ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Rescuing qkV dysmyelination by a single isoform of the selective RNA-binding protein QKI.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- Metabolic signatures in sciatic nerve of PMP22 transgenic rats provide insights into the pathogenesis of charcot-marie-tooth disease type 1 A.Scientific reports · 2026Article
- Quaking Protein in Myelin Maintenance and Regeneration in the Central Nervous System.Molecular neurobiology · 2025Review
- The Quaking RNA-binding proteins as regulators of cell differentiation.Wiley interdisciplinary reviews. RNA · 2022Review
- The Long Non-Coding RNACells · 2022Review
- Mature myelin maintenance requires Qki to coactivate PPARβ-RXRα-mediated lipid metabolism.The Journal of clinical investigation · 2020Article
- Generation and characterisation of a parkin-Pacrg knockout mouse line and a Pacrg knockout mouse line.Scientific reports · 2018Article
- Noise-Induced Dysregulation ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Genetic and Epigenetic Alterations Underlie Oligodendroglia Susceptibility and White Matter Etiology in Psychiatric Disorders.Frontiers in genetics · 2018Review
- mTORC1 Activation by Loss ofFrontiers in cellular neuroscience · 2018Article
- Novel schizophrenia risk factor pathways regulate FEZ1 to advance oligodendroglia development.Translational psychiatry · 2017Review
- RNA-binding Protein Quaking StabilizesThe Journal of biological chemistry · 2017Article
- Inherited and acquired disorders of myelin: The underlying myelin pathology.Experimental neurology · 2016Review
- Oligodendroglial defects during quakingviable cerebellar development.Developmental neurobiology · 2016Article
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- A cytoplasmic quaking I isoform regulates the hnRNP F/H-dependent alternative splicing pathway in myelinating glia.Nucleic acids research · 2014Article
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- Solution structure of the QUA1 dimerization domain of pXqua, the Xenopus ortholog of Quaking.PloS one · 2013Article
- HuD promotes BDNF expression in brain neurons via selective stabilization of the BDNF long 3'UTR mRNA.PloS one · 2013Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Alternative splicing of the qkI transcript generates multiple isoforms of the selective RNA-binding protein QKI, which play key roles in controlling the homeostasis of their mRNA targets. QKI deficiency in oligodendrocytes of homozygous quakingviable (qkV/qkV) mutant mice results in severe hypomyelination, indicating the essential function of QKI in myelinogenesis. However, the molecular mechanisms by which QKI controls myelination remain elusive. We report here that QKI-6 is the most abundant isoform in brain and is preferentially reduced in the qkV/qkV mutant during normal myelinogenesis. To test whether QKI-6 is the predominant isoform responsible for advancing CNS myelination, we developed transgenic mice that express Flag-QKI-6 specifically in the oligodendroglia lineage, driven by the proteolipid protein (PLP) promoter. When introduced into the qkV/qkV mutant, the QKI-6 transgene rescues the severe tremor and hypomyelination phenotype. Electron microscopic studies further revealed that the Flag-QKI-6 transgene is sufficient for restoring compact myelin formation with normal lamellar periodicity and thickness. Interestingly, Flag-QKI-6 preferentially associates with the mRNA encoding the myelin basic protein (MBP) and rescues MBP expression from the beginning of myelinogenesis. In contrast, Flag-QKI-6 binds the PLP mRNA with lower efficiency and has a minimal impact on PLP expression until much later, when the expression level of QKI-6 in the transgenic animal significantly exceeds what is needed for normal myelination. Together, our results demonstrate that QKI-6 is the major isoform responsible for CNS myelination, which preferentially promotes MBP expression in oligodendrocytes.
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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.