Transposon-triggered epigenetic chromatin dynamics modulate EFR-related pathogen response.

Infectious diseases drive wild plant evolution and impact crop yield. Plants, like animals, sense biotic threats through pattern recognition receptors (PRRs). Overly robust immune responses can harm plants; thus, understanding the tuning of defense response mechanisms is crucial for developing pathogen-resistant crops. In this study, we found that an inverted-repeat transposon (EFR-associated IR, Ea-IR) located between the loci encoding PRRs ELONGATION FACTOR-TU RECEPTOR (EFR) and myosin XI-k (XI-k) in Arabidopsis affects chromatin organization, promoting the formation of a repressive chromatin loop. Upon pathogen infection, chromatin changes around EFR and XI-k correlate with increased EFR transcription. Pathogen-induced chromatin opening causes RNA polymerase II readthrough, producing a longer, Ea-IR-containing XI-k transcript, processed by Dicer-like enzymes into small RNAs, which reset chromatin to a repressive state attenuating the immune response after infection. Arabidopsis accessions lacking Ea-IR have higher basal EFR levels and resistance to pathogens. We show a scenario in which a transposon, chromatin organization and gene expression interact to fine-tune immune responses, during both the course of infection and the course of evolution.