|
||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
By


From the * Department of Bacteriology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108, Japan; and the Shigella, the causative agents of bacillary dysentery, are capable of invading mammalian cells
that are not normally phagocytic. Uptake of bacteria by the mammalian cells is directed by bacterial factors named IpaB, IpaC, and IpaD invasins, in which Ipa invasins secreted into the bacterial environment can interact with
Department of Veterinary Science, College of
Agriculture, University of Osaka Prefecture, Sakai, Osaka 593, Japan
5
1 integrin. We report here that Shigella invasion of epithelial cells requires rho activity, a ras-related GTP-binding protein. The invasive capacity of
Shigella flexneri for Chinese hamster ovary (CHO) cells and other epithelial cells were greatly
reduced when treated with Clostridium botulinum exoenzyme C3 transferase. Conversely, uptake of bacteria by CHO cells was promoted upon microinjection of an activated rho variant,
Val14RhoA. Attachment of S. flexneri to CHO cells can elicit tyrosine phosphorylation of
pp125FAK and paxillin, localized accumulation of F-actin, vinculin, and talin, and activation of
protein kinase C, which were all blocked by the treatment with C3 transferase. Our results indicate that cellular signal transduction regulated by rho is essential for Shigella invasion of epithelial cells.
This article has been cited by other articles:
| TABLE OF CONTENTS |
|