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Dysregulated Dynein-Mediated Trafficking of Nephrin Causes INF2-related Podocytopathy
Journal article   Open access   Peer reviewed

Dysregulated Dynein-Mediated Trafficking of Nephrin Causes INF2-related Podocytopathy

Hua Sun, Chandra Perez-Gill, Johannes S Schlöndorff, Balajikarthick Subramanian and Martin R Pollak
Journal of the American Society of Nephrology, Vol.32(2), pp.307-322
02/01/2021
DOI: 10.1681/ASN.2020081109
PMCID: PMC8054882
PMID: 33443052
url
https://doi.org/10.1681/ASN.2020081109View
Published (Version of record) Open Access

Abstract

FSGS caused by mutations in is characterized by a podocytopathy with mistrafficked nephrin, an essential component of the slit diaphragm. Because INF2 is a formin-type actin nucleator, research has focused on its actin-regulating function, providing an important but incomplete insight into how these mutations lead to podocytopathy. A yeast two-hybridization screen identified the interaction between INF2 and the dynein transport complex, suggesting a newly recognized role of INF2 in regulating dynein-mediated vesicular trafficking in podocytes. Live cell and quantitative imaging, fluorescent and surface biotinylation-based trafficking assays in cultured podocytes, and a new puromycin aminoglycoside nephropathy model of transgenic mice were used to demonstrate altered dynein-mediated trafficking of nephrin in INF2 associated podocytopathy. Pathogenic mutations disrupt an interaction of INF2 with dynein light chain 1, a key dynein component. The best-studied mutation, R218Q, diverts dynein-mediated postendocytic sorting of nephrin from recycling endosomes to lysosomes for degradation. Antagonizing dynein-mediated transport can rescue this effect. Augmented dynein-mediated trafficking and degradation of nephrin underlies puromycin aminoglycoside-induced podocytopathy and FSGS . mutations enhance dynein-mediated trafficking of nephrin to proteolytic pathways, diminishing its recycling required for maintaining slit diaphragm integrity. The recognition that dysregulated dynein-mediated transport of nephrin in R218Q knockin podocytes opens an avenue for developing targeted therapy for INF2-mediated FSGS.
Animals Cell Culture Techniques Cytoplasmic Dyneins - metabolism Formins - genetics Glomerulosclerosis, Focal Segmental - etiology Glomerulosclerosis, Focal Segmental - metabolism Glomerulosclerosis, Focal Segmental - pathology Membrane Proteins - metabolism Mice Mutation - genetics Podocytes - metabolism Podocytes - pathology Protein Transport

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