Expression Profiling during Arabidopsis/Downy Mildew Interaction Reveals a Highly-Expressed Effector That Attenuates Responses to Salicylic Acid

SHUTA ASAI; GANASHYAM RALLAPALLI; SOPHIE J. M. PIQUEREZ; MARIE-CECILE CAILLAUD; OLIVER J FURZER; NAVEED ISHAQUE; LENNART WIRTHMUELLER; GEORGINA FABRO; KEN SHIRASU; JONATHAN D. G. JONES

PLOS PATHOGENS

PUBLIC LIBRARY SCIENCE

Lugar: San Francisco; Año: 2014 vol. 10

1553-7366

Plants have evolved strong innate immunity mechanisms, but successful pathogens evade or suppress plant immunity viaeffectors delivered into the plant cell. Hyaloperonospora arabidopsidis (Hpa) causes downy mildew on Arabidopsis thaliana,and a genome sequence is available for isolate Emoy2. Here, we exploit the availability of genome sequences for Hpa andArabidopsis to measure gene-expression changes in both Hpa and Arabidopsis simultaneously during infection. Using ahigh-throughput cDNA tag sequencing method, we reveal expression patterns of Hpa predicted effectors and Arabidopsisgenes in compatible and incompatible interactions, and promoter elements associated with Hpa genes expressed duringinfection. By resequencing Hpa isolate Waco9, we found it evades Arabidopsis resistance gene RPP1 through deletion of thecognate recognized effector ATR1. Arabidopsis salicylic acid (SA)-responsive genes including PR1 were activated not only atearly time points in the incompatible interaction but also at late time points in the compatible interaction. By histochemicalanalysis, we found that Hpa suppresses SA-inducible PR1 expression, specifically in the haustoriated cells into which hosttranslocatedeffectors are delivered, but not in non-haustoriated adjacent cells. Finally, we found a highly-expressed Hpaeffector candidate that suppresses responsiveness to SA. As this approach can be easily applied to host-pathogeninteractions for which both host and pathogen genome sequences are available, this work opens the door towardstranscriptome studies in infection biology that should help unravel pathogen infection strategies and the mechanisms bywhich host defense responses are overcome.