ArticleThe Journal of physiology2014
Deficiency of slow skeletal muscle troponin T causes atrophy of type I slow fibres and decreases tolerance to fatigue.
Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 44 citations in OpenAlex.
- Potential cytotoxicity of truncated slow skeletal muscle troponin T (ssTnT) in a loss of function TNNT1 myopathy mouse model.The FEBS journal · 2025Article
- The highly conserved C-terminal end segment of troponin T binds tropomyosin and actin to function in modulating contractile kinetics.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Pathogenic TNNT1 variants are associated with aberrant thin filament compliance and myofibre hyper-contractility.The Journal of physiology · 2025Article
- Congenital myopathies: pathophysiological mechanisms and promising therapies.Journal of translational medicine · 2024Review
- Transcriptomic and metabolomic dissection of skeletal muscle of crossbred Chongming white goats with different meat production performance.BMC genomics · 2024Article
- Integrating miRNA and full-length transcriptome profiling to elucidate the mechanism of muscle growth in Muscovy ducks reveals key roles for miR-301a-3p/ANKRD1.BMC genomics · 2024Article
- Motor neurons and endothelial cells additively promote development and fusion of human iPSC-derived skeletal myocytes.Skeletal muscle · 2024Article
- FUS-Mediated Inhibition of Myogenesis Elicited by Suppressing TNNT1 Production.Molecular and cellular biology · 2024Article
- WiTNNess: An international natural history study of infantile-onset TNNT1 myopathy.Annals of clinical and translational neurology · 2023Observational
- Differentially Expressed Genes and Molecular Susceptibility to Human Age-Related Diseases.International journal of molecular sciences · 2023Article
- Skeletal muscle proteome analysis underpins multifaceted mitochondrial dysfunction in Friedreich's ataxia.Frontiers in neuroscience · 2023Article
- Early Divergence of the C-Terminal Variable Region of Troponin T Via a Pair of Mutually Exclusive Alternatively Spliced Exons Followed by a Selective Fixation in Vertebrate Heart.Journal of molecular evolution · 2022Article
- Global Landscape of m6A Methylation of Differently Expressed Genes in Muscle Tissue of Liaoyu White Cattle and Simmental Cattle.Frontiers in cell and developmental biology · 2022Article
- Gene Expression Profiling of Skeletal Muscles.Genes · 2021Article
- Troponin Variants as Markers of Skeletal Muscle Health and Diseases.Frontiers in physiology · 2021Review
- Ovine congenital progressive muscular dystrophy (OCPMD) is a model of TNNT1 congenital myopathy.Acta neuropathologica communications · 2020Article
- In vivo characterization of skeletal muscle function in nebulin-deficient mice.Muscle & nerve · 2020Article
- Exploring the Mechanism of Skeletal Muscle in a Tacrolimus-Induced Posttransplantation Diabetes Mellitus Model on Gene Expression Profiles.Journal of diabetes research · 2020Article
- The loss of slow skeletal muscle isoform of troponin T in spindle intrafusal fibres explains the pathophysiology of Amish nemaline myopathy.The Journal of physiology · 2019Article
- Nemaline myopathies: a current view.Journal of muscle research and cell motility · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The total loss of slow skeletal muscle troponin T (ssTnT encoded by TNNT1 gene) due to a nonsense mutation in codon Glu(180) causes a lethal form of recessively inherited nemaline myopathy (Amish nemaline myopathy, ANM). To investigate the pathogenesis and muscle pathophysiology of ANM, we studied the phenotypes of partial and total loss of ssTnT in Tnnt1 gene targeted mice. An insertion of neomycin resistance cassette in intron 10 of Tnnt1 gene caused an approximately 60% decrease in ssTnT protein expression whereas cre-loxP-mediated deletion of exons 11-13 resulted in total loss of ssTnT, as seen in ANM muscles. In diaphragm and soleus muscles of the knockdown and knockout mouse models, we demonstrated that ssTnT deficiency resulted in significantly decreased levels of other slow fibre-specific myofilament proteins whereas fast fibre-specific myofilament proteins were increased correspondingly. Immunohistochemical studies revealed that ssTnT deficiency produced significantly smaller type I slow fibres and compensatory growth of type II fast fibres. Along with the slow fibre atrophy and the changes in myofilament protein isoform contents, ssTnT deficiency significantly reduced the tolerance to fatigue in soleus muscle. ssTnT-deficient soleus muscle also contains significant numbers of small-sized central nuclei type I fibres, indicating active regeneration. The data provide strong support for the essential role of ssTnT in skeletal muscle function and the causal effect of its loss in the pathology of ANM. This observation further supports the hypothesis that the function of slow fibres can be restored in ANM patients if a therapeutic supplement of ssTnT is achieved.
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