ArticleGenetics2003
Suppression of muscle hypercontraction by mutations in the myosin heavy chain gene of Drosophila melanogaster.
Article in Genetics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 78 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
- Developmental remodelling ofOpen biology · 2025Article
- Titin-dependent biomechanical feedback tailors sarcomeres to specialized muscle functions in insects.Science advances · 2025Article
- Insufficient wing development possibly contributes to flightlessness of the silkwormProceedings. Biological sciences · 2025Article
- Bruno 1/CELF regulates splicing and cytoskeleton dynamics to ensure correct sarcomere assembly in Drosophila flight muscles.PLoS biology · 2024Article
- Article
- Rbfox1 is required for myofibril development and maintaining fiber type-specific isoform expression inLife science alliance · 2022Article
- Article
- Impaired muscle morphology in aDisease models & mechanisms · 2020Article
- Suppression of myopathic lamin mutations by muscle-specific activation of AMPK and modulation of downstream signaling.Human molecular genetics · 2019Article
- Article
- Myosin storage myopathy mutations yield defective myosin filament assembly in vitro and disrupted myofibrillar structure and function in vivo.Human molecular genetics · 2017Article
- Overexpression of miRNA-9 Generates Muscle Hypercontraction Through Translational Repression of Troponin-T inG3 (Bethesda, Md.) · 2017Article
- Flightin maintains myofilament lattice organization required for optimal flight power and courtship song quality inProceedings. Biological sciences · 2017Article
- Muscles provide protection during microbial infection by activating innate immune response pathways in Drosophila and zebrafish.Disease models & mechanisms · 2016Article
- Article
- Intrinsic disorder and multiple phosphorylations constrain the evolution of the flightin N-terminal region.Journal of proteomics · 2016Article
- Article
- Metabolite localization in living drosophila using High Resolution Magic Angle Spinning NMR.Scientific reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The indirect flight muscles (IFM) of Drosophila melanogaster provide a good genetic system with which to investigate muscle function. Flight muscle contraction is regulated by both stretch and Ca(2+)-induced thin filament (actin + tropomyosin + troponin complex) activation. Some mutants in troponin-I (TnI) and troponin-T (TnT) genes cause a "hypercontraction" muscle phenotype, suggesting that this condition arises from defects in Ca(2+) regulation and actomyosin-generated tension. We have tested the hypothesis that missense mutations of the myosin heavy chain gene, Mhc, which suppress the hypercontraction of the TnI mutant held-up(2) (hdp(2)), do so by reducing actomyosin force production. Here we show that a "headless" Mhc transgenic fly construct that reduces the myosin head concentration in the muscle thick filaments acts as a dose-dependent suppressor of hypercontracting alleles of TnI, TnT, Mhc, and flightin genes. The data suggest that most, if not all, mutants causing hypercontraction require actomyosin-produced forces to do so. Whether all Mhc suppressors act simply by reducing the force production of the thick filament is discussed with respect to current models of myosin function and thin filament activation by the binding of calcium to the troponin complex.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.