ArticleKidney international2013
Myo1c is an unconventional myosin required for zebrafish glomerular development.
Article in Kidney international, 2013. 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, 21 citations in OpenAlex.
- MYO1C is a urinary extracellular vesicle biomarker and mediator of podocyte injury in diabetic nephropathy.JCI insight · 2026Article
- Recessive variants in MYO1C as a potential novel cause of proteinuric kidney disease.Pediatric nephrology (Berlin, Germany) · 2024Article
- Recessive variants in MYO1C as a potential novel cause of proteinuric kidney disease.Research square · 2024Article
- The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes.Kidney international · 2019Article
- High-content screening assay-based discovery of paullones as novel podocyte-protective agents.American journal of physiology. Renal physiology · 2018Article
- Targeting Neph1 and ZO-1 protein-protein interaction in podocytes prevents podocyte injury and preserves glomerular filtration function.Scientific reports · 2017Article
- Myosin-1 inhibition by PClP affects membrane shape, cortical actin distribution and lipid droplet dynamics in early Zebrafish embryos.PloS one · 2017Article
- Structural Analysis of the Myo1c and Neph1 Complex Provides Insight into the Intracellular Movement of Neph1.Molecular and cellular biology · 2016Article
- Podocyte endocytosis in the regulation of the glomerular filtration barrier.American journal of physiology. Renal physiology · 2015Review
- Human Kidney Disease-causing INF2 Mutations Perturb Rho/Dia Signaling in the Glomerulus.EBioMedicine · 2014Article
- Using zebrafish to study podocyte genesis during kidney development and regeneration.Genesis (New York, N.Y. : 2000) · 2014Review
- Slit diaphragm protein Neph1 and its signaling: a novel therapeutic target for protection of podocytes against glomerular injury.The Journal of biological chemistry · 2014Article
- Molecular Mechanisms of Podocyte Development Revealed by Zebrafish Kidney Research.Cell & developmental biology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The targeting and organization of podocyte slit diaphragm proteins nephrin and neph1 is critical for development and maintenance of a functional glomerular filtration barrier. Myo1c is a non-muscle myosin motor protein that interacts directly with nephrin and neph1, and mediates their intracellular transport to the podocyte intercellular junction. Here we investigated the necessity of Myo1c in podocyte development using zebrafish as a model system. Immunofluorescence microscopy and in situ RNA hybridization analysis of zebrafish embryos showed that Myo1c is widely expressed in various tissues including the zebrafish glomerulus. Knockdown of the Myo1c gene in zebrafish using antisense morpholino derivatives resulted in an abnormal developmental phenotype that included pericardial edema and dilated renal tubules. Ultrastructural analysis of the glomerulus in Myo1c-depleted zebrafish showed abnormal podocyte morphology and absence of the slit diaphragm. Consistent with these observations, the glomerular filter permeability appeared altered in zebrafish in which Myo1c expression was attenuated. The specificity of Myo1c knockdown was confirmed by a rescue experiment in which co-injection of Myo1c morpholino derivatives with orthologous Myo1c mRNA prepared from mouse cDNA lessened phenotypic abnormalities including edema in Myo1c morphants. Thus, our results demonstrate that Myo1c is necessary for podocyte morphogenesis.
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