Arp2/3 complex-deficient mouse fibroblasts are viable and have normal leading-edge actin structure and function

被引：48

作者：

Di Nardo, A

Cicchetti, G

Falet, H

Hartwig, JH

Stossel, TP

Kwiatkowski, DJ

机构：

[1] Harvard Univ, Sch Med, Div Hematol, Brigham & Womens Hosp, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA

[3] Elsevier Inc, Burlington, MA 01803 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2005年 / 102卷 / 45期

关键词：

RNA interference; motility; ruffling;

D O I：

10.1073/pnas.0508228102

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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 Arp2/3 complex function in wild-type cells retained normal PDGF-induced ruffling. The Arp2/3 complex can be dispensable for leading-edge actin remodeling.

引用

页码：16263 / 16268

页数：6