A transposon-induced epigenetic change controls EFR-mediated pathogen susceptibility

Plants have evolved a complex two-layer immune system to battle pathogens. In the first layer, which resembles human innate immunity, plants utilize pattern-recognition receptors (PRRs) located on the cell surface to detect the presence of conserved pathogen (or microbe)-associated molecular patterns (PAMPs/MAMPs) leading to PAMP-triggered immunity (PTI). While some PRRs are present in all higher plant species, others have evolved only in certain plant families. The ELONGATION FACTOR-TU RECEPTOR (EFR), which recognizes the abundant bacterial protein EF-Tu, is specific to the Brassicaceae family. EFR activation triggers a cascade of signaling events that initiate plant immune responses. Recently, we found that the insertion of TE-derived inverted repeats (IRs) near genes cause changes in the local chromatin organization that profoundly impact the activity of neighboring loci. Here we show that an IR located between the genes encoding EFR and Myosin XI-k, a protein previously associated with root organogenesis, ER dynamics, and penetration resistant to fungus, controls EFR expression by shaping the local chromatin topology.