Characterizing interactors of Hpa effector HaRxL106 reveals a novel regulatory role for RCD1 in NPR1-mediated immunity

LENNART WIRTHMUELLER; SHUTA ASAI; FABRO GEORGINA; SHYAM RALAPALLI; MARIE-CECILE CAILLAUD; MARK BANFIELD; JONATHAN D. G. JONES

Fallen Leaf Lake

Simposio; Immuno modulation by plant associated organisms 30th New Phytologist Symposium; 2012

New Phytologyst Journal

The HaRxL106 effector protein from the oomycete pathogen Hyaloperonospora arabidopsidis (Hpa) suppresses basal defense gene expression when constitutively expressed in Arabidopsis thaliana. HaRxL106 also suppresses autoimmunity triggered by the constitutively active TIR-NB-LRR protein variant snc1-1 but has no effect on resistance mediated by two other TIR-NB-LRR proteins, RPP2 and RPP4. The HaRxL106 effector protein localizes exclusively to the nucleus and interacts with several nuclear host proteins, including alpha‐importins and RADICAL INDUCED CELL DEATH1 (RCD1). Whereas alpha-importin single knock outs only weakly compromise resistance to virulent Hpa races, rcd1 mutants exhibit loss of basal resistance comparable to an npr1 mutant. A comparative transcriptomics approach revealed a partially overlapping gene set mis-regulated in transgenic lines expressing HaRxL106 and in rcd1 mutants. Particularly, NPR1 target genes were underexpressed in both genetic backgrounds before and 24h after infection with virulent Pseudomonas syringae DC3000. As NPR1 transcript levels were not affected by HaRxL106 or rcd1 our data suggest that RCD1 is required for NPR1 protein function. We will report on our analysis of transgenic lines expressing NPR1-GFP in an rcd1 mutant background. We hypothesize that HaRxL106 may target RCD1 to suppress NPR1-mediated local and systemic defense.