ArticleThe Journal of cell biology1991
Muscle abnormalities in Drosophila melanogaster heldup mutants are caused by missing or aberrant troponin-I isoforms.
Article in The Journal of cell biology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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59 citing papers in PubMed, 103 citations in OpenAlex.
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- A role for actin flexibility in thin filament-mediated contractile regulation and myopathy.Nature communications · 2020Article
- Multi-modal and multiscale imaging approaches reveal novel cardiovascular pathophysiology inBiology open · 2019Article
- Suppression of myopathic lamin mutations by muscle-specific activation of AMPK and modulation of downstream signaling.Human molecular genetics · 2019Article
- Reductions in ATPase activity, actin sliding velocity, and myofibril stability yield muscle dysfunction in Drosophila models of myosin-based Freeman-Sheldon syndrome.Molecular biology of the cell · 2019Article
- Overexpression of miRNA-9 Generates Muscle Hypercontraction Through Translational Repression of Troponin-T inG3 (Bethesda, Md.) · 2017Article
- Distortion of the Actin A-Triad Results in Contractile Disinhibition and Cardiomyopathy.Cell reports · 2017Article
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- Vimar Is a Novel Regulator of Mitochondrial Fission through Miro.PLoS genetics · 2016Article
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- Pseudo-acetylation of K326 and K328 of actin disrupts Drosophila melanogaster indirect flight muscle structure and performance.Frontiers in physiology · 2015Article
- Galactokinase is a novel modifier of calcineurin-induced cardiomyopathy in Drosophila.Genetics · 2014Article
- An ongoing role for structural sarcomeric components in maintaining Drosophila melanogaster muscle function and structure.PloS one · 2014Article
- Elevated expression of the integrin-associated protein PINCH suppresses the defects of Drosophila melanogaster muscle hypercontraction mutants.PLoS genetics · 2013Article
- Modeling dilated cardiomyopathies in Drosophila.Trends in cardiovascular medicine · 2012Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the molecular bases of muscle abnormalities in four Drosophila melanogaster heldup mutants. We find that the heldup gene encodes troponin-I, one of the principal regulatory proteins associated with skeletal muscle thin filaments. heldup3, heldup4, and heldup5 mutants, all of which have grossly abnormal flight muscle myofibrils, lack mRNAs encoding one or more troponin-I isoforms. In contrast, heldup2, an especially interesting mutant wherein flight muscles are atrophic, synthesizes the complete mRNA complement. By sequencing mutant troponin-I cDNAs we demonstrate that the molecular basis for muscle degeneration in heldup2 is conversion of an invariant alanine residue to valine. We finally show that degeneration of heldup2 thin filament/Z-disc networks can be prevented by eliminating thick filaments from flight muscles using a null allele of the sarcomeric myosin heavy chain gene. This latter observation suggests that actomyosin interactions exacerbate the structural or functional defect resulting from the troponin-I mutation.
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