ArticleGenetics1994
Recovery of dominant, autosomal flightless mutants of Drosophila melanogaster and identification of a new gene required for normal muscle structure and function.
Article in Genetics, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 47 citations in OpenAlex.
- TET exhibits enzymatic-independent and-dependent functions during Drosophila flight muscle development and aging.Skeletal muscle · 2025Article
- Angel wing: a class of alternative splicing regulators in animals.Nucleic acids research · 2025Article
- An insight on Drosophila myogenesis and its assessment techniques.Molecular biology reports · 2020Review
- Suppression of myopathic lamin mutations by muscle-specific activation of AMPK and modulation of downstream signaling.Human molecular genetics · 2019Article
- Article
- A New Behavioral Test and Associated Genetic Tools Highlight the Function of Ventral Abdominal Muscles in AdultFrontiers in cellular neuroscience · 2017Article
- Article
- E2F function in muscle growth is necessary and sufficient for viability in Drosophila.Nature communications · 2016Article
- Reduced expression of CDP-DAG synthase changes lipid composition and leads to male sterility in Drosophila.Open biology · 2016Article
- Binding partners of the kinase domains in Drosophila obscurin and their effect on the structure of the flight muscle.Journal of cell science · 2015Article
- Article
- DAAM is required for thin filament formation and Sarcomerogenesis during muscle development in Drosophila.PLoS genetics · 2014Article
- The function of the M-line protein obscurin in controlling the symmetry of the sarcomere in the flight muscle of Drosophila.Journal of cell science · 2012Article
- In vitro motility of native thin filaments from Drosophila indirect flight muscles reveals that the held-up 2 TnI mutation affects calcium activation.Journal of muscle research and cell motility · 2010Article
- Mining phenotypes for gene function prediction.BMC bioinformatics · 2008Article
- Other model organisms for sarcomeric muscle diseases.Advances in experimental medicine and biology · 2008Review
- Article
- small bristles is required for the morphogenesis of multiple tissues during Drosophila development.Genetics · 2001Article
- A direct screen identifies new flight muscle mutants on the Drosophila second chromosome.Genetics · 1999Article
- Transformation of Drosophila melanogaster with the wild-type myosin heavy-chain gene: rescue of mutant phenotypes and analysis of defects caused by overexpression.The Journal of cell biology · 1994Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To identify further mutations affecting muscle function and development in Drosophila melanogaster we recovered 22 autosomal dominant flightless mutations. From these we have isolated eight viable and lethal alleles of the muscle myosin heavy chain gene, and seven viable alleles of the indirect flight muscle (IFM)-specific Act88F actin gene. The Mhc mutations display a variety of phenotypic effects, ranging from reductions in myosin heavy chain content in the indirect flight muscles only, to reductions in the levels of this protein in other muscles. The Act88F mutations range from those which produce no stable actin and have severely abnormal myofibrillar structure, to those which accumulate apparently normal levels of actin in the flight muscles but which still have abnormal myofibrils and fly very poorly. We also recovered two recessive flightless mutants on the third chromosome. The remaining five dominant flightless mutations are all lethal alleles of a gene named lethal(3)Laker. The Laker alleles have been characterized and the gene located in polytene bands 62A10,B1-62B2,4. Laker is a previously unidentified locus which is haplo-insufficient for flight. In addition, adult wild-type heterozygotes and the lethal larval trans-heterozygotes show abnormalities of muscle structure indicating that the Laker gene product is an important component of muscle.
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