Agents that inhibit Rho, Rac, and Cdc42 do not block formation of actin pedestals in HeLa cells infected with enteropathogenic Escherichia coli

Infect Immun. 1998 Apr;66(4):1755-8. doi: 10.1128/IAI.66.4.1755-1758.1998.

Abstract

Enteropathogenic Escherichia coli (EPEC) induces formation of actin pedestals in infected host cells. Agents that inhibit the activity of Rho, Rac, and Cdc42, including Clostridium difficile toxin B (ToxB), compactin, and dominant negative Rho, Rac, and Cdc42, did not inhibit formation of actin pedestals. In contrast, treatment of HeLa cells with ToxB inhibited EPEC invasion. Thus, Rho, Rac, and Cdc42 are not required for assembly of actin pedestals; however, they may be involved in EPEC uptake by HeLa cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Actins / chemistry*
  • Bacterial Proteins*
  • Bacterial Toxins / pharmacology
  • Cell Cycle Proteins / antagonists & inhibitors*
  • Escherichia coli / pathogenicity*
  • GTP-Binding Proteins / antagonists & inhibitors*
  • HeLa Cells
  • Humans
  • Membrane Proteins / antagonists & inhibitors*
  • cdc42 GTP-Binding Protein, Saccharomyces cerevisiae
  • rac GTP-Binding Proteins
  • rhoB GTP-Binding Protein

Substances

  • Actins
  • Bacterial Proteins
  • Bacterial Toxins
  • Cell Cycle Proteins
  • Membrane Proteins
  • toxB protein, Clostridium difficile
  • GTP-Binding Proteins
  • cdc42 GTP-Binding Protein, Saccharomyces cerevisiae
  • rac GTP-Binding Proteins
  • rhoB GTP-Binding Protein