Arabidopsis Downy Mildew effector HaRxL106 suppresses plant immunity by binding to RADICAL-INDUCED CELL DEATH1

LENNART WIRTHMUELLER; SHUTA ASAI; GHANASYAM RALLAPALLI; JAN SKLENAR; GEORGINA FABRO; DAE SUNG KIM; RUTH LINTHRMANN; PINJA JASPERS; MICHAEL WRZACZEK; JAAKKO KANGASJÄRVI; DANIEL MCLEAN; FRANK MENKE; MARK BANFIELD; JONATHAN D G JONES

NEW PHYTOLOGIST

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2018

0028-646X

he 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 RADICAL39INDUCED 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