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ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier.

  • Schell C Institute of Surgical Pathology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany; Department of Medicine IV, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany; Berta-Ottenstein Programme, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany.
  • Sabass B Institute of Complex Systems-2, Forschungszentrum Jülich, Jülich 52428, Germany.
  • Helmstaedter M Department of Medicine IV, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany.
  • Geist F Department of Medicine IV, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany.
  • Abed A Department of Medicine IV, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany.
  • Yasuda-Yamahara M Department of Medicine IV, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany; Department of Medicine, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan.
  • Sigle A Department of Medicine IV, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany.
  • Maier JI Institute of Surgical Pathology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany; Department of Medicine IV, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany.
  • Grahammer F Department of Medicine IV, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany; III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany.
  • Siegerist F Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald 17487, Germany.
  • Artelt N Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald 17487, Germany.
  • Endlich N Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald 17487, Germany.
  • Kerjaschki D Department of Pathology, Medical University of Vienna, Vienna 1090, Austria.
  • Arnold HH Cell and Molecular Biology, Technical University of Braunschweig, Braunschweig 38106, Germany.
  • Dengjel J BIOSS Center for Biological Signaling Studies, Albert-Ludwigs-University Freiburg, Freiburg 79106, Germany; Department of Biology, University of Fribourg, Fribourg 1700, Switzerland; Department of Dermatology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79104, Germany.
  • Rogg M Department of Medicine IV, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany.
  • Huber TB Department of Medicine IV, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany; III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany; BIOSS Center for Biological Signaling Studies, Albert-Ludwigs-University Freiburg, Freiburg 79106, Germany. Electronic address: t.huber@uke.de.
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  • 2018-12-04
Published in:
  • Developmental cell. - 2018
Arp2/3
N-WASP
actin networks
actomyosin
cell process generation
focal adhesion
glomerular epithelial cells
kidney filtration barrier
podocytes
Actin Cytoskeleton
Actin-Related Protein 3
Actins
Actomyosin
Animals
Cell Adhesion
Focal Adhesions
Glomerular Filtration Barrier
Humans
Kidney
Mice
Mice, Knockout
Podocytes
Signal Transduction
Wiskott-Aldrich Syndrome Protein, Neuronal
English 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.
Language
  • English
Open access status
hybrid
Identifiers
Persistent URL
https://sonar.ch/global/documents/277831
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