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

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

Proc Natl Acad Sci U S A

Division of Hematology, Brigham and Women's Hospital, and Department of Medicine, Harvard Medical School, One Blackfan Circle, Boston, MA 02115, USA.

Published: November 2005

AI Article Synopsis

  • - Silencing Arp3 protein expression by up to 90% significantly reduces the movement of Listeria monocytogenes and actin nucleation in mouse embryonic fibroblasts, indicating the importance of the Arp2/3 complex in these processes.
  • - Despite the lack of Arp2/3 complex, the cells can maintain normal structures and functions such as lamellipodial actin networks, movement, spreading, and ruffling responses.
  • - Cells with reduced Arp3 that were treated with certain peptides still showed normal ruffling in response to PDGF, suggesting that the Arp2/3 complex is not essential for actin remodeling at the leading edge of the cell.

Article Abstract

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1283463PMC
http://dx.doi.org/10.1073/pnas.0508228102DOI Listing

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