Epigenetic regulation of TaFIP phytocytokine clusters confers basal resistance via receptor kinase TaFIPR in wheat

In both plant and animal innate immunity, rapid biosynthesis of cytokine-like peptides is essential for activating immune responses through plasma membrane receptor kinases. Peptide homeostasis is tightly controlled at multiple regulatory levels to avoid adverse effects caused by excessive phytocytokine production. However, the mechanisms underlying the rapid transition between transcriptional activation and repression of phytocytokine genes in response to immune stimuli remain largely unknown. Here we identify previously uncharacterized phytocytokine clusters in wheat, termed TaFIPs, which are rapidly induced by Fusarium infection. TaFIP genes are epigenetically regulated by H3K4me3 and H3K27me3 bivalent histone marks enabling rapid transcriptional shifts. Functionally, the leucine-rich repeat receptor kinase TaFIPR directly recognizes and binds TaFIPs to activate multiple immune responses, thereby enhancing wheat resistance to Fusarium infection. Our findings reveal an epigenetic mechanism that fine-tunes phytocytokine-mediated immunity in wheat.