ArticleGenetics2007
Aberrant splicing of an alternative exon in the Drosophila troponin-T gene affects flight muscle development.
Article in Genetics, 2007. 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, 59 citations in OpenAlex.
- Signalling networks orchestrating the development of Drosophila indirect flight muscles.Histochemistry and cell biology · 2026Review
- Fine-tuning striated muscle performance: conserved sarcomere-level mechanisms across insect and vertebrate systems.Frontiers in physiology · 2026Review
- Parvin is essential for indirect flight muscle (IFM) performance and Zasp52 localisation to the Z-disc in Drosophila melanogaster.Cell and tissue research · 2025Article
- Identification and Characterization ofInternational journal of molecular sciences · 2025Article
- Bruno 1/CELF regulates splicing and cytoskeleton dynamics to ensure correct sarcomere assembly in Drosophila flight muscles.PLoS biology · 2024Article
- Differential gene expression and microRNA profile in corpora allata-corpora cardiaca of Aedes aegypti mosquitoes with weak juvenile hormone signalling.BMC genomics · 2024Article
- 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
- Rbfox1 is required for myofibril development and maintaining fiber type-specific isoform expression inLife science alliance · 2022Article
- Transcriptional Profiles of Diploid MutantInsects · 2021Article
- The glutamic acid-rich-long C-terminal extension of troponin T has a critical role in insect muscle functions.The Journal of biological chemistry · 2020Article
- Invertebrate troponin: Insights into the evolution and regulation of striated muscle contraction.Archives of biochemistry and biophysics · 2019Review
- A tissue communication network coordinating innate immune response during muscle stress.Journal of cell science · 2018Article
- Novel functions for integrin-associated proteins revealed by analysis of myofibril attachment ineLife · 2018Article
- Overexpression of miRNA-9 Generates Muscle Hypercontraction Through Translational Repression of Troponin-T inG3 (Bethesda, Md.) · 2017Article
- Molecular plasticity and functional enhancements of leg muscles in response to hypergravity in the fruit flyThe Journal of experimental biology · 2017Article
- Muscles provide protection during microbial infection by activating innate immune response pathways in Drosophila and zebrafish.Disease models & mechanisms · 2016Article
- miR-434-3p and DNA hypomethylation co-regulate eIF5A1 to increase AChRs and to improve plasticity in SCT rat skeletal muscle.Scientific reports · 2016Article
- Effects of age and hindlimb immobilization and remobilization on fast troponin T precursor mRNA alternative splicing in rat gastrocnemius muscle.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2016Article
- Article
- The RNA-binding protein Arrest (Bruno) regulates alternative splicing to enable myofibril maturation in Drosophila flight muscle.EMBO reports · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During myofibrillogenesis, many muscle structural proteins assemble to form the highly ordered contractile sarcomere. Mutations in these proteins can lead to dysfunctional muscle and various myopathies. We have analyzed the Drosophila melanogaster troponin T (TnT) up1 mutant that specifically affects the indirect flight muscles (IFM) to explore troponin function during myofibrillogenesis. The up1 muscles lack normal sarcomeres and contain "zebra bodies," a phenotypic feature of human nemaline myopathies. We show that the up(1) mutation causes defective splicing of a newly identified alternative TnT exon (10a) that encodes part of the TnT C terminus. This exon is used to generate a TnT isoform specific to the IFM and jump muscles, which during IFM development replaces the exon 10b isoform. Functional differences between the 10a and 10b TnT isoforms may be due to different potential phosphorylation sites, none of which correspond to known phosphorylation sites in human cardiac TnT. The absence of TnT mRNA in up1 IFM reduces mRNA levels of an IFM-specific troponin I (TnI) isoform, but not actin, tropomyosin, or troponin C, suggesting a mechanism controlling expression of TnT and TnI genes may exist that must be examined in the context of human myopathies caused by mutations of these thin filament proteins.
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