ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier

Podocytes, highly specialized epithelial cells, build the outer part of the kidney filtration barrier and withstand high mechanical forces through a complex network of cellular protrusions. Here, we show that Arp2/3-dependent actin polymerization controls actomyosin contractility and focal adhesion...

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Veröffentlicht in:Developmental cell Jg. 47; H. 6; S. 741
Hauptverfasser: Schell, Christoph, Sabass, Benedikt, Helmstaedter, Martin, Geist, Felix, Abed, Ahmed, Yasuda-Yamahara, Mako, Sigle, August, Maier, Jasmin I, Grahammer, Florian, Siegerist, Florian, Artelt, Nadine, Endlich, Nicole, Kerjaschki, Dontscho, Arnold, Hans-Henning, Dengjel, Jörn, Rogg, Manuel, Huber, Tobias B
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 17.12.2018
Schlagworte:
Actin Cytoskeleton - metabolism
Actin-Related Protein 3 - metabolism
Actin-Related Protein 3 - physiology
Actins - metabolism
Actomyosin - metabolism
Animals
Cell Adhesion
Focal Adhesions - metabolism
Glomerular Filtration Barrier - metabolism
Glomerular Filtration Barrier - physiology
Humans
Kidney - metabolism
Kidney - physiology
Mice
Mice, Knockout
Podocytes - metabolism
Podocytes - physiology
Signal Transduction
Wiskott-Aldrich Syndrome Protein, Neuronal - metabolism
focal adhesion
Arp2/3
cell process generation
podocytes
actomyosin
kidney filtration barrier
glomerular epithelial cells
actin networks
N-WASP
ISSN:1878-1551, 1878-1551
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Zusammenfassung:Podocytes, highly specialized epithelial cells, build the outer part of the kidney filtration barrier and withstand high mechanical forces through a complex network of cellular protrusions. Here, we show that Arp2/3-dependent actin polymerization controls actomyosin contractility and focal adhesion maturation of podocyte protrusions and thereby regulates formation, maintenance, and capacity to adapt to mechanical requirements of the filtration barrier. We find that N-WASP-Arp2/3 define the development of complex arborized podocyte protrusions in vitro and in vivo. Loss of dendritic actin networks results in a pronounced activation of the actomyosin cytoskeleton and the generation of over-maturated but less efficient adhesion, leading to detachment of podocytes. Our data provide a model to explain podocyte protrusion morphology and their mechanical stability based on a tripartite relationship between actin polymerization, contractility, and adhesion.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1878-1551
1878-1551
DOI:10.1016/j.devcel.2018.11.011