Enhanced defense responses in Arabidopsis induced by the cell wall protein fractions from Pythium oligandrum require SGT1, RAR1, NPR1 and JAR1.

The cell wall protein fraction (CWP) is purified from the non-pathogenic biocontrol agent Pythium oligandrum and is composed of two glycoproteins (POD-1 and POD-2), which are structurally similar to class III elicitins. In tomato plants treated with CWP, jasmonic acid (JA)- and ethylene (ET)-dependent signaling pathways are activated, and resistance to Ralstonia solanaceraum is enhanced. To dissect CWP-induced defense mechanisms, we investigated defense gene expression and resistance to bacterial pathogens in Arabidopsis thaliana ecotype Col-0 treated with CWP. When the leaves of Col-0 were infiltrated with CWP, neither visible necrosis nor salicylic acid (SA)-responsive gene (PR-1 and PR-5) expression was induced. In contrast, JA-responsive gene (PDF1.2 and JR2) expression was up-regulated and the resistance to R. solanaceraum and Pseudomonas syringae pv. tomato DC3000 was enhanced in response to CWP. Such CWP-induced defense responses were completely compromised in CWP-treated coi1-1 and jar1-1 mutants with an impaired JA signaling pathway. The induction of defense-related gene expression after CWP treatment was partially compromised in ET-insensitive ein2-1 mutants, but not in SA signaling mutants or nahG transgenic plants. Global gene expression analysis using cDNA array also suggested that several other JA- and ET-responsive genes, but not SA-responsive genes, were up-regulated in response to CWP. Further analysis of CWP-induced defense responses using another eight mutants with impaired defense signaling pathways indicated that, interestingly, the induction of JA-responsive gene expression and enhanced resistance to two bacterial pathogens in response to CWP were completely compromised in rar1-1, rar1-21, sgt1a-1, sgt1b (edm1) and npr1-1 mutants. Thus, the CWP-induced defense system appears to be regulated by JA-mediated and SGT1-, RAR1- and NPR1-dependent signaling pathways.