JCB logo
Epitomics: The Rabbit Monoclonal Company
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published 20 August 2001. doi:10.1083/jcb.200101113
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 482K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Witke, W.
Right arrow Articles by Southwick, F. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Witke, W.
Right arrow Articles by Southwick, F. S.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
© The Rockefeller University Press, 0021-9525/2001/8/775 $5.00
The Journal of Cell Biology, Volume 154, Number 4, August 20, 2001 775-784


Article

Comparisons of CapG and gelsolin-null macrophages : demonstration of a unique role for CapG in receptor-mediated ruffling, phagocytosis, and vesicle rocketing



Walter Witke1, Wei Li2, David J. Kwiatkowski1 and Frederick S. Southwick2

1 Hematology Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115
2 Infectious Disease Division, Department of Medicine, University of Florida College of Medicine, Gainesville, FL 32610

Address correspondence to David Kwiatkowski, Division of Experimental Medicine, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Ave., Boston, MA 02115. Tel.: (617) 278-0384. Fax: (617) 734-2248. E-mail: dkwiatkowski{at}rics.bwh.harvard.edu

Capping the barbed ends of actin filaments is a critical step for regulating actin-based motility in nonmuscle cells. The in vivo function of CapG, a calcium-sensitive barbed end capping protein and member of the gelsolin/villin family, has been assessed using a null Capg allele engineered into mice. Both CapG-null mice and CapG/gelsolin double-null mice appear normal and have no gross functional abnormalities. However, the loss of CapG in bone marrow macrophages profoundly inhibits macrophage colony stimulating factor–stimulated ruffling; reintroduction of CapG protein by microinjection fully restores this function. CapG-null macrophages also demonstrate ~50% impairment of immunoglobulin G, and complement-opsonized phagocytosis and lanthanum-induced vesicle rocketing. These motile functions are not impaired in gelsolin-null macrophages and no additive effects are observed in CapG/gelsolin double-null macrophages, establishing that CapG function is distinct from, and does not overlap with, gelsolin in macrophages. Our observations indicate that CapG is required for receptor-mediated ruffling, and that it is a major functional component of macrophage phagocytosis. These primary effects on macrophage motile function suggest that CapG may be a useful target for the regulation of macrophage-mediated inflammatory responses.

Key Words: CapG; gelsolin; macrophages; ruffling; phagocytosis


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents