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

Journal Article · · Nature Communications
DOI:https://doi.org/10.1038/ncomms13099· OSTI ID:1903892
 [1];  [2];  [3];  [4];  [4];  [4];  [5];  [3];  [4]
  1. Duke Univ., Durham, NC (United States); OSTI
  2. Duke Univ., Durham, NC (United States); Sinai University (Egypt)
  3. Michigan State Univ., East Lansing, MI (United States)
  4. Duke Univ., Durham, NC (United States)
  5. Michigan State Univ., East Lansing, MI (United States); Western Michigan Univ., Kalamazoo MI (United States)
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.
Research Organization:
Michigan State Univ., East Lansing, MI (United States). MSU-DOE Plant Research Laboratory
Sponsoring Organization:
Gordon and Betty Moore Foundation; Howard Hughes Medical Institute; National Institutes of Health (NIH); USDOE
OSTI ID:
1903892
Journal Information:
Nature Communications, Journal Name: Nature Communications Journal Issue: 1 Vol. 7; ISSN 2041-1723
Publisher:
Nature Publishing GroupCopyright Statement
Country of Publication:
United States
Language:
English

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