Abstract
Plant pathogenic oomycete species pose a worldwide threat to crop production and ecosystems. During infection, oomycete pathogens secrete a series of effectors to manipulate plant immunity. Many of these effectors, which are indicated as avirluence gene candidates, will use components of immunity pathway to induce cell death in plants. This response given by plants is known as effector-triggered immunity (ETI). The identification of avirulence genes from pathogenic oomycete species opens a way to investigating their virulence function and uncovering related R gene repertoires in resistant plants. In this study, we screened eight cell death-inducing effectors from oomycete species in N. benthamiana and tested the requirements of ETI signaling components to induce cell death. SGT1 was required for PsAvh163- and PcRXLR25-mediated cell death, while silencing NbHSP90 abolished PcRXLR25-, PsAvh163-, PsAvh241- and PsCRN63-triggered cell death. The cell death induced by the tested effectors does not depend on EDS1, NDR1, NRG1 and ADR1. PcRXLR25- and PsAvh163-induced cell death was found to require NRC2/3/4, indicating that these two effectors are avirulence protein candidates. Finally, we found that auto-activated NRC2/3/4 also required SGT1 and HSP90 to induce hypersensitive response.
Highlights
Oomycete pathogens continue to hamper crop production and damage ecosystems on a global scale (Pais et al 2013)
hypersensitive response (HR) induced by PcRXLR25 and PsAvh163 required NRC2/3/4
Eight effectors listed as INF1, PoNLP5, PoNLP7, PcRxLR25, PsAvh105, PsAvh163, PsAvh241 and PsCRN63 were chosen in this assay (Additional file 1: Table S1)
Summary
Oomycete pathogens continue to hamper crop production and damage ecosystems on a global scale (Pais et al 2013). Oomycetes belong to heterokont/chromist clade (Riisberg et al 2009), within the ’Straminipila-Alveolata-Rhizaria’ superkingdom (Burki et al 2008). For successful colonization in host plants, oomycete pathogens deliver diverse groups of effectors into plant cells to subvert host immunity (Dou and Zhou 2012). Oomycete pathogens mostly secrete two classes of effectors: apoplastic effectors such as necrosis and ethyleneinducing peptide-like proteins (NLPs), and cytoplasmic effectors such as RXLRs (Arg-X-Leu-Arg, where X is any amino acid) and CRNs (crinkling and necrosis proteins) (Dou and Zhou 2012). Hundreds of effectors are encoded by oomycete pathogens and many of them trigger hypersensitive response (HR)-like phenotype in
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