Abstract
Pathogens secrete effector proteins to suppress host immunity, mediate nutrient uptake and subsequently enable parasitism. However, on non-adapted hosts, effectors can be detected as non-self by host immune receptors and activate non-host immunity. Nevertheless, the molecular mechanisms of effector triggered non-host resistance remain unknown. Here, we report that a small cysteine-rich protein PstSCR1 from the wheat rust pathogen Puccinia striiformis f. sp. tritici (Pst) activates immunity in the non-host solanaceous model plant Nicotiana benthamiana. PstSCR1 homologs were found to be conserved in Pst, and in its closest relatives, Puccinia graminis f. sp. tritici and Puccinia triticina. When PstSCR1 was expressed in N. benthamiana with its signal peptide, it provoked the plant immune system, whereas no stimulation was observed when it was expressed without its signal peptide. PstSCR1 expression in N. benthamiana significantly reduced infection capacity of the oomycete pathogens. Moreover, apoplast-targeted PstSCR1 triggered plant cell death in a dose dependent manner. However, in Brassinosteroid insensitive 1-Associated Kinase 1 (SERK3/BAK1) silenced N. benthamiana, cell death was remarkably decreased. Finally, purified PstSCR1 protein activated defence related gene expression in N. benthamiana. Our results show that a Pst-secreted protein, PstSCR1 can activate surface mediated immunity in non-adapted hosts and contribute to non-host resistance.
Highlights
Surface localized pattern recognition receptors (PRRs) mediate pathogen associated molecular pattern (PAMP)-triggered immunity (PTI) against a variety of plant pathogens[1,2,3]
We noted that PstSCR1 protein sequence has three conserved (Y/F/W)x(C) motifs (Supplementary Fig. S1), one of which is located at the N-terminus as described in many wheat rust and other fungal effector candidates[29,30,31,32]
In order to test whether PstSCR1 is expressed during Puccinia striiformis f. sp. tritici (Pst) infection of wheat, we employed qPCR (Supplementary Fig. S2) using infected samples collected at different time points (24-h, 72-h, 8-d and 10-d)
Summary
Surface localized pattern recognition receptors (PRRs) mediate pathogen associated molecular pattern (PAMP)-triggered immunity (PTI) against a variety of plant pathogens[1,2,3]. Some effectors are known to stimulate cell death through surface localized immune receptors[8, 15,16,17,18]. Discovering how effectors operate in different subcellular compartments is critical for understanding the mechanisms of host-pathogen interactions that will eventually lead to new ways of engineering plant disease resistance. Petre et al have reported that N. benthamiana is a feasible experimental tool to functionally analyse candidate effectors from Pst, a fungal pathogen of wheat[28]. In this work, using N. benthamiana as a model system, we studied subcellular localization, function and response to pathogen infections of PstSCR1, which was previously predicted as a candidate effector[23]. In non-adapted hosts, effectors can assist to explore the components of non-host resistance and discover novel participants of plant immunity
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