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Arabidopsis downy mildew effector HaRxL106 suppresses plant immunity by binding to RADICAL-INDUCED CELL DEATH1
Authors:
Lennart
Wirthmueller
(John Innes Centre)
,
Shuta
Asai
(The Sainsbury Laboratory)
,
Ghanasyam
Rallapalli
(The Sainsbury Laboratory)
,
Jan
Sklenar
(The Sainsbury Laboratory)
,
Georgina
Fabro
(The Sainsbury Laboratory)
,
Dae Sung
Kim
(The Sainsbury Laboratory)
,
Ruth
Lintermann
(Freie Universität Berlin)
,
Pinja
Jaspers
(University of Helsinki)
,
Michael
Wrzaczek
(University of Helsinki)
,
Jaakko
Kangasjärvi
(University of Helsinki)
,
Daniel
Maclean
(The Sainsbury Laboratory)
,
Frank L. H.
Menke
(The Sainsbury Laboratory)
,
Mark J.
Banfield
(John Innes Centre)
,
Jonathan D. G.
Jones
(The Sainsbury Laboratory)
Co-authored by industrial partner:
No
Type:
Journal Paper
Journal:
New Phytologist
, VOL 220
, PAGES 232 - 248
State:
Published (Approved)
Published:
August 2018
Diamond Proposal Number(s):
7641

Abstract: The oomycete pathogen Hyaloperonospora arabidopsidis (Hpa) causes downy mildew disease on Arabidopsis. To colonize its host, Hpa translocates effector proteins that suppress plant immunity into infected host cells. Here, we investigate the relevance of the interaction between one of these effectors, HaRxL106, and Arabidopsis RADICAL‐INDUCED CELL DEATH1 (RCD1). We use pathogen infection assays as well as molecular and biochemical analyses to test the hypothesis that HaRxL106 manipulates RCD1 to attenuate transcriptional activation of defense genes. We report that HaRxL106 suppresses transcriptional activation of salicylic acid (SA)‐induced defense genes and alters plant growth responses to light. HaRxL106‐mediated suppression of immunity is abolished in RCD1 loss‐of‐function mutants. We report that RCD1‐type proteins are phosphorylated, and we identified Mut9‐like kinases (MLKs), which function as phosphoregulatory nodes at the level of photoreceptors, as RCD1‐interacting proteins. An mlk1,3,4 triple mutant exhibits stronger SA‐induced defense marker gene expression compared with wild‐type plants, suggesting that MLKs also affect transcriptional regulation of SA signaling. Based on the combined evidence, we hypothesize that nuclear RCD1/MLK complexes act as signaling nodes that integrate information from environmental cues and pathogen sensors, and that the Arabidopsis downy mildew pathogen targets RCD1 to prevent activation of plant immunity.
Journal Keywords: Arabidopsis thaliana; Hyaloperonospora arabidopsidis; oomycete pathogen; pathogen effector; plant innate immunity; RADICAL‐INDUCED CELL DEATH1; salicylic acid (SA)
Subject Areas:
Biology and Bio-materials
Instruments:
I04-Macromolecular Crystallography
,
I24-Microfocus Macromolecular Crystallography
Documents:
n546546ph.pdf