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Authors
Kage, FriedaWinterhoff, Moritz
Dimchev, Vanessa
Mueller, Jan
Thalheim, Tobias
Freise, Anika
Brühmann, Stefan
Kollasser, Jana
Block, Jennifer
Dimchev, Georgi
Geyer, Matthias
Schnittler, Hans-Joachim
Brakebusch, Cord
Stradal, Theresia E B
Carlier, Marie-France
Sixt, Michael
Käs, Josef
Faix, Jan
Rottner, Klemens
Issue Date
2017-03-22
Metadata
Show full item recordAbstract
Migration frequently involves Rac-mediated protrusion of lamellipodia, formed by Arp2/3 complex-dependent branching thought to be crucial for force generation and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors targeting to the lamellipodium tip and shown here to nucleate and elongate actin filaments with complementary activities in vitro. In migrating B16-F1 melanoma cells, both formins contribute to the velocity of lamellipodium protrusion. Loss of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width, actin filament density and -bundling, without changing patterns of Arp2/3 complex incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost completely abolishes protrusion forces exerted by lamellipodia and modifies their ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3 in fibroblasts reduces both migration and capability of cells to move against viscous media. Together, we conclude that force generation in lamellipodia strongly depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent filament branching.Citation
FMNL formins boost lamellipodial force generation. 2017, 8:14832 Nat CommunAffiliation
Helmholtz Centre for infection research, Inhoffenstr.7, 38124 Braunschweig, Germany.Journal
Nature communicationsPubMed ID
28327544Type
ArticleLanguage
enISSN
2041-1723ae974a485f413a2113503eed53cd6c53
10.1038/ncomms14832
Scopus Count
The following license files are associated with this item:
- Creative Commons
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-sa/4.0/
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