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ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier

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ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier. / 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.

In: DEV CELL, Vol. 47, No. 6, 17.12.2018, p. 741-757.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Schell, C, Sabass, B, Helmstaedter, M, Geist, F, Abed, A, Yasuda-Yamahara, M, Sigle, A, Maier, JI, Grahammer, F, Siegerist, F, Artelt, N, Endlich, N, Kerjaschki, D, Arnold, H-H, Dengjel, J, Rogg, M & Huber, TB 2018, 'ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier', DEV CELL, vol. 47, no. 6, pp. 741-757. https://doi.org/10.1016/j.devcel.2018.11.011

APA

Schell, C., Sabass, B., Helmstaedter, M., Geist, F., Abed, A., Yasuda-Yamahara, M., Sigle, A., Maier, J. I., Grahammer, F., Siegerist, F., Artelt, N., Endlich, N., Kerjaschki, D., Arnold, H-H., Dengjel, J., Rogg, M., & Huber, T. B. (2018). ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier. DEV CELL, 47(6), 741-757. https://doi.org/10.1016/j.devcel.2018.11.011

Vancouver

Schell C, Sabass B, Helmstaedter M, Geist F, Abed A, Yasuda-Yamahara M et al. ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier. DEV CELL. 2018 Dec 17;47(6):741-757. https://doi.org/10.1016/j.devcel.2018.11.011

Bibtex

@article{c8c6598a94644e3a8ad0210a08a2331f,
title = "ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier",
abstract = "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.",
keywords = "Journal Article",
author = "Christoph Schell and Benedikt Sabass and Martin Helmstaedter and Felix Geist and Ahmed Abed and Mako Yasuda-Yamahara and August Sigle and Maier, {Jasmin I} and Florian Grahammer and Florian Siegerist and Nadine Artelt and Nicole Endlich and Dontscho Kerjaschki and Hans-Henning Arnold and J{\"o}rn Dengjel and Manuel Rogg and Huber, {Tobias B}",
note = "Copyright {\textcopyright} 2018 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2018",
month = dec,
day = "17",
doi = "10.1016/j.devcel.2018.11.011",
language = "English",
volume = "47",
pages = "741--757",
journal = "DEV CELL",
issn = "1534-5807",
publisher = "Cell Press",
number = "6",

}

RIS

TY - JOUR

T1 - ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier

AU - Schell, Christoph

AU - Sabass, Benedikt

AU - Helmstaedter, Martin

AU - Geist, Felix

AU - Abed, Ahmed

AU - Yasuda-Yamahara, Mako

AU - Sigle, August

AU - Maier, Jasmin I

AU - Grahammer, Florian

AU - Siegerist, Florian

AU - Artelt, Nadine

AU - Endlich, Nicole

AU - Kerjaschki, Dontscho

AU - Arnold, Hans-Henning

AU - Dengjel, Jörn

AU - Rogg, Manuel

AU - Huber, Tobias B

N1 - Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2018/12/17

Y1 - 2018/12/17

N2 - 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.

AB - 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.

KW - Journal Article

U2 - 10.1016/j.devcel.2018.11.011

DO - 10.1016/j.devcel.2018.11.011

M3 - SCORING: Journal article

C2 - 30503751

VL - 47

SP - 741

EP - 757

JO - DEV CELL

JF - DEV CELL

SN - 1534-5807

IS - 6

ER -