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Roles of Arp2/3 complex and mDia2 in actin‐based protrusions
Author(s) -
Svitkina Tatyana,
Yang Changsong,
Korobova Farida,
Gerboth Silke,
Scita Giorgio
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1029.12
Subject(s) - filopodia , lamellipodium , formins , microbiology and biotechnology , pseudopodia , mdia1 , actin , actin remodeling , actin remodeling of neurons , protein filament , biology , chemistry , microfilament , actin cytoskeleton , cytoskeleton , cell , genetics
Actin polymerization is a key mechanism of force generation in cells. Actin filament nucleators, formins and the Arp2/3 complex, are believed to have non‐overlapping functions in inducing actin filament bundles and dendritic networks, respectively. We investigated roles of the Arp2/3 complex and an mDia2 formin in lamellipodia and filopodia, cellular protrusions containing dendritic and bundled actin filaments, respectively. Contrary to the above paradigm, we have found that mDia2 is an important player in lamellipodia, while Arp2/3 complex significantly contributes to generation of filopodia. The contribution of mDia2 to lamellipodial protrusion was related to generation of long filaments in the lamellipodial network. These long filaments displayed a high tendency to converge into bundles during elongation, thereby producing filopodia. Depletion of the Arp2/3 complex by siRNA in neuronal cells, as expected, inhibited lamellipodia, but remarkably, also filopodia. Correlative structural and kinetic analyses suggested that Arp2/3‐nucleated filaments become incorporated into filopodial bundles in the course of elongation, and that this process contributes significantly to filopodia initiation. Together, our data show that each of two distinct actin nucleators, Arp2/3 complex and mDia2, jointly participate in generation of both lamellipodia and filopodia. Supported by NIH grant GM 070898 to TMS.