AEM
Home Help [Feedback] [For Subscribers] [Archive] [Search] --
AEM Accepts, published online ahead of print on 2 March 2007
This Article
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
AEM.02664-06v1
73/9/2919    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mc Gann, P.
Right arrow Articles by Boor, K. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mc Gann, P.
Right arrow Articles by Boor, K. J.
Agricola
Right arrow Articles by Mc Gann, P.
Right arrow Articles by Boor, K. J.

 Previous Article  |  Next Article 

Appl. Environ. Microbiol. doi:10.1128/AEM.02664-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The alternative sigma factor {sigma}B and the virulence gene regulator PrfA both regulate transcription of Listeria monocytogenes internalins

Patrick Mc Gann, Martin Wiedmann, and Kathryn J. Boor*

Department of Food Science, Cornell University, Ithaca, New York 14853, USA

* To whom correspondence should be addressed. Email: kjb4{at}cornell.edu.


   Abstract

Some Listeria monocytogenes internalins are recognized as contributing to invasion of mammalian tissue culture cells. While PrfA is well-established as a positive regulator of L. monocytogenes virulence gene expression, the stress responsive {sigma}B has been recognized only recently as contributing to expression of virulence genes, including some that encode internalins. To measure the relative contributions of PrfA and {sigma}B to internalin gene transcription, we used RT-PCR to quantify transcript levels for eight internalin genes (inlA, inlB, inlC, inlC2, inlD, inlE, inlF and inlG) in L. monocytogenes 10403S and in isogenic {Delta}prfA, {Delta}sigB and {Delta}sigB{Delta}prfA strains. Strains were grown under defined conditions to produce (i) active PrfA; (ii) active {sigma}B and active PrfA; (iii) inactive PrfA; and (iv) active {sigma}B and inactive PrfA. Under the conditions tested, {sigma}B and PrfA contributed differentially to expression of the various internalins such that (i) both {sigma}B and PrfA contributed to inlA and inlB transcription, (ii) only PrfA contributed to inlC transcription, (iii) only {sigma}B contributed to inlC2 and inlD transcription, and (iv) neither {sigma}B nor PrfA contributed to inlF and inlG transcription. Transcript levels were undetectable for inlE. The important role for {sigma}B in regulating expression of L. monocytogenes internalins suggests that exposure of this organism to environmental stress conditions, such as those encountered in the gastrointestinal tract, may activate internalin transcription. Interplay between {sigma}B and PrfA also appears to be critical for regulating transcription of some virulence genes, including inlA, inlB, and prfA.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] --
J. Bacteriol. Microbiol. Mol. Biol. Rev. Eukaryot. Cell All ASM Journals

Copyright © 2007 by the American Society for Microbiology. All rights reserved.