Abstract
Summary The fungus Zymoseptoria tritici is a strictly apoplastic, host‐specific pathogen of wheat leaves and causal agent of septoria tritici blotch (STB) disease. All other plants are considered nonhosts, but the mechanism of nonhost resistance (NHR) to Z. tritici has not been addressed previously. We sought to develop Nicotiana benthamiana as a system to study NHR against Z. tritici.Fluorescence microscopy and quantitative reverse transcription polymerase chain reactions were used to establish the interaction between Z. tritici and N. benthamiana. Agrobacterium‐mediated transient expression was used to screen putative Z. tritici effector genes for recognition in N. benthamiana, and virus‐induced gene silencing (VIGS) was employed to determine the role of two receptor‐like kinases (RLKs), NbBAK1 and NbSOBIR1, in Z. tritici effector recognition.Numerous Z. tritici putative effectors (14 of 63 tested) induced cell death or chlorosis in N. benthamiana. For most, phenotypes were light‐dependent and required effector secretion to the leaf apoplastic space. Moreover, effector‐induced host cell death was dependent on NbBAK1 and NbSOBIR1.Our results indicate widespread recognition of apoplastic effectors from a wheat‐infecting fungal pathogen in a taxonomically distant nonhost plant species presumably by cell surface immune receptors. This suggests that apoplastic recognition of multiple nonadapted pathogen effectors may contribute to NHR.
Highlights
Plants are able to resist infection or colonization by the majority of would-be pathogens and pests they encounter, including bacteria, fungi, oomycetes, viruses and invertebrate pests
By implementing a highlevel transient Agrobacterium-mediated protein expression system, we found that recognition of Z. tritici candidate effectors is surprisingly common in this nonhost species
We present evidence that perception of some Z. tritici effectors in this nonhost plant occurs at the plasma membrane-apoplast interface, and is dependent on the previously described plant defence associated receptor-like kinases (RLKs), NbBAK1 and NbSOBIR1
Summary
Plants are able to resist infection or colonization by the majority of would-be pathogens and pests they encounter, including bacteria, fungi, oomycetes, viruses and invertebrate pests. The fact that disease is relatively rare, suggests that plants have highly effective and robust means of repelling the vast majority of microbes they encounter This most durable form of plant defence is termed nonhost resistance (NHR) and describes the resistance of a potential host to all isolates/races of a potential pathogen. Direct recognition of some pathogen effectors or their actions by plant disease resistance (R) proteins represents a second level of defence termed effector-triggered immunity (ETI) This is often characterized by a localized host cell death (known as the hypersensitive response, HR) that is thought to spatially restrict or encase pathogens. Immune recognition of an effector leads to host susceptibility rather than resistance
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