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A team of Brassica researchers from the University of Hertfordshire have proposed a new classification for a type of plant defence mechanism: effector-triggered defence (ETD). This new understanding of how plants defend themselves against some destructive pathogens may help breed new, more successful disease-resistant crops.
Henrik Stotz is first author of the paper describing ETD, currently In Press in Trends in Plant Science. He explains, “In the same way that humans have developed immune responses against human disease pathogens, crops can be bred for resistance against disease pathogens, but we need to improve our understanding of effective resistance mechanisms within plants. Our research enhances the traditional understanding of the plant defence system and describes how plants protect themselves against the pathogens that grow in the space outside plant cells (the apoplast) – a new concept called effector-triggered defence or ETD.”
Traditionally, plant pathogen defence is broken into two broad forms: pathogen-triggered immunity (PTI) and effector-triggered immunity (ETI). PTI is the first action the plant takes against a pathogen and is triggered when the pathogen lands on the plant. The pathogen releases molecules called effectors into the plant cells, which the plant recognises and reacts against (ETI). If the effectors are not recognised, the pathogen can spread with little resistance.
The team from Hertfordshire, led by Bruce Fitt, argue that one line of defence, R gene-mediated host resistance against fungal pathogens that grow in the space between cells, is not adequately explained by either mechanism.
Effector-triggered defence (ETD) is mediated by R genes encoding cell surface-bound receptor-like proteins that engage the receptor-like kinase SOBIR1 – an extracellular recognition. The response is host cell death after an extended period of endophytic pathogen growth. This is in contrast to ETI, in which detection of the pathogen occurs within cells and usually triggers fast host cell death.