Effector-triggered defence against apoplastic fungal pathogens

Henrik Stotz, Georgia Mitrousia, Pierre de Wit, Bruce D.L. Fitt

Research output: Contribution to journalLiterature reviewpeer-review

102 Citations (Scopus)
232 Downloads (Pure)

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
Original languageEnglish
Pages (from-to)491-500
Number of pages10
JournalTrends in Plant Science
Volume19
Issue number8
Early online date22 May 2014
DOIs
Publication statusPublished - 1 Aug 2014

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