O s EIL 2 balances rice immune responses against (hemi)biotrophic and necrotrophic pathogens via the salicylic acid and jasmonic acid synergism
Summary Plants typically activate distinct defense pathways against various pathogens. Heightened resistance to one pathogen often coincides with increased susceptibility to another pathogen. However, the underlying molecular basis of this antagonistic response remains unclear. Here, we demonstrate...
Saved in:
Published in | The New phytologist |
---|---|
Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
10.05.2024
|
Online Access | Get full text |
Cover
Loading…
Summary: | Summary
Plants typically activate distinct defense pathways against various pathogens. Heightened resistance to one pathogen often coincides with increased susceptibility to another pathogen. However, the underlying molecular basis of this antagonistic response remains unclear.
Here, we demonstrate that mutants defective in the transcription factor
ETHYLENE‐INSENSITIVE 3‐LIKE 2
(
OsEIL2
) exhibited enhanced resistance to the biotrophic bacterial pathogen
Xanthomonas oryzae
pv
oryzae
and to the hemibiotrophic fungal pathogen
Magnaporthe oryzae
, but enhanced susceptibility to the necrotrophic fungal pathogen
Rhizoctonia solani
.
Furthermore, necrotroph‐induced OsEIL2 binds to the promoter of
OsWRKY67
with high affinity, leading to the upregulation of salicylic acid (SA)/jasmonic acid (JA) pathway genes and increased SA/JA levels, ultimately resulting in enhanced resistance.
However, biotroph‐ and hemibiotroph‐induced OsEIL2 targets
OsERF083
, resulting in the inhibition of SA/JA pathway genes and decreased SA/JA levels, ultimately leading to reduced resistance. Our findings unveil a previously uncharacterized defense mechanism wherein two distinct transcriptional regulatory modules differentially mediate immunity against pathogens with different lifestyles through the transcriptional reprogramming of phytohormone pathway genes. |
---|---|
ISSN: | 0028-646X 1469-8137 |
DOI: | 10.1111/nph.19809 |