The Polycomb-Group Repressor MEDEA Attenuates Pathogen Defense

Abstract

Plants recruit positive and negative regulators for fine tuning the balance between growth and development. Negative regulators of pathogen defense generally modulate defense hormone biosynthesis and signaling. Here, we report a mechanism for attenuation of the defense response in Arabidopsis (<i>Arabidopsis thaliana</i>), which is mediated by the polycomb-group repressor MEDEA (MEA). Our results showed that pathogen inoculation or exogenous application of salicylic acid, methyl jasmonate, or the bacterial 22-amino acid domain of flagellin peptide induces the expression of <i>MEA</i><i>MEA</i> expression was higher when plants were inoculated with the avirulent strain of <i>Pseudomonas syringae</i> pv. <i>tomato</i> (<i>Pst</i>) carrying the <i>AvrRpt2</i> effector (<i>Pst-AvrRpt2</i>) compared to the virulent <i>Pst</i> strain. <i>MEA</i> remains suppressed during the vegetative phase via DNA and histone (H3K27) methylation, and only the maternal copy is expressed in the female gametophyte and endosperm via histone and DNA demethylation. In contrast, <i>Pst-AvrRpt2</i> induces high levels of <i>MEA</i> expression via hyper-accumulation of H3K4me3 at the <i>MEA</i> locus. <i>MEA</i>-overexpressing transgenic plants are susceptible to the fungal pathogen <i>Botrytis cinerea</i> and bacterial pathogens <i>Pst</i> and <i>Pst-AvrRpt2</i>, whereas <i>mea</i> mutant plants are more resistant to bacterial pathogens. <i>AvrRpt2</i>-mediated immunity requires the function of RESISTANCE TO P. SYRINGAE2 (RPS2) in Arabidopsis. Using transcriptional analysis and chromatin immunoprecipitation, we established that MEA directly targets <i>RPS2</i> and suppresses its transcription. We screened an Arabidopsis cDNA library using MEA as the bait in a yeast two-hybrid assay and identified DROUGHT-INDUCED19, a transcription factor that interacts with MEA and recruits it at the <i>RPS2</i> promoter. The results identified a previously unknown mechanism of defense response attenuation in plants.