Effector-triggered defence against apoplastic fungal pathogens

P474 - The plant immune system was originally defined as including pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI). After arrival of a potential pathogen, PTI is rapidly activated by recognition of PAMPs by pattern recognition receptors (PRRs) located on the cell surface. PTI has also been defined as PRR-triggered immunity. In resistant hosts, ETI is initiated by intracellular host recognition of pathogen effectors. Haustoria-forming pathogens generally deliver their effectors into the host cell, whereas apoplastic fungal pathogens deliver effectors into the apoplast to target extracellular or membrane proteins. However, it is not generally believed that resistance against apoplastic pathogens should be considered as PTI as some considerit as ETI. To explain interactions between apoplastic fungal pathogens and their host plants and reconcile these opposing views, it is proposed that this resistance is referred to as effector- triggered defence (ETD). EDT is mediated by R genes encoding cell surface-localized receptor-like proteins (RLPs) that engage the receptor-like kinase SOBIR1. In contrasts, intracellular effectors are directly or indirectly recognised by intracellular nucleotide binding site (NBS) leucine-rich repeat (LRR) receptors (NLRs). Whereas ETI is usually associated with fast, hypersensitive host cell death, ETD often triggers host cell death only after a period of endophytic pathogen growth. This resistance does not generally eliminate these apoplastic pathogens since there are cases that they are subsequently able to complete their sexual life cycle on the resistant host.