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Wiley InterScience

The Plant Journal

The Plant Journal

Volume 53 Issue 5, Pages 763 - 775

Published Online: 14 Nov 2007

Journal compilation © 2010 Blackwell Publishing Ltd and the Society for Experimental Biology



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Interplay between MAMP-triggered and SA-mediated defense responses
Kenichi Tsuda 1 , Masanao Sato 1,2 , Jane Glazebrook 1 , Jerry D. Cohen 3 and Fumiaki Katagiri 1,*
  1 Department of Plant Biology, Microbial and Plant Genomics Institute, University of Minnesota, 1500 Gortner Avenue, St Paul, MN 55108, USA,
  2 Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Komaba 3-8-1, Meguro-ku, Tokyo 153-8902, Japan, and
  3 Department of Horticultural Science, Microbial and Plant Genomics Institute, University of Minnesota, 1970 Folwell Avenue, St Paul, MN 55108, USA
Correspondence to   *(fax +1 612 624 6264; e-mail katagiri@umn.edu).
Copyright Journal compilation © 2008 Blackwell Publishing Ltd and the Society for Experimental Biology
KEYWORDS
MAMP • salicylic acid (SA) • expression profiling • SID2PAD4Arabidopsis thaliana

ABSTRACT

Plants respond to pathogen infection using an innate immune system with at least two distinct recognition mechanisms. One mechanism recognizes microbe-associated molecular patterns (MAMPs). The other is based on resistance (R) genes and specifically recognizes certain pathogen virulence factors, including those delivered through the type III secretion system (TTSS) of bacteria. Salicylic acid (SA)-mediated responses are an important part of the R gene-mediated defense. Substantial overlaps between MAMP-triggered and SA-mediated responses have been reported. However, interactions between MAMP-triggered and SA-mediated signaling mechanisms have not been well documented. Here we report intimate interactions between MAMP-triggered and SA-mediated signaling. We found that SA accumulated at a higher level 6 h after treatment with a MAMP, flg22 or inoculation with Pseudomonas syringae pv. tomato DC3000 (PstDC3000) hrcC mutant, which is deficient in TTSS function. Disruptions of SA signaling components, such as SID2 and PAD4, strongly affected MAMP-triggered responses monitored by expression profiling. We found two groups of genes that were induced by PstDC3000 hrcC in an SA-dependent manner. One group was SID2-dependent at all time points, whereas the other was SID2-independent at early time points and SID2-dependent at later time points. Thus, the expression of the latter genes responds to MAMPs through both SA-independent and SA-dependent signaling mechanisms. Strong resistance to PstDC3000 hrcC was dependent on SA signaling. These results indicate that the SA increase triggered by MAMPs is a major component of the MAMP-triggered signaling mechanism, explaining the overlapping spectra of MAMP-triggered and SA-mediated responses.


Received 6 July 2007; revised 28 October 2007; accepted 31 October 2007.

DIGITAL OBJECT IDENTIFIER (DOI)
10.1111/j.1365-313X.2007.03369.x About DOI

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