Is localized acquired resistance the mechanism for effector-triggered disease resistance in plants?

Plant nucleotide-binding leucine-rich repeat receptors (NLRs) are intracellular immune receptors that are activated by their direct or indirect interactions with virulence effectors. NLR activation triggers a strong immune response and consequent disease resistance. However, the NLR-driven immune response can be targeted by virulence effectors. It is thus unclear how immune activation can occur concomitantly with virulence effector suppression of immunity. Recent observations suggest that the activation of effector-triggered immunity does not sustain defence gene expression in tissues in contact with the hemi-biotrophic pathogen Pseudomonas syringae pv. tomato. Instead, strong defence was observed on the border of the infection area. This response is reminiscent of localized acquired resistance (LAR). LAR is a strong defence response occurring in a similar to 2 mm area around cells in contact with the pathogen and probably serves to prevent the spread of pathogens. Here we propose that effector-triggered immunity is essentially a quarantining mechanism to prevent systemic pathogen spread and disease, and that the induction of LAR is a key component of this mechanism.

Automated summary

Plant nucleotide-binding leucine-rich repeat receptors (NLRs) are immune receptors that are activated by direct or indirect interactions with virulence effectors. The activation of NLRs triggers a strong immune response and disease resistance. However, the immune response can be suppressed by virulence effectors, and recent observations suggest that localized acquired resistance (LAR) plays a key role in preventing pathogen spread.