Erwinia carotovora subsp. carotovora and Erwinia-Derived Elicitors HrpN and PehA Trigger Distinct but Interacting Defense Responses and Cell Death in Arabidopsis

Abstract

We have used an hrp-positive strain of the soft rot pathogen Erwinia carotovora subsp. carotovora to elucidate plant responses to this bacterial necrotroph. Purified virulence determinants, harpin (HrpN) and polygalacturonase (PehA), were used as tools to facilitate this analysis. We show that HrpN elicits lesion formation in Arabidopsis and tobacco and triggers systemic resistance in Arabidopsis. Establishment of resistance is accompanied by the expression of salicylic acid (SA)-dependent, but also jasmonate/ethylene (JA/ET)-dependent, marker genes PR1 and PDF1.2, respectively, suggesting that both SA-dependent and JA/ET-dependent defense pathways are activated. Use of pathway-specific mutants and transgenic NahG plants show that both pathways are required for the induction of resistance. Arabidopsis plants treated simultaneously with both elictors PehA, known to trigger only JA/ET-dependent defense signaling, and HrpN react with accelerated and enhanced induction of the marker genes PR1 and PDF1.2 both locally and systemically. This mutual amplification of defense gene expression involves both SA-dependent and JA/ET-dependent defense signaling. The two elicitors produced by E. carotovora subsp. carotovora also cooperate in triggering increased production of superoxide and lesion formation.

The WRKY70 Transcription Factor: A Node of Convergence for Jasmonate-Mediated and Salicylate-Mediated Signals in Plant Defense[W]

“…These pathways are not necessarily linear, but the signals mediated by the major endogenous signal molecules SA, JA, or JA/ET appear to form a network of synergistic and antagonistic interactions (Glazebrook, 2001;Kunkel and Brooks, 2002;Spoel et al, 2003). Some pathogens, like the Gramnegative bacterial necrotroph E. c. carotovora, appear to be capable of triggering both SA-and JA-or JA/ET-mediated defense responses (Kariola et al, 2003), and E. c. carotovora hence provides an excellent model for studies of the interaction between different signal pathways. Furthermore, induced resistance to this pathogen can be obtained either by SA-mediated or JA/ET-mediated defenses (Palva et al, 1994;NormanSetterblad et al, 2000;Kariola et al, 2003).…”

“…Some pathogens, like the Gramnegative bacterial necrotroph E. c. carotovora, appear to be capable of triggering both SA-and JA-or JA/ET-mediated defense responses (Kariola et al, 2003), and E. c. carotovora hence provides an excellent model for studies of the interaction between different signal pathways. Furthermore, induced resistance to this pathogen can be obtained either by SA-mediated or JA/ET-mediated defenses (Palva et al, 1994;NormanSetterblad et al, 2000;Kariola et al, 2003). Here, we show that E. c. carotovora elicitors indeed cause alterations in the endogenous SA/JA balance and trigger accumulation of mRNAs for both the SAR marker PR1 and the JA-responsive gene AtCOR1 ( Figure 1B).…”

“…In this study, we identified WRKY70 as a key factor controlling plant response to Erwinia carotovora subsp carotovora, a bacterial necrotroph that can trigger both SA-and JA-dependent defense signaling (Kariola et al, 2003). Resistance to this pathogen can be induced by activation of either SA-mediated (Palva et al, 1994;Kariola et al, 2003) or JA/ET-mediated (Norman-Setterblad et al, 2000;Kariola et al, 2003) defense pathways.…”

“…Resistance to this pathogen can be induced by activation of either SA-mediated (Palva et al, 1994;Kariola et al, 2003) or JA/ET-mediated (Norman-Setterblad et al, 2000;Kariola et al, 2003) defense pathways. We characterized the expression of WRKY70 in response to plant hormones and pathogen elicitors and generated WRKY70 transgenic plants to identify target genes controlled by WRKY70.…”

The AtrbohD-Mediated Oxidative Burst Elicited by Oligogalacturonides in Arabidopsis Is Dispensable for the Activation of Defense Responses Effective against Botrytis cinerea

“…Because some reports have suggested that the jar1-1 mutation is leaky (Staswick et al, 1998;Kariola et al, 2003), we also analyzed the coronatine insensitive1 (coi1) mutant, which is severely impaired in JA-mediated responses (Xie et al, 1998). Induction of RetOx and CYP81F2 by OGs in wild-type and coi1 seedlings was indistinguishable, whereas AtWRKY40 expression was slightly reduced in coi1 (Supplemental Fig.…”