Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity

Lijing Liu, Fathi-Mohamed Sonbol, Bethany Huot, Yangnan Gu, John Withers, Musoki Mwimba, Jian Yao, Sheng Yang He and Xinnian Dong ()
Additional contact information
Lijing Liu: Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University
Fathi-Mohamed Sonbol: Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University
Bethany Huot: and Cell and Molecular Biology Program, Michigan State University
Yangnan Gu: Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University
John Withers: Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University
Musoki Mwimba: Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University
Jian Yao: Howard Hughes Medical Institute, Michigan State University
Sheng Yang He: Howard Hughes Medical Institute, Michigan State University
Xinnian Dong: Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University

Nature Communications, 2016, vol. 7, issue 1, 1-10

Abstract: Abstract It is an apparent conundrum how plants evolved effector-triggered immunity (ETI), involving programmed cell death (PCD), as a major defence mechanism against biotrophic pathogens, because ETI-associated PCD could leave them vulnerable to necrotrophic pathogens that thrive on dead host cells. Interestingly, during ETI, the normally antagonistic defence hormones, salicylic acid (SA) and jasmonic acid (JA) associated with defence against biotrophs and necrotrophs respectively, both accumulate to high levels. In this study, we made the surprising finding that JA is a positive regulator of RPS2-mediated ETI. Early induction of JA-responsive genes and de novo JA synthesis following SA accumulation is activated through the SA receptors NPR3 and NPR4, instead of the JA receptor COI1. We provide evidence that NPR3 and NPR4 may mediate this effect by promoting degradation of the JA transcriptional repressor JAZs. This unique interplay between SA and JA offers a possible explanation of how plants can mount defence against a biotrophic pathogen without becoming vulnerable to necrotrophic pathogens.

Date: 2016
References: Add references at CitEc
Citations: View citations in EconPapers (3)

Downloads: (external link)
https://www.nature.com/articles/ncomms13099 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13099

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms13099

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().