Involvement of the intermediate filament protein cytokeratin-18 in actin pedestal formation during EPEC infection

EMBO Rep. 2004 Jan;5(1):104-10. doi: 10.1038/sj.embor.7400038.

Abstract

While remaining extracellular, enteropathogenic Escherichia coli (EPEC) establish direct links with the cytoskeleton of the target epithelial cell leading to the formation of actin-rich pedestals underneath attached bacteria. The translocated adaptor protein Tir forms the transmembrane bridge between the cytoskeleton and the bacterium; the extracellular domain of Tir functions as a receptor for the bacterial adhesin intimin, while the intracellular amino and carboxy termini interact with a number of focal adhesion and other cytoskeletal proteins; and recruitment of some is dependent on phosphorylation of Tyr 474. Using Tir as bait and HeLa cell cDNA library as prey in a yeast two-hybrid screen, we identified cytokeratin 18 as a novel Tir partner protein. Cytokeratin 18 is recruited to the EPEC-induced pedestal and has a direct role in actin accretion and cytoskeleton reorganization. This study is the first to implicate intermediate filaments in microfilament reorganization following EPEC infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Escherichia coli / genetics
  • Escherichia coli / metabolism
  • Escherichia coli / pathogenicity*
  • Escherichia coli Infections / microbiology
  • Escherichia coli Proteins / genetics
  • Escherichia coli Proteins / metabolism*
  • HeLa Cells
  • Humans
  • Immunohistochemistry
  • Immunoprecipitation
  • Keratins / metabolism*
  • Phosphorylation
  • Plasmids
  • RNA, Small Interfering / genetics
  • Receptors, Cell Surface / genetics
  • Receptors, Cell Surface / metabolism*
  • Transfection

Substances

  • Actins
  • Escherichia coli Proteins
  • RNA, Small Interfering
  • Receptors, Cell Surface
  • Tir protein, E coli
  • Keratins