Journal
TRENDS IN PLANT SCIENCE
Volume 19, Issue 8, Pages 491-500Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tplants.2014.04.009
Keywords
apoplastic fungal pathogens; cell wall; extracellular matrix; receptor-like protein; R gene-mediated resistance
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Funding
- European Union [302202]
- UK Biotechnology and Biological Sciences Research Council [RD-2009-3676]
- Department for the Environment, Food and Rural Affairs [OREGIN - 1F0144]
- HGCA
- Royal Netherlands Academy of Arts and Sciences
- Perry Foundation
- Biotechnology and Biological Sciences Research Council [BB/I017585/2, BBS/E/C/00004693, BB/D015200/1, BB/E001610/1, BB/I017585/1] Funding Source: researchfish
- Engineering and Physical Sciences Research Council [TS/I000747/1, TS/I000747/2] Funding Source: researchfish
- BBSRC [BB/E001610/1, BB/I017585/2, BB/D015200/1, BB/I017585/1] Funding Source: UKRI
- EPSRC [TS/I000747/1, TS/I000747/2] Funding Source: UKRI
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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.
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