ArticleMolecular biology of the cell2012
UNC-89 (obscurin) binds to MEL-26, a BTB-domain protein, and affects the function of MEI-1 (katanin) in striated muscle of Caenorhabditis elegans.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- The varied functions of the giant muscle scaffold protein obscurin.Frontiers in cell and developmental biology · 2025Review
- STRIPAK regulation of katanin microtubule severing in the Caenorhabditis elegans embryo.Genetics · 2022Article
- Article
- The Role of Cullin-RING Ligases in Striated Muscle Development, Function, and Disease.International journal of molecular sciences · 2020Review
- A Region of UNC-89 (Obscurin) Lying between Two Protein Kinase Domains Is a Highly Elastic Spring Required for Proper Sarcomere Organization.Journal of molecular biology · 2020Article
- The M-band: The underestimated part of the sarcomere.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Supporting the heart: Functions of the cardiomyocyte's non-sarcomeric cytoskeleton.Journal of molecular and cellular cardiology · 2019Review
- Murine obscurin and Obsl1 have functionally redundant roles in sarcolemmal integrity, sarcoplasmic reticulum organization, and muscle metabolism.Communications biology · 2019Article
- Protein phosphatase 2A is crucial for sarcomere organization in Caenorhabditis elegans striated muscle.Molecular biology of the cell · 2018Article
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- Pressure Overload in Mice With Haploinsufficiency of Striated Preferentially Expressed Gene Leads to Decompensated Heart Failure.Frontiers in physiology · 2018Article
- Article
- Obscure functions: the location-function relationship of obscurins.Biophysical reviews · 2017Review
- Cullin E3 Ligase Activity Is Required for Myoblast Differentiation.Journal of molecular biology · 2017Article
- Binding of Myomesin to Obscurin-Like-1 at the Muscle M-Band Provides a Strategy for Isoform-Specific Mechanical Protection.Structure (London, England : 1993) · 2017Article
- The SH3 domain of UNC-89 (obscurin) interacts with paramyosin, a coiled-coil protein, in Caenorhabditis elegans muscle.Molecular biology of the cell · 2016Article
- Titin and obscurin: giants holding hands and discovery of a new Ig domain subset.Journal of molecular biology · 2015Article
- The non-catalytic domains of Drosophila katanin regulate its abundance and microtubule-disassembly activity.PloS one · 2015Article
- Membrane-myofibril cross-talk in myofibrillogenesis and in muscular dystrophy pathogenesis: lessons from the zebrafish.Frontiers in physiology · 2014Article
- The ubiquitin proteasome system in Caenorhabditis elegans and its regulation.Redox biology · 2014Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The ubiquitin proteasome system is involved in degradation of old or damaged sarcomeric proteins. Most E3 ubiquitin ligases are associated with cullins, which function as scaffolds for assembly of the protein degradation machinery. Cullin 3 uses an adaptor to link to substrates; in Caenorhabditis elegans, one of these adaptors is the BTB-domain protein MEL-26 (maternal effect lethal). Here we show that MEL-26 interacts with the giant sarcomeric protein UNC-89 (obscurin). MEL-26 and UNC-89 partially colocalize at sarcomeric M-lines. Loss of function or gain of function of mel-26 results in disorganization of myosin thick filaments similar to that found in unc-89 mutants. It had been reported that in early C. elegans embryos, a target of the CUL-3/MEL-26 ubiquitylation complex is the microtubule-severing enzyme katanin (MEI-1). Loss of function or gain of function of mei-1 also results in disorganization of thick filaments similar to unc-89 mutants. Genetic data indicate that at least some of the mel-26 loss-of-function phenotype in muscle can be attributed to increased microtubule-severing activity of MEI-1. The level of MEI-1 protein is reduced in an unc-89 mutant, suggesting that the normal role of UNC-89 is to inhibit the CUL-3/MEL-26 complex toward MEI-1.
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