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.

doi:10.1016/j.devcel.2018.11.011

Cited by 42 publications

(44 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Collectively, Arp2/3-mediated formation of lamellipodia and associated retrograde actin flow seems critical for proper formation and alignment of focal adhesions contributing to directed migration both in vitro and in vivo. Interestingly a similar cellular phenotype has also been observed in a podocyte-specific deletion of Arp3 (Schell et al, 2018).…”

Section: Development • Accepted Manuscriptsupporting

confidence: 65%

The Arp2/3 complex is critical for colonisation of the mouse skin by melanoblasts

et al. 2020

Self Cite

View full text Add to dashboard Cite

The Arp2/3 complex is essential for the assembly of branched filamentous actin but its role in physiology and development is surprisingly little understood. Melanoblasts deriving from the neural crest migrate along the developing embryo and traverse the dermis to reach the epidermis colonising the skin and eventually homing within the hair follicles. We have previously established that Rac1 and Cdc42 direct melanoblast migration in vivo. We hypothesised that the Arp2/3 complex might be the main downstream effector of these small GTPases. Arp3 depletion in the melanocyte lineage results in severe pigmentation defects in dorsal and ventral regions of the mouse skin. Arp3 null melanoblasts demonstrate proliferation and migration defects and fail to elongate as their wild-type counterparts. Conditional deletion of Arp3 in primary melanocytes causes improper proliferation, spreading, migration and adhesion to extracellular matrix. Collectively, our results suggest that the Arp2/3 complex is absolutely indispensable in the melanocyte lineage in mouse development, and indicate a significant role in developmental processes that require tight regulation of actin-mediated motility.

show abstract

Section: Development • Accepted Manuscriptsupporting

confidence: 65%

The Arp2/3 complex is critical for colonisation of the mouse skin by melanoblasts

et al. 2020

Self Cite

View full text Add to dashboard Cite

show abstract

“…Thus, networks of actin filaments (F-actin) and the F-actin-activated motor protein non-muscle myosin II (NMII) specify cell shape by exerting forces on the plasma membrane to control membrane tension and curvature [5][6][7][8]. These actomyosin networks determine cell shapes and interactions during tissue morphogenesis in development [6,[9][10][11][12][13] and their dysregulation has been implicated in cancer, [14][15][16], hearing disorders [17], podocyte filtration in the kidney [17,18], and neurodegeneration [19], among other physical issues. Local, nanoscale changes in actomyosin organization can lead to micron-scale changes in membrane curvature and cell shape to support normal cell function [20].…”

Section: Introductionmentioning

confidence: 99%

Non-uniform distribution of myosin-mediated forces governs red blood cell membrane curvature through tension modulation

et al. 2020

View full text Add to dashboard Cite

The biconcave disk shape of the mammalian red blood cell (RBC) is unique to the RBC and is vital for its circulatory function. Due to the absence of a transcellular cytoskeleton, RBC shape is determined by the membrane skeleton, a network of actin filaments cross-linked by spectrin and attached to membrane proteins. While the physical properties of a uniformly distributed actin network interacting with the lipid bilayer membrane have been assumed to control RBC shape, recent experiments reveal that RBC biconcave shape also depends on the contractile activity of nonmuscle myosin IIA (NMIIA) motor proteins. Here, we use the classical Helfrich-Canham model for the RBC membrane to test the role of heterogeneous force distributions along the membrane and mimic the contractile activity of sparsely distributed NMIIA filaments. By incorporating this additional contribution to the Helfrich-Canham energy, we find that the RBC biconcave shape depends on the ratio of forces per unit volume in the dimple and rim regions of the RBC. Experimental measurements of NMIIA densities at the dimple and rim validate our prediction that (a) membrane forces must be nonuniform along the RBC membrane and (b) the force density must be larger in the dimple than the rim to produce the observed membrane curvatures. Furthermore, we predict that RBC membrane tension and the orientation of the applied forces play important roles in regulating this force-shape landscape. Our findings of heterogeneous force distributions on the plasma membrane for RBC shape maintenance may also have implications for shape maintenance in different cell types.

show abstract

“…actin filaments (F-actin) and the F-actin-activated motor protein non-muscle myosin II (NMII) specify cell shape by exerting forces on the plasma membrane to control membrane tension and curvature [5][6][7][8] . These actomyosin networks determine cell shapes and interactions during tissue morphogenesis in development [6,[9][10][11][12][13] and their dysregulation has been implicated in cancer, [14][15][16] , hearing disorders [17] , podocyte filtration in the kidney [17,18] , and neurodegeneration [19] , among other physical issues. Local, nanoscale changes in actomyosin organization can lead to micron-scale changes in membrane curvature and cell shape to support normal cell function [20] .…”

mentioning

confidence: 99%

Non-uniform distribution of myosin-mediated forces governs red blood cell membrane curvature through tension modulation

Alimohamadi

Smith

Nowak

et al. 2019

Preprint

View full text Add to dashboard Cite

The biconcave disk shape of the mammalian red blood cell (RBC) is unique to the RBC and is vital for its circulatory function. Due to the absence of a transcellular cytoskeleton, RBC shape is determined by the membrane skeleton, a network of actin filaments cross-linked by spectrin and attached to membrane proteins. While the physical properties of a uniformly distributed actin network interacting with the lipid bilayer membrane have been assumed to control RBC shape, recent experiments reveal that RBC biconcave shape also depends on the contractile activity of nonmuscle myosin IIA (NMIIA) motor proteins. Here, we use the classical Helfrich-Canham model for the RBC membrane to test the role of heterogeneous force distributions along the membrane and mimic the contractile activity of sparsely distributed NMIIA filaments. By incorporating this additional contribution to the Helfrich-Canham energy, we find that the RBC biconcave shape depends on the ratio of forces per unit volume in the dimple and rim regions of the RBC. Experimental measurements of NMIIA densities at the dimple and rim validate our prediction that (a) membrane forces must be non-uniform along the RBC membrane and (b) the force density must be larger in the dimple than the rim to produce the observed membrane curvatures. Furthermore, we predict that RBC membrane tension and the orientation of the applied forces play important roles in regulating this force-shape landscape. Our findings of heterogeneous force distributions on the plasma membrane for RBC shape maintenance may also have implications for shape maintenance in different cell types.

show abstract

ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier

Cited by 42 publications

References 75 publications

The Arp2/3 complex is critical for colonisation of the mouse skin by melanoblasts

The Arp2/3 complex is critical for colonisation of the mouse skin by melanoblasts

Non-uniform distribution of myosin-mediated forces governs red blood cell membrane curvature through tension modulation

Non-uniform distribution of myosin-mediated forces governs red blood cell membrane curvature through tension modulation

Contact Info

Product

Resources

About