ArticleProceedings of the National Academy of Sciences of the United States of America2012
Thin, a Trim32 ortholog, is essential for myofibril stability and is required for the integrity of the costamere in Drosophila.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 45 citations in OpenAlex.
- TET exhibits enzymatic-independent and-dependent functions during Drosophila flight muscle development and aging.Skeletal muscle · 2025Article
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- Congenital myopathies: pathophysiological mechanisms and promising therapies.Journal of translational medicine · 2024Review
- Identification of CryAB as a target of NUAK kinase activity in Drosophila muscle tissue.Genetics · 2023Article
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- A conserved STRIPAK complex is required for autophagy in muscle tissue.Molecular biology of the cell · 2023Article
- Drosophila Tropomodulin is required for multiple actin-dependent processes within developing myofibers.Development (Cambridge, England) · 2023Article
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- The E3 ligase Thin controls homeostatic plasticity through neurotransmitter release repression.eLife · 2022Article
- Article
- Integration of proteomic and genetic approaches to assess developmental muscle atrophy.The Journal of experimental biology · 2021Article
- A large-scale transgenic RNAi screen identifies transcription factors that modulate myofiber size in Drosophila.PLoS genetics · 2021Article
- TRIM32: A Multifunctional Protein Involved in Muscle Homeostasis, Glucose Metabolism, and Tumorigenesis.Biomolecules · 2021Review
- Costameric integrin and sarcoglycan protein levels are altered in aMolecular biology of the cell · 2021Article
- Roles for RNA export factor, Nxt1, in ensuring muscle integrity and normal RNA expression in Drosophila.G3 (Bethesda, Md.) · 2021Article
- Impaired muscle morphology in aDisease models & mechanisms · 2020Article
- Drosophila NUAK functions with Starvin/BAG3 in autophagic protein turnover.PLoS genetics · 2020Article
- Article
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- Thin is required for cell death in the Drosophila abdominal muscles by targeting DIAP1.Cell death & disease · 2018Article
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6 authors at 3 institutions in 1 country.
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Abstract
Myofibril stability is required for normal muscle function and maintenance. Mutations that disrupt myofibril stability result in individuals who develop progressive muscle wasting, or muscular dystrophy, and premature mortality. Here we present our investigations of the Drosophila l(2)thin [l(2)tn] mutant. The "thin" phenotype exhibits features of the human muscular disease phenotype in that tn mutant larvae show progressive muscular degeneration. Loss-of-function and rescue experiments determined that l(2)tn is allelic to the tn locus [previously annotated as both CG15105 and another b-box affiliate (abba)]. tn encodes a TRIM (tripartite motif) containing protein highly expressed in skeletal muscle and is orthologous to the human limb-girdle muscular dystrophy type 2H disease gene Trim32. Thin protein is localized at the Z-disk in muscle, but l(2)tn mutants showed no genetic interaction with mutants affecting the Z-line-associated protein muscle LIM protein 84B. l(2)tn, along with loss-of-function mutants generated for tn, showed no relative mislocalization of the Z-disk proteins α-Actinin and muscle LIM protein 84B. In contrast, tn mutants had significant disorganization of the costameric orthologs β-integrin, Spectrin, Talin, and Vinculin, and we present the initial description for the costamere, a key muscle stability complex, in Drosophila. Our studies demonstrate that myofibrils progressively unbundle in flies that lack Thin function through progressive costamere breakdown. Due to the high conservation of these structures in animals, we demonstrate a previously unknown role for TRIM32 proteins in myofibril stability.
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