ArticleBMC neuroscience2013
Lack of exon 10 in the murine tau gene results in mild sensorimotor defects with aging.
Article in BMC neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 24 citations in OpenAlex.
- Limitations and Applications of Rodent Models in Tauopathy and Synucleinopathy Research.Journal of neurochemistry · 2025Review
- The six brain-specific TAU isoforms and their role in Alzheimer's disease and related neurodegenerative dementia syndromes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- Can accelerated ageing models inform us on age-related tauopathies?Aging cell · 2023Review
- The collateral activity of RfxCas13d can induce lethality in a RfxCas13d knock-in mouse model.Genome biology · 2023Article
- IntelliCage: the development and perspectives of a mouse- and user-friendly automated behavioral test system.Frontiers in behavioral neuroscience · 2023Review
- The physiological roles of tau and Aβ: implications for Alzheimer's disease pathology and therapeutics.Acta neuropathologica · 2020Review
- High-resolution temporal and regional mapping of MAPT expression and splicing in human brain development.PloS one · 2018Article
- Atypical, non-standard functions of the microtubule associated Tau protein.Acta neuropathologica communications · 2017Review
- Absence of Tau triggers age-dependent sciatic nerve morphofunctional deficits and motor impairment.Aging cell · 2016Article
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundComplex species-specific, developmental- and tissue-dependent mechanisms regulate alternative splicing of tau, thereby diversifying tau protein synthesis. The functional role of alternative splicing of tau e.g. exon 10 has never been examined in vivo, although genetic studies suggest that it is important to neurodegenerative disease.
resultsGene-targeting was used to delete exon 10 in murine tau on both alleles (E10-/-) to study its functional role. Moreover, mice devoid of exon 10 (E10+/-) on one allele were generated to investigate the effects of 1:1 balanced expression of 4R-/3R-tau protein, since equal amounts of 4R-/3R-tau protein are synthesized in human brain. Middle-aged E10-/- mice displayed sensorimotor disturbances in the rotarod when compared to age-matched E10+/- and wild-type mice, and their muscular grip strength was less than that of E10+/- mice. The performance of E10+/- mice and wild-type mice (E10+/+) was similar in sensorimotor tests. Cognitive abilities or anxiety-like behaviours did not depend on exon 10 in tau, and neither pathological inclusions nor gene-dependent morphological abnormalities were found.
conclusionAblation of exon 10 in the murine tau gene alters alternative splicing and tau protein synthesis which results in mild sensorimotor phenotypes with aging. Presumably related microtubule-stabilizing genes rescue other functions.
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