ArticleThe Journal of cell biology1999
Specific myosin heavy chain mutations suppress troponin I defects in Drosophila muscles.
Article in The Journal of cell biology, 1999. 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, 36 citations in OpenAlex.
- The mechanism of thin filament regulation: Models in conflict?The Journal of general physiology · 2019Review
- Article
- Two Drosophila myosin transducer mutants with distinct cardiomyopathies have divergent ADP and actin affinities.The Journal of biological chemistry · 2011Article
- Low temperature dynamic mapping reveals unexpected order and disorder in troponin.The Journal of biological chemistry · 2010Article
- Mutual rescues between two dominant negative mutations in cardiac troponin I and cardiac troponin T.The Journal of biological chemistry · 2010Article
- Myosin transducer mutations differentially affect motor function, myofibril structure, and the performance of skeletal and cardiac muscles.Molecular biology of the cell · 2008Article
- Other model organisms for sarcomeric muscle diseases.Advances in experimental medicine and biology · 2008Review
- Characterization of a hypercontraction-induced myopathy in Drosophila caused by mutations in Mhc.The Journal of cell biology · 2004Article
- Drosophila muscle regulation characterized by electron microscopy and three-dimensional reconstruction of thin filament mutants.Biophysical journal · 2004Article
- Transcription of Drosophila troponin I gene is regulated by two conserved, functionally identical, synergistic elements.Molecular biology of the cell · 2004Article
- Disruption of Caenorhabditis elegans muscle structure and function caused by mutation of troponin I.Biophysical journal · 2004Article
- Suppression of muscle hypercontraction by mutations in the myosin heavy chain gene of Drosophila melanogaster.Genetics · 2003Article
- Requirement of the calcineurin subunit gene canB2 for indirect flight muscle formation in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
We show that specific mutations in the head of the thick filament molecule myosin heavy chain prevent a degenerative muscle syndrome resulting from the hdp2 mutation in the thin filament protein troponin I. One mutation deletes eight residues from the actin binding loop of myosin, while a second affects a residue at the base of this loop. Two other mutations affect amino acids near the site of nucleotide entry and exit in the motor domain. We document the degree of phenotypic rescue each suppressor permits and show that other point mutations in myosin, as well as null mutations, fail to suppress the hdp2 phenotype. We discuss mechanisms by which the hdp2 phenotypes are suppressed and conclude that the specific residues we identified in myosin are important in regulating thick and thin filament interactions. This in vivo approach to dissecting the contractile cycle defines novel molecular processes that may be difficult to uncover by biochemical and structural analysis. Our study illustrates how expression of genetic defects are dependent upon genetic background, and therefore could have implications for understanding gene interactions in human disease.
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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.