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


Journal

Nature plants
ISSN: 2055-0278
Titre abrégé: Nat Plants
Pays: England
ID NLM: 101651677

Informations de publication

Date de publication:
08 2023
Historique:
received: 30 01 2023
accepted: 23 06 2023
medline: 21 8 2023
pubmed: 4 8 2023
entrez: 3 8 2023
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 37537398
doi: 10.1038/s41477-023-01466-1
pii: 10.1038/s41477-023-01466-1
doi:

Substances chimiques

Carrier Proteins 0

Types de publication

Journal Article Review Research Support, U.S. Gov't, Non-P.H.S. Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1184-1190

Subventions

Organisme : National Science Foundation (NSF)
ID : IOS-1758400

Informations de copyright

© 2023. Springer Nature Limited.

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Auteurs

Pierre Jacob (P)

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

Junko Hige (J)

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

Jeffery L Dangl (JL)

Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. dangl@email.unc.edu.
Howard Hughes Medical Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. dangl@email.unc.edu.

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