Human QKI, a potential regulator of mRNA expression of human oligodendrocyte-related genes involved in schizophrenia
Open accessAbstract
The quaking viable mouse mutation (qk v ) is a deletion including the 5′ regulatory region of the quaking gene ( Qki ), which causes body tremor and severe dysmyelination in mouse. The function of the human quaking gene, called quaking homolog KH domain RNA-binding (mouse) ( QKI ), is not well known. We have previously shown that QKI is a new candidate gene for schizophrenia. Here we show that human QKI mRNA levels can account for a high proportion (47%) of normal interindividual mRNA expression variation (and covariation) of six oligodendrocyte-related genes ( PLP1 , MAG , MBP , TF , SOX10 , and CDKN1B ) in 55 human brain autopsy samples from individuals without psychiatric diagnoses. In addition, the tightly coexpressed myelin-related genes ( PLP1 , MAG , and TF ) have decreased mRNA levels in 55 schizophrenic patients, as compared with 55 control individuals, and most of this difference (68–96%) can be explained by variation in the relative mRNA levels of QKI-7kb , the same QKI splice variant previously shown to be down-regulated in patients with schizophrenia. Taken together, our results suggest that QKI levels may regulate oligodendrocyte differentiation and maturation in human brain, in a similar way as in mouse. Moreover, we hypothesize that previously observed decreased activity of myelin-related genes in schizophrenia might be caused by disturbed QKI splicing.
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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 [77]
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 [77]
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 [77]
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- Authors
- Åberg, K., Saetre, P., Jareborg, N., & Jazin, E.
- Affiliations
- Uppsala University (SE)
- AstraZeneca (Sweden) (SE)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2006-05-09
- Volume
- 103
- Issue
- 19
- Pages
- 7482-7487
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1987002276
- Cited by
- 208
- References
- 35
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 10 · 2023: 7 · 2022: 15 · 2021: 6 · 2020: 10 · 2019: 11 · 2018: 11 · 2017: 14 · 2016: 10 · 2015: 9 · 2014: 10 · 2013: 10 · 2012: 10
- FWCI
- 8.37
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- QKI, schizophrenia, oligodendrocytes, myelin genes, PLP1, myelin basic protein, myelin-associated glycoprotein, SOX10, p27, TF, gene expression variation, oligodendrocyte differentiation, dysmyelination, candidate genes
- MeSH terms
- Animals, Autopsy, Base Sequence, Binding Sites, Gene Expression Regulation, Humans, Molecular Sequence Data, Myelin Proteins, Myelin Sheath, Oligodendroglia, RNA, Messenger, Schizophrenia, Transcription, Genetic, Genetic Variation, Open Reading Frames, Sequence Alignment, RNA-Binding Proteins, Conserved Sequence
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