Fig. 7: A proposed model for a self-buffered immune response mechanism controlled by the Ea-IR-mediated regulation of chromatin organization and transcription at EFR locus.

In a resting state, Arabidopsis plants with the Ea-IR insertion between EFR and Xl-k genes from the repressive Loop^EFR chromatin loop, which encompasses EFR-encoding sequences. This loop dampens the background activity of the immune system and also promotes the termination of Xl-k transcription. Upon pathogen infection, the repressive Loop^EFR opens, allowing for enhanced EFR transcription, which increases immunity and allows Pol II readthrough at the Xl-k termination site. The hairpin at the 3′ end of the long Xl-k transcript isoform is processed by DCL1 and DCL3 into epigenetically active siRNAs. These siRNAs can subsequently initiate the remethylation of Ea-IR sequences, promoting the reformation of Loop^EFR and thereby resetting chromatin topology to a homeostatic state with a steady but reduced immune response. Open Loop^EFR or the absence of Ea-IR allows for the formation of a second, apparently innocuous Loop^Xl-k.