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

This Article Full Text Full Text (PDF, 2647K) PPT slides of all figures Supplemental Material Index View Video 4 Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Robbins, J. R. Articles by Theriot, J. A. Search for Related Content PubMed PubMed Citation Articles by Robbins, J. R. Articles by Theriot, J. A. Pubmed/NCBI databases Substance via MeSH Related Collections Related Article Social Bookmarking                            What's this?

© The Rockefeller University Press, 0021-9525/1999//1333 $5.00
The Journal of Cell Biology, Volume 146, Number 6, , 1999 1333-1350

Listeria monocytogenes Exploits Normal Host Cell Processes to Spread from Cell to Cell

^a Department of Biochemistry, Stanford University School of Medicine
^b Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, California 94305-5307
^c Department of Microbiology, University of Colorado Health Sciences Center, Denver, Colorado 80262
^d Tropical Disease Research Unit, University of California, San Francisco, California 94121
^e Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305-5307
Department of Biochemistry, Beckman Center, Stanford School of Medicine, Stanford, CA 94305-5307.(650) 723-6783(650) 725-7968

theriot{at}cmgm.stanford.edu

The bacterial pathogen, Listeria monocytogenes, grows in the cytoplasm of host cells and spreads intercellularly using a form of actin-based motility mediated by the bacterial protein ActA. Tightly adherent monolayers of MDCK cells that constitutively express GFP-actin were infected with L. monocytogenes, and intercellular spread of bacteria was observed by video microscopy. The probability of formation of membrane-bound protrusions containing bacteria decreased with host cell monolayer age and the establishment of extensive cell-cell contacts. After their extension into a recipient cell, intercellular membrane-bound protrusions underwent a period of bacterium-dependent fitful movement, followed by their collapse into a vacuole and rapid vacuolar lysis. Actin filaments in protrusions exhibited decreased turnover rates compared with bacterially associated cytoplasmic actin comet tails. Recovery of motility in the recipient cell required 1–2 bacterial generations. This delay may be explained by acid-dependent cleavage of ActA by the bacterial metalloprotease, Mpl. Importantly, we have observed that low levels of endocytosis of neighboring MDCK cell surface fragments occurs in the absence of bacteria, implying that intercellular spread of bacteria may exploit an endogenous process of paracytophagy.

Key Words: Listeria monocytogenes • ActA • actin • epithelial cells • bacterial pathogenesis

© 1999 The Rockefeller University Press

The online version of this article contains supplemental material.

CiteULike

Complore

Connotea

Del.icio.us

Digg

Facebook

Reddit

Technorati

Twitter

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