RT Journal Article
SR Electronic
T1 Clathrin is required for Scar/Wave-mediated lamellipodium formation
JF Journal of Cell Science
JO J. Cell Sci.
FD The Company of Biologists Ltd
SP 3414
OP 3427
DO 10.1242/jcs.081083
VO 124
IS 20
A1 Gautier, Jérémie J.
A1 Lomakina, Maria E.
A1 Bouslama-Oueghlani, Lamia
A1 Derivery, Emmanuel
A1 Beilinson, Helen
A1 Faigle, Wolfgang
A1 Loew, Damarys
A1 Louvard, Daniel
A1 Echard, Arnaud
A1 Alexandrova, Antonina Y.
A1 Baum, Buzz
A1 Gautreau, Alexis
YR 2011
UL http://jcs.biologists.org/content/124/20/3414.abstract
AB The Scar/Wave complex (SWC) generates lamellipodia through Arp2/3-dependent polymerisation of branched actin networks. In order to identify new SWC regulators, we conducted a screen in Drosophila cells combining proteomics with functional genomics. This screen identified Clathrin heavy chain (CHC) as a protein that binds to the SWC and whose depletion affects lamellipodium formation. This role of CHC in lamellipodium formation can be uncoupled from its role in membrane trafficking by several experimental approaches. Furthermore, CHC is detected in lamellipodia in the absence of the adaptor and accessory proteins of endocytosis. We found that CHC overexpression decreased membrane recruitment of the SWC, resulting in reduced velocity of protrusions and reduced cell migration. By contrast, when CHC was targeted to the membrane by fusion to a myristoylation sequence, we observed an increase in membrane recruitment of the SWC, protrusion velocity and cell migration. Together these data suggest that, in addition to its classical role in membrane trafficking, CHC brings the SWC to the plasma membrane, thereby controlling lamellipodium formation.