Abstract
R gene-mediated host resistance against apoplastic fungal pathogens is not adequately explained by the terms pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) or effector-triggered immunity (ETI). Therefore, it is proposed that this type of resistance is termed 'effector-triggered defence' (ETD). Unlike PTI and ETI, ETD is mediated by R genes encoding cell surface-localised receptor-like proteins (RLPs) that engage the receptor-like kinase SOBIR1. In contrast to this extracellular recognition, ETI is initiated by intracellular detection of pathogen effectors. ETI is usually associated with fast, hypersensitive host cell death, whereas ETD often triggers host cell death only after an elapsed period of endophytic pathogen growth. In this opinion, we focus on ETD responses against foliar fungal pathogens of crops.
Highlights
Resistance against apoplastic leaf pathogens of crops Breeding agricultural crops for resistance against pathogens is essential to secure global food production
Unlike PTI and effector-triggered immunity (ETI), effector-triggered defence’ (ETD) is mediated by R genes encoding cell surfacelocalised receptor-like proteins (RLPs) that engage the receptor-like kinase SOBIR1
We focus on ETD responses against foliar fungal pathogens of crops
Summary
AThese hemibiotrophic pathogens are in order with most ‘biotrophic’ first and most ‘necrotropic’ last. NSTB genes are not associated with host cell death, but do reduce pathogen biomass and asexual sporulation without preventing sexual sporulation. Whereas PTI operates against both apoplastic and cell-penetrating filamentous pathogens (referred to as ‘haustorial pathogens’), the mode of R gene-mediated resistance against them differs between the two types of pathogen (Box 1). Some dothideomycetes are saprophytes, many are epiphytes, endophytes, or pathogens of plants [2] Apoplastic pathogens, such as C. fulvum, L. maculans, Z. tritici, P. brassicae, V. inaequalis, and R. commune, do not trigger an effective host defence response during the early stages of invasion (Table 1, Figure 2A–C) but slowly colonise the apoplast to adapt to the constitutive antimicrobial compounds present.
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