The long non-coding RNA Gomafu is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing
Abstract
Schizophrenia (SZ) is a complex disease characterized by impaired neuronal functioning. Although defective alternative splicing has been linked to SZ, the molecular mechanisms responsible are unknown. Additionally, there is limited understanding of the early transcriptomic responses to neuronal activation. Here, we profile these transcriptomic responses and show that long non-coding RNAs (lncRNAs) are dynamically regulated by neuronal activation, including acute downregulation of the lncRNA Gomafu, previously implicated in brain and retinal development. Moreover, we demonstrate that Gomafu binds directly to the splicing factors QKI and SRSF1 (serine/arginine-rich splicing factor 1) and dysregulation of Gomafu leads to alternative splicing patterns that resemble those observed in SZ for the archetypal SZ-associated genes DISC1 and ERBB4. Finally, we show that Gomafu is downregulated in post-mortem cortical gray matter from the superior temporal gyrus in SZ. These results functionally link activity-regulated lncRNAs and alternative splicing in neuronal function and suggest that their dysregulation may contribute to neurological disorders.
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QKI is an established regulator of oligodendrocyte-gene splicing and is located in this module.
“an established regulator of oligodendrocyte-gene splicing also located in this module (77, 78).”
From Transcriptome-wide isoform-level dysregulation in ASD, schizophrenia, and bipolar disorder (2018) · cites this paper as [78]
MIAT is known to interact with QKI.
“MIAT is also known to interact with QKI”
From Transcriptome-wide isoform-level dysregulation in ASD, schizophrenia, and bipolar disorder (2018) · cites this paper as [78]
These analyses predict critical roles for these non-coding genes in oligodendrocyte function and potentially in psychiatric conditions.
“These analyses predict critical roles for these or these often overlooked non-coding genes in oligodendrocyte function (77, 78) and potentially in psychiatric conditions.”
From Transcriptome-wide isoform-level dysregulation in ASD, schizophrenia, and bipolar disorder (2018) · cites this paper as [78]
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Self-citation
- Authors
- Barry, G., Briggs, J. A., Vanichkina, D. P., Poth, E. M., Beveridge, N. J., Ratnu, V. S., Nayler, S. P., Nones, K., Hu, J., Bredy, T. W., Nakagawa, S., Rigo, F., Taft, R. J., Cairns, M. J., Blackshaw, S., Wolvetang, E. J., & Mattick, J. S.
- Affiliations
- The University of Queensland (AU)
- Johns Hopkins University (US)
- Schizophrenia Research Institute (AU)
- RIKEN (JP)
- Ionis Pharmaceuticals (United States) (US)
- Garvan Institute of Medical Research (AU)
- Corresponding author
- Mattick, J S
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2013-04-30
- Volume
- 19
- Issue
- 4
- Pages
- 486-494
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- OpenAlex
- W2074495242
- Cited by
- 394
- References
- 72
- Citations by year
- 2026: 7 · 2025: 13 · 2024: 21 · 2023: 23 · 2022: 24 · 2021: 43 · 2020: 37 · 2019: 33 · 2018: 40 · 2017: 43 · 2016: 42 · 2015: 35 · 2014: 22 · 2013: 11
- FWCI
- 12.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- NOVA (University of Newcastle Australia) (submittedVersion)
- Funders
- Japan Society for the Promotion of Science (26113005, 21228003)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Keywords
- long non-coding RNA, schizophrenia, alternative splicing, neuronal activation, QKI, SRSF1, splicing factors, DISC1, ErbB4, superior temporal gyrus, cortical gray matter, transcriptome
- MeSH terms
- Serine-Arginine Splicing Factors, Animals, Cells, Cultured, Cerebral Cortex, Embryo, Mammalian, Gene Expression Regulation, Humans, Mice, Inbred C57BL, Nerve Tissue Proteins, Neurons, Nuclear Proteins, Schizophrenia, Oligonucleotides, Antisense, RNA-Binding Proteins, Alternative Splicing, Proteome, Electrophoretic Mobility Shift Assay, Microarray Analysis, Immunoprecipitation, Mice, RNA, Long Noncoding, ErbB Receptors, Receptor, ErbB-4
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