University of Hertfordshire

By the same authors

Effector-triggered defence against apoplastic fungal pathogens

Research output: Contribution to journalLiterature review

Documents

  • 906813

    Final published version, 1 MB, PDF document

Links

View graph of relations
Original languageEnglish
Number of pages10
Pages (from-to)491-500
JournalTrends in Plant Science
Journal publication date1 Aug 2014
Volume19
Issue8
Early online date22 May 2014
DOIs
Publication statusPublished - 1 Aug 2014

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

Notes

Copyright 2014 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license CC BY 3.0 (http://creativecommons.org/licenses/by/3.0/). h

ID: 7110641