Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity.
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.
Duke Scholars
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Related Subject Headings
- Signal Transduction
- Salicylic Acid
- Receptors, Cell Surface
- Protein Binding
- Plant Immunity
- Oxylipins
- Models, Biological
- Gene Expression Regulation, Plant
- Cyclopentanes
- Arabidopsis Proteins
Citation
Published In
DOI
EISSN
ISSN
Publication Date
Volume
Start / End Page
Related Subject Headings
- Signal Transduction
- Salicylic Acid
- Receptors, Cell Surface
- Protein Binding
- Plant Immunity
- Oxylipins
- Models, Biological
- Gene Expression Regulation, Plant
- Cyclopentanes
- Arabidopsis Proteins