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

Nature Plants volume 9, pages 1184–1190 (2023)Cite this article

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Abstract

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 ~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.

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Fig. 1: ETI does not restore defence gene expression that has been suppressed by virulence effectors.
Fig. 2: ETI does not inhibit pathogen growth locally but limits pathogen propagation.
Fig. 3: Does ETI induce LAR to prevent systemic pathogen spread?.

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Acknowledgements

We thank T. Nobori, J. G. Ellis, G. L. Coaker and T. Nuernberger for constructive critical reading of the manuscript and members of the Dangl lab for useful discussions. This research was supported by the National Science Foundation (grant no. IOS-1758400 to J.L.D.) and the Howard Hughes Medical Institute (HHMI). J.L.D. is an HHMI Investigator. This article is subject to HHMI’s Open Access to Publications policy. HHMI lab heads have previously granted a non-exclusive CC BY 4.0 licence to the public and a sublicensable licence to HHMI in their research articles. Pursuant to those licences, the author-accepted manuscript of this article can be made freely available under a CC BY4.0 licence immediately upon publication.

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  1. Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

    Pierre Jacob, Junko Hige & Jeffery L. Dangl

  2. Howard Hughes Medical Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

    Pierre Jacob, Junko Hige & Jeffery L. Dangl

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P.J. conceptualized the project, wrote the original draft, reviewed and edited the manuscript, and conducted the formal analysis. J.H. conducted the investigation. J.L.D. conceptualized the project, reviewed and edited the manuscript, acquired the funding and supervised the project.

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Correspondence to Jeffery L. Dangl.

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Jacob, P., Hige, J. & Dangl, J.L. Is localized acquired resistance the mechanism for effector-triggered disease resistance in plants?. Nat. Plants 9, 1184–1190 (2023). https://doi.org/10.1038/s41477-023-01466-1

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