Abstract
Plants have evolved strong innate immunity mechanisms, but successful pathogens evade or suppress plant immunity via effectors 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 and Arabidopsis to measure gene-expression changes in both Hpa and Arabidopsis simultaneously during infection. Using a high-throughput cDNA tag sequencing method, we reveal expression patterns of Hpa predicted effectors and Arabidopsis genes in compatible and incompatible interactions, and promoter elements associated with Hpa genes expressed during infection. By resequencing Hpa isolate Waco9, we found it evades Arabidopsis resistance gene RPP1 through deletion of the cognate recognized effector ATR1. Arabidopsis salicylic acid (SA)-responsive genes including PR1 were activated not only at early time points in the incompatible interaction but also at late time points in the compatible interaction. By histochemical analysis, we found that Hpa suppresses SA-inducible PR1 expression, specifically in the haustoriated cells into which host-translocated effectors are delivered, but not in non-haustoriated adjacent cells. Finally, we found a highly-expressed Hpa effector candidate that suppresses responsiveness to SA. As this approach can be easily applied to host-pathogen interactions for which both host and pathogen genome sequences are available, this work opens the door towards transcriptome studies in infection biology that should help unravel pathogen infection strategies and the mechanisms by which host defense responses are overcome.
Highlights
During co-evolution with pathogens, plants have evolved multiple immune signaling mechanisms that successful pathogens have evolved to evade or suppress
We report here gene expression changes in both Arabidopsis and its parasite Hyaloperonospora arabidopsidis (Hpa) simultaneously during infection using a high-throughput RNA sequencing method
We found that Hpa suppresses responsiveness to salicylic acid (SA) in haustoriated cells into which host-translocated effectors are delivered
Summary
During co-evolution with pathogens, plants have evolved multiple immune signaling mechanisms that successful pathogens have evolved to evade or suppress. The first layer is based on recognition of broadly conserved pathogen molecules (pathogen/ microbe-associated molecular patterns, PAMP/MAMPs) by plant cell surface pattern-recognition receptors (PRRs), resulting in PAMP- (or pattern)-triggered immunity (PTI) [1]. PTI can be suppressed by pathogen proteins, termed effectors, that are delivered into the apoplast or plant cell cytoplasm, resulting in effector-triggered susceptibility. Plants carry a second layer of defense, so-called effector triggered immunity (ETI), in which cytoplasmic disease resistance (R) proteins recognize directly or indirectly the presence of pathogen effectors. A hallmark of ETI is the hypersensitive response (HR), which involves programmed cell death at pathogen infection sites and helps resist biotrophic pathogens
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