ArticleThe Journal of cell biology1996
Alterations in flight muscle ultrastructure and function in Drosophila tropomyosin mutants.
Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 50 citations in OpenAlex.
- Suppression of myopathic lamin mutations by muscle-specific activation of AMPK and modulation of downstream signaling.Human molecular genetics · 2019Article
- The tymbal muscle of cicada has flight muscle-type sarcomeric architecture and protein expression.Zoological letters · 2017Article
- A novel tropomyosin isoform functions at the mitotic spindle and Golgi in Drosophila.Molecular biology of the cell · 2015Article
- Tropomodulins and tropomyosins: working as a team.Journal of muscle research and cell motility · 2013Review
- Evolutionarily conserved surface residues constitute actin binding sites of tropomyosin.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Structure, function and evolution of insect flight muscle.Biophysics (Nagoya-shi, Japan) · 2011Review
- Functional identity of the gamma tropomyosin gene: Implications for embryonic development, reproduction and cell viability.Bioarchitecture · 2011Article
- Article
- The structural role of high molecular weight tropomyosins in dipteran indirect flight muscle and the effect of phosphorylation.Journal of muscle research and cell motility · 2006Article
- The essential role of PP1beta in Drosophila is to regulate nonmuscle myosin.Molecular biology of the cell · 2004Article
- Gamma tropomyosin gene products are required for embryonic development.Molecular and cellular biology · 2004Article
- The interaction of tropomodulin with tropomyosin stabilizes thin filaments in cardiac myocytes.The Journal of cell biology · 2003Article
- Tropomyosin inhibits ADF/cofilin-dependent actin filament dynamics.The Journal of cell biology · 2002Article
- Varieties of elastic protein in invertebrate muscles.Journal of muscle research and cell motility · 2002Review
- Thin filaments elongate from their pointed ends during myofibril assembly in Drosophila indirect flight muscle.The Journal of cell biology · 2001Article
- A tropomyosin-2 mutation suppresses a troponin I myopathy in Drosophila.Molecular biology of the cell · 2001Article
- Overexpression of miniparamyosin causes muscle dysfunction and age-dependant myofibril degeneration in the indirect flight muscles of Drosophila melanogaster.Journal of muscle research and cell motility · 2001Article
- Thin filament protein dynamics in fully differentiated adult cardiac myocytes: toward a model of sarcomere maintenance.The Journal of cell biology · 1999Article
- Interaction of troponin-H and glutathione S-transferase-2 in the indirect flight muscles of Drosophila melanogaster.Journal of muscle research and cell motility · 1998Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Drosophila indirect flight muscle (IFM) contains two different types of tropomyosin: a standard 284-amino acid muscle tropomyosin, Ifm-TmI, encoded by the TmI gene, and two > 400 amino acid tropomyosins, TnH-33 and TnH-34, encoded by TmII. The two IFM-specific TnH isoforms are unique tropomyosins with a COOH-terminal extension of approximately 200 residues which is hydrophobic and rich in prolines. Previous analysis of a hypomorphic TmI mutant, Ifm(3)3, demonstrated that Ifm-TmI is necessary for proper myofibrillar assembly, but no null TmI mutant or TmII mutant which affects the TnH isoforms have been reported. In the current report, we show that four flightless mutants (Warmke et al., 1989) are alleles of TmI, and characterize a deficiency which deletes both TmI and TmII. We find that haploidy of TmI causes myofibrillar disruptions and flightless behavior, but that haploidy of TmII causes neither. Single fiber mechanics demonstrates that power output is much lower in the TmI haploid line (32% of wild-type) than in the TmII haploid line (73% of wild-type). In myofibers nearly depleted of Ifm-TmI, net power output is virtually abolished (< 1% of wild-type) despite the presence of an organized fibrillar core (approximately 20% of wild-type). The results suggest Ifm-TmI (the standard tropomyosin) plays a key role in fiber structure, power production, and flight, with reduced Ifm-TmI expression producing corresponding changes of IFM structure and function. In contrast, reduced expression of the TnH isoforms has an unexpectedly mild effect on IFM structure and function.
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