ArticleThe Journal of cell biology1998
Ca2+-dependent muscle dysfunction caused by mutation of the Caenorhabditis elegans troponin T-1 gene.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Pervasive non-triplet alternative splicing drives functional isoform diversity.Nature communications · 2026Article
- DamID identifies targets of CEH-60/PBX that are associated with neuron development and muscle structure in Caenorhabditis elegans.PloS one · 2020Article
- Regulation of structure and function of sarcomeric actin filaments in striated muscle of the nematode Caenorhabditis elegans.Anatomical record (Hoboken, N.J. : 2007) · 2014Review
- Roles of the troponin isoforms during indirect flight muscle development in Drosophila.Journal of genetics · 2014Article
- Molecular characterisation of colour formation in the prawn Fenneropenaeus merguiensis.PloS one · 2013Article
- Caenorhabditis elegans gelsolin-like protein 1 is a novel actin filament-severing protein with four gelsolin-like repeats.The Journal of biological chemistry · 2008Article
- Other model organisms for sarcomeric muscle diseases.Advances in experimental medicine and biology · 2008Review
- Aberrant splicing of an alternative exon in the Drosophila troponin-T gene affects flight muscle development.Genetics · 2007Article
- Genes that control ray sensory neuron axon development in the Caenorhabditis elegans male.Genetics · 2006Article
- Structure and sequence of the human fast skeletal troponin T (TNNT3) gene: insight into the evolution of the gene and the origin of the developmentally regulated isoforms.Comparative and functional genomics · 2003Article
- MUP-4 is a novel transmembrane protein with functions in epithelial cell adhesion in Caenorhabditis elegans.The Journal of cell biology · 2001Article
- A tropomyosin-2 mutation suppresses a troponin I myopathy in Drosophila.Molecular biology of the cell · 2001Article
- A novel nemaline myopathy in the Amish caused by a mutation in troponin T1.American journal of human genetics · 2000Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the functions of troponin T (CeTnT-1) in Caenorhabditis elegans embryonic body wall muscle. TnT tethers troponin I (TnI) and troponin C (TnC) to the thin filament via tropomyosin (Tm), and TnT/Tm regulates the activation and inhibition of myosin-actin interaction in response to changes in intracellular [Ca2+]. Loss of CeTnT-1 function causes aberrant muscle trembling and tearing of muscle cells from their exoskeletal attachment sites (Myers, C.D., P.-Y. Goh, T. StC. Allen, E.A. Bucher, and T. Bogaert. 1996. J. Cell Biol. 132:1061-1077). We hypothesized that muscle tearing is a consequence of excessive force generation resulting from defective tethering of Tn complex proteins. Biochemical studies suggest that such defective tethering would result in either (a) Ca2+-independent activation, due to lack of Tn complex binding and consequent lack of inhibition, or (b) delayed reestablishment of TnI/TnC binding to the thin filament after Ca2+ activation and consequent abnormal duration of force. Analyses of animals doubly mutant for CeTnT-1 and for genes required for Ca2+ signaling support that CeTnT-1 phenotypes are dependent on Ca2+ signaling, thus supporting the second model and providing new in vivo evidence that full inhibition of thin filaments in low [Ca2+] does not require TnT.
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