ArticleHuman molecular genetics2014
Inhibition of protein translation by the DISC1-Boymaw fusion gene from a Scottish family with major psychiatric disorders.
Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
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- Chimeric RNAs Discovered by RNA Sequencing and Their Roles in Cancer and Rare Genetic Diseases.Genes · 2022Review
- Metaplastic Effects of Ketamine and MK-801 on Glutamate Receptors Expression in Rat Medial Prefrontal Cortex and Hippocampus.Molecular neurobiology · 2021Article
- Chronic nicotine, but not suramin or resveratrol, partially remediates the mania-like profile of dopamine transporter knockdown mice.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2021Article
- Astrocyte Bioenergetics and Major Psychiatric Disorders.Advances in neurobiology · 2021Review
- Astrocyte DISC1 contributes to cognitive function in a brain region-dependent manner.Human molecular genetics · 2020Article
- Knock-in of Mutated hTAU Causes Insulin Resistance, Inflammation and Proteostasis Disturbance in a Mouse Model of Frontotemporal Dementia.Molecular neurobiology · 2020Article
- Novel genome-wide associations for anhedonia, genetic correlation with psychiatric disorders, and polygenic association with brain structure.Translational psychiatry · 2019Article
- Ribosomal biogenesis as an emerging target of neurodevelopmental pathologies.Journal of neurochemistry · 2019Review
- Sensorimotor gating deficits in "two-hit" models of schizophrenia risk factors.Schizophrenia research · 2018Review
- DISC1 regulates lactate metabolism in astrocytes: implications for psychiatric disorders.Translational psychiatry · 2018Article
- Expression of mutant DISC1 in Purkinje cells increases their spontaneous activity and impairs cognitive and social behaviors in mice.Neurobiology of disease · 2017Article
- Chronic Stress Increases Prefrontal Inhibition: A Mechanism for Stress-Induced Prefrontal Dysfunction.Biological psychiatry · 2016Article
- DISC1 causes associative memory and neurodevelopmental defects in fruit flies.Molecular psychiatry · 2016Article
- Disrupted-in-schizophrenia 1 (DISC1) and Syntaphilin collaborate to modulate axonal mitochondrial anchoring.Molecular brain · 2016Article
- Utility and validity of DISC1 mouse models in biological psychiatry.Neuroscience · 2016Review
- A critical period of vulnerability to adolescent stress: epigenetic mediators in mesocortical dopaminergic neurons.Human molecular genetics · 2016Article
- The involvement of N-methyl-D-aspartate receptor (NMDAR) subunit NR1 in the pathophysiology of schizophrenia.Acta biochimica et biophysica Sinica · 2016Review
- DISC1-dependent Regulation of Mitochondrial Dynamics Controls the Morphogenesis of Complex Neuronal Dendrites.The Journal of biological chemistry · 2016Article
- Balanced translocation linked to psychiatric disorder, glutamate, and cortical structure/function.NPJ schizophrenia · 2016Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The t(1; 11) translocation appears to be the causal genetic lesion with 70% penetrance for schizophrenia, major depression and other psychiatric disorders in a Scottish family. Molecular studies identified the disruption of the disrupted-in-schizophrenia 1 (DISC1) gene by chromosome translocation at chromosome 1q42. Our previous studies, however, revealed that the translocation also disrupted another gene, Boymaw (also termed DISC1FP1), on chromosome 11. After translocation, two fusion genes [the DISC1-Boymaw (DB7) and the Boymaw-DISC1 (BD13)] are generated between the DISC1 and Boymaw genes. In the present study, we report that expression of the DB7 fusion gene inhibits both intracellular NADH oxidoreductase activities and protein translation. We generated humanized DISC1-Boymaw mice with gene targeting to examine the in vivo functions of the fusion genes. Consistent with the in vitro studies on the DB7 fusion gene, protein translation activity is decreased in the hippocampus and in cultured primary neurons from the brains of the humanized mice. Expression of Gad67, Nmdar1 and Psd95 proteins are also reduced. The humanized mice display prolonged and increased responses to the NMDA receptor antagonist, ketamine, on various mouse genetic backgrounds. Abnormal information processing of acoustic startle and depressive-like behaviors are also observed. In addition, the humanized mice display abnormal erythropoiesis, which was reported to associate with depression in humans. Expression of the DB7 fusion gene may reduce protein translation to impair brain functions and thereby contribute to the pathogenesis of major psychiatric disorders.
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