ArticleMolecular biology of the cell2001
Golgi complex reorganization during muscle differentiation: visualization in living cells and mechanism.
Article in Molecular biology of the cell, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 113 citations in OpenAlex.
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- A coordinated transcriptional program controls de novo Golgi biogenesis.The EMBO journal · 2026Article
- Protein Kinase D2 Regulates GRASP65 Phosphorylation and Golgi Ribbon Unlinking During G2/M Transition.Cells · 2026Article
- The Dynamic Role of the Golgi Apparatus in Neuronal Function and Alzheimer's Disease.Sub-cellular biochemistry · 2026Review
- Siamese Twins: The Multimodular Mechanisms of Golgi Maturation and Glycan Synthesis Are Coupled at Their Core.Sub-cellular biochemistry · 2026Review
- The Impact of Golgi Organization on Cell Cycle and Cancer Development.Sub-cellular biochemistry · 2026Review
- Alternatively spliced MAP4 isoforms have key roles in maintaining microtubule organization and skeletal muscle function.iScience · 2024Article
- Tail-anchored membrane protein SLMAP3 is essential for targeting centrosomal proteins to the nuclear envelope in skeletal myogenesis.Open biology · 2024Article
- The Golgi checkpoint: Golgi unlinking during G2 is necessary for spindle formation and cytokinesis.Life science alliance · 2024Article
- Reevaluating Golgi fragmentation and its implications in wound repair.Cell regeneration (London, England) · 2024Review
- Split but merge: Golgi fragmentation in physiological and pathological conditions.Molecular biology reports · 2024Review
- Rab6-mediated retrograde trafficking from the Golgi: the trouble with tubules.Small GTPases · 2023Review
- Microtubule plus-end tracking proteins: novel modulators of cardiac sodium channels and arrhythmogenesis.Cardiovascular research · 2023Article
- Insights into Cell-Specific Functions of Microtubules in Skeletal Muscle Development and Homeostasis.International journal of molecular sciences · 2023Review
- Golgi Complex form and Function: A Potential Hub Role Also in Skeletal Muscle Pathologies?International journal of molecular sciences · 2022Article
- Tissue-Specific Variations in Transcription Factors Elucidate Complex Immune System Regulation.Genes · 2022Article
- Review
- Reconstitution of muscle cell microtubule organization in vitro.Cytoskeleton (Hoboken, N.J.) · 2021Article
- The ESCRT-0 subcomplex component Hrs/Hgs is a master regulator of myogenesis via modulation of signaling and degradation pathways.BMC biology · 2021Article
- Unscrambling exit site patterns on the endoplasmic reticulum as a quenched demixing process.Biophysical journal · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
During skeletal muscle differentiation, the Golgi complex (GC) undergoes a dramatic reorganization. We have now visualized the differentiation and fusion of living myoblasts of the mouse muscle cell line C2, permanently expressing a mannosidase-green fluorescent protein (GFP) construct. These experiments reveal that the reorganization of the GC is progressive (1-2 h) and is completed before the cells start fusing. Fluorescence recovery after photobleaching (FRAP), immunofluorescence, and immunogold electron microscopy demonstrate that the GC is fragmented into elements localized near the endoplasmic reticulum (ER) exit sites. FRAP analysis and the ER relocation of endogenous GC proteins by phospholipase A2 inhibitors demonstrate that Golgi-ER cycling of resident GC proteins takes place in both myoblasts and myotubes. All results support a model in which the GC reorganization in muscle reflects changes in the Golgi-ER cycling. The mechanism is similar to that leading to the dispersal of the GC caused, in all mammalian cells, by microtubule-disrupting drugs. We propose that the trigger for the dispersal results, in muscle, from combined changes in microtubule nucleation and ER exit site localization, which place the ER exit sites near microtubule minus ends. Thus, changes in GC organization that initially appear specific to muscle cells, in fact use pathways common to all mammalian cells.
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Registered trials
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.