Eukaryotic Cell
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH

EC Accepts, published online ahead of print on 1 December 2006
This Article
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
EC.00330-05v1
6/3/546    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 Google Scholar
Google Scholar
Right arrow Articles by Fudal, I.
Right arrow Articles by Lebrun, M.-H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fudal, I.
Right arrow Articles by Lebrun, M.-H.

 Previous Article  |  Next Article 

Eukaryotic Cell doi:10.1128/EC.00330-05
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Expression of M. grisea avirulence gene ACE1 is connected to the initiation of appressorium mediated penetration

Isabelle Fudal, Jérôme Collemare, Heidi U. Böhnert, Delphine Melayah, and Marc-Henri Lebrun*

UMR2847 CNRS-Bayer CropsScience, Lyon, France

* To whom correspondence should be addressed. Email: marc-henri.lebrun{at}bayercropscience.com.


   Abstract

Magnaporthe grisea is responsible for a devastating fungal disease of rice called blast. Current control of this disease relies on resistant rice cultivars that recognize M. grisea signals corresponding to specific secreted proteins encoded by avirulence genes. M. grisea ACE1 avirulence gene differs from others, since it controls the biosynthesis of a secondary metabolite likely recognized by rice cultivars carrying Pi33 resistance gene. Using a transcriptional fusion between ACE1 promoter and eGFP, we showed that ACE1 is only expressed in appressoria during fungal penetration into rice and barley leaves, onion skin and cellophane membranes. ACE1 is almost not expressed in appressoria differentiated on Teflon and Mylar artificial membranes. ACE1 expression is not induced by cellophane and plant cell wall components demonstrating that it does not require typical host plant compounds. cAMP signaling mutants {Delta}cpkA and {Delta}mac1 sum1-99 and tetraspanin mutant {Delta}pls1::hph differentiate melanized appressoria with normal turgor but are unable to penetrate into host plant leaves. ACE1 is normally expressed in these mutants suggesting that it does not require cAMP signaling or a successful penetration event. ACE1 is not expressed in appressoria of the buf1::hph mutant defective for melanin biosynthesis and appressorial turgor. Addition of hyper-osmotic solutes to buf1::hph appressoria restores appressorial development and ACE1 expression. Treatments of young wild type appressoria with actin and tubulin inhibitors reduce both fungal penetration and ACE1 expression. These experiments suggest that ACE1 appressorium specific expression does not depend on host plant signals, but is connected to the onset of appressorium mediated penetration.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Appl. Environ. Microbiol. Infect. Immun. J. Bacteriol.
Mol. Cell Biol. Microbiol. Mol. Biol. Rev. ALL ASM JOURNALS
Copyright © 2006 by the American Society for Microbiology.