Article
- Systems Analysis of the 22q11.2 Microdeletion Syndrome Converges on a Mitochondrial Interactome Necessary for Synapse Function and Behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Deletion of Dtnbp1 in mice impairs threat memory consolidation and is associated with enhanced inhibitory drive in the amygdala.Translational psychiatry · 2019Article
- Developmental Genes and Regulatory Proteins, Domains of Cognitive Impairment in Schizophrenia Spectrum Psychosis and Implications for Antipsychotic Drug Discovery: The Example of Dysbindin-1 Isoforms and Beyond.Frontiers in pharmacology · 2019Review
- Coupling of microtubule motors with AP-3 generated organelles in axons by NEEP21 family member calcyon.Molecular biology of the cell · 2018Article
- Variations in Dysbindin-1 are associated with cognitive response to antipsychotic drug treatment.Nature communications · 2018Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
Neurodevelopmental disorders arise from single or multiple gene defects. However, the way multiple loci interact to modify phenotypic outcomes remains poorly understood. Here, we studied phenotypes associated with mutations in the schizophrenia susceptibility gene dysbindin (dysb), in isolation or in combination with null alleles in the dysb network component Blos1. In humans, the Blos1 ortholog Bloc1s1 encodes a polypeptide that assembles, with dysbindin, into the octameric BLOC-1 complex. We biochemically confirmed BLOC-1 presence in Drosophila neurons, and measured synaptic output and complex adaptive behavior in response to BLOC-1 perturbation. Homozygous loss-of-function alleles of dysb, Blos1, or compound heterozygotes of these alleles impaired neurotransmitter release, synapse morphology, and homeostatic plasticity at the larval neuromuscular junction, and impaired olfactory habituation. This multiparameter assessment indicated that phenotypes were differentially sensitive to genetic dosages of loss-of-function BLOC-1 alleles. Our findings suggest that modification of a second genetic locus in a defined neurodevelopmental regulatory network does not follow a strict additive genetic inheritance, but rather, precise stoichiometry within the network determines phenotypic outcomes.
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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.