ArticleThe Journal of biological chemistry2016
DISC1-dependent Regulation of Mitochondrial Dynamics Controls the Morphogenesis of Complex Neuronal Dendrites.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Bioenergetic impairment in schizophrenia: role of mitochondrial signaling in synaptic dysfunction - a systematic review.Frontiers in cell and developmental biology · 2026Pooled it
- Mitochondria‑endoplasmic reticulum contact site nexus: Molecular integration, disease pathogenesis and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- The schizophrenia associated protein DISC1 forms a multivalent tetrameric hub via conserved UVR dimers.Nature communications · 2026Article
- Rheumatoid arthritis-associated depression: focusing on the interactions between mitochondria and endoplasmic reticulum.Frontiers in pharmacology · 2025Review
- Is it possible to prevent excessive synaptic pruning in schizophrenia? Possibilities and limitations.Frontiers in synaptic neuroscience · 2025Review
- Mitochondrial Dysfunction as a Biomarker of Illness State in Bipolar Disorder: A Critical Review.Brain sciences · 2024Review
- Ancestral retrovirus envelope protein ERVWE1 upregulates circ_0001810, a potential biomarker for schizophrenia, and induces neuronal mitochondrial dysfunction via activating AK2.Cell & bioscience · 2024Article
- TransgenicCurrent issues in molecular biology · 2024Article
- Genome-wide Association Analysis of Schizophrenia and Vitamin D Levels Shows Shared Genetic Architecture and Identifies Novel Risk Loci.Schizophrenia bulletin · 2023Article
- Genome-Wide Selection Signal Analysis to Investigate Wide Genomic Heredity Divergence between Eurasian Wild Boar and Domestic Pig.Animals : an open access journal from MDPI · 2023Article
- Schizophrenia Synaptic Pathology and Antipsychotic Treatment in the Framework of Oxidative and Mitochondrial Dysfunction: Translational Highlights for the Clinics and Treatment.Antioxidants (Basel, Switzerland) · 2023Review
- Article
- Efficacy of Serotonin and Dopamine Activity Modulators in the Treatment of Negative Symptoms in Schizophrenia: A Rapid Review.Biomedicines · 2023Review
- Fatty Acid Metabolism-Related lncRNAs are Potential Biomarkers for Predicting Prognoses and Immune Responses in Patients with Skin Cutaneous Melanoma.Clinical, cosmetic and investigational dermatology · 2023Article
- The interplay of dopamine metabolism abnormalities and mitochondrial defects in the pathogenesis of schizophrenia.Translational psychiatry · 2022Review
- Article
- Review
- Article
- Mutations in DISC1 alter IPNeuronal signaling · 2021Review
- Haloperidol rescues the schizophrenia-like phenotype in adulthood after rotenone administration in neonatal rats.Psychopharmacology · 2021Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
The DISC1 protein is implicated in major mental illnesses including schizophrenia, depression, bipolar disorder, and autism. Aberrant mitochondrial dynamics are also associated with major mental illness. DISC1 plays a role in mitochondrial transport in neuronal axons, but its effects in dendrites have yet to be studied. Further, the mechanisms of this regulation and its role in neuronal development and brain function are poorly understood. Here we have demonstrated that DISC1 couples to the mitochondrial transport and fusion machinery via interaction with the outer mitochondrial membrane GTPase proteins Miro1 and Miro2, the TRAK1 and TRAK2 mitochondrial trafficking adaptors, and the mitochondrial fusion proteins (mitofusins). Using live cell imaging, we show that disruption of the DISC1-Miro-TRAK complex inhibits mitochondrial transport in neurons. We also show that the fusion protein generated from the originally described DISC1 translocation (DISC1-Boymaw) localizes to the mitochondria, where it similarly disrupts mitochondrial dynamics. We also show by super resolution microscopy that DISC1 is localized to endoplasmic reticulum contact sites and that the DISC1-Boymaw fusion protein decreases the endoplasmic reticulum-mitochondria contact area. Moreover, disruption of mitochondrial dynamics by targeting the DISC1-Miro-TRAK complex or upon expression of the DISC1-Boymaw fusion protein impairs the correct development of neuronal dendrites. Thus, DISC1 acts as an important regulator of mitochondrial dynamics in both axons and dendrites to mediate the transport, fusion, and cross-talk of these organelles, and pathological DISC1 isoforms disrupt this critical function leading to abnormal neuronal development.
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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.