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| TR |
TITLE |
AUTHORS |
KEYWORDS |
MATERIALS & METHODS
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MICROSCOPIC
TECHNIQUES |
SPECIES |
MORPHOLOGY |
CELL
LINE |
| 632 |
Arp2
3 complex-deficient mouse fibroblasts are viable and have normal leading-edge actin structure
and function |
Alessia
Di Nardo, Gregor Cicchetti, Herve Falet, John H. Hartwig, Thomas P. Stossel, and David J. Kwiatkowski |
RNA
interference, motility, ruffling |
Cells were seeded on 35-mm glass-bottom
dishes (MatTek, Ashland, MA) and microinjected with 1 pg of CFP-CA or
CFP-VCA vector DNA by using a MO-150 micromanipulator and an IM200 pressure injector (Narishige,
Tokyo).
|
video
microscopy, electron microscopy |
mouse |
|
embryonic
fibroblasts |
| |
RNA interference silencing of up to 90%
of Arp3 protein expression, a major subunit of the Arp2 3 complex, proportionately decreases
the intracellular motility of Listeria monocytogenes and actin nucleation activity ascribable
to the Arp2 3 complex in mouse embryonic fibroblasts. However, the Arp2 3-deficient cells exhibit
unimpaired lamellipodial actin network structure, translational locomotion, spreading, actin
assembly, and ruffling responses. In addition, Arp3-silenced cells expressing neural Wiskott–Aldrich
syndrome protein-derived peptides that inhibit Arp23 complex function in wild-type cells retained
normal PDGF-induced ruffling. The Arp23 complex can be dispensable for leading-edge actin remodeling. |
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