ArticleHuman molecular genetics2016
Disrupted in schizophrenia 1 (DISC1) is a constituent of the mammalian mitochondrial contact site and cristae organizing system (MICOS) complex, and is essential for oxidative phosphorylation.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Reductive Stress and Dysregulated Energy Metabolism in Schizophrenia: Mechanisms and Therapeutic Targets.Biological psychiatry · 2026Review
- Effects of an indole chemical, mitochonic acid 5, in a mouse model of mitochondrial disease onset.Scientific reports · 2026Article
- From brain bioenergetics to hypothalamic glucoregulation: A shared-systems hypothesis for intrinsic dysglycemia in schizophrenia.Reviews in endocrine & metabolic disorders · 2026Review
- mtDNA leakage promotes neuron-glia crosstalk to induce epilepsy by cGAS-STING-driven neuroinflammation and serine metabolic reprogramming.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Exploring the roots of schizophrenia: Current research and future directions (Review).Experimental and therapeutic medicine · 2026Review
- Molecular machineries shaping the mitochondrial inner membrane.Nature reviews. Molecular cell biology · 2025Review
- Mitochondrial Oxidative Phosphorylation System Dysfunction in Schizophrenia.International journal of molecular sciences · 2025Review
- Peering into the mind: unraveling schizophrenia's secrets using models.Molecular psychiatry · 2025Review
- Ethnicity-related differences in mitochondrial regulation by insulin stimulation in diabetes.Journal of cellular physiology · 2024Review
- The serum small non-coding RNA (SncRNA) landscape as a molecular biomarker of age associated muscle dysregulation and insulin resistance in older adults.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- 3D reconstruction of murine mitochondria reveals changes in structure during aging linked to the MICOS complex.Aging cell · 2023Article
- Transcriptomic analysis reveals mitochondrial pathways associated with distinct adolescent behavioral phenotypes and stress response.Translational psychiatry · 2023Article
- Cellular Models in Schizophrenia Research.International journal of molecular sciences · 2021Review
- Mitophagy in Human Diseases.International journal of molecular sciences · 2021Review
- Functional brain defects in a mouse model of a chromosomal t(1;11) translocation that disrupts DISC1 and confers increased risk of psychiatric illness.Translational psychiatry · 2021Article
- Astrocyte Bioenergetics and Major Psychiatric Disorders.Advances in neurobiology · 2021Review
- Mitophagy: A New Player in Stem Cell Biology.Biology · 2020Review
- Astrocyte DISC1 contributes to cognitive function in a brain region-dependent manner.Human molecular genetics · 2020Article
- Cristae undergo continuous cycles of membrane remodelling in a MICOS-dependent manner.EMBO reports · 2020Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disrupted in Schizophrenia-1 (DISC1) has been associated with a broad spectrum of mental disorders. DISC1 is a multi-compartmentalized protein found in the cytoplasm, centrosome, nuclei and mostly enriched in mitochondria. In order to shed light on DISC1 mitochondrial function, we have studied its topology within the organelle. We show in here that in mammals DISC1 resides in the 'Mitochondrial contact site and Cristae Organizing system' (MICOS) complex, involved in cristae organization. DISC1 knockdown in SH-SY5Y cells causes MICOS disassembly and fragmentation of the mitochondrial morphology network. Moreover, DISC1 depleted cells have decreased mitochondrial DNA (mtDNA) content and steady state levels of oxidative phosphorylation (OXPHOS) subunits. As a consequence, OXPHOS complexes and supercomplexes are partially disassembled in DISC1 knockdown cells, which suffer severe bioenergetic defects, evidenced by impaired oxygen consumption, adenosine triphosphate synthesis and mitochondrial membrane potential. Transfection of recombinant full-length human DISC1 restores MICOS complex assembly and rescues OXPHOS function, meanwhile overexpression of the DISC1 truncated form Δ597-854, known to be pathogenic, fails to rescue the bioenergetic impairment caused by DISC1 knockdown. These results should contribute to reveal DISC1 physiological function and potential pathogenic role in severe mental illnesses.
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