miR159b, an epigenetic target of RSI1/FLD, negatively regulates systemic acquired resistance

Plants retain memories of past infections to mount a robust defense in the form of systemic acquired resistance (SAR) during subsequent pathogen invasions. Primary infected tissues generate a group of compounds that serve as mobile signals for SAR development. Downstream processes subsequent to mobile signal perception are little known. Epigenetic regulator reduced systemic immunity1/FLOWERING LOCUS D (RSI1/FLD) is essential for activating SAR and functions downstream of signal perception in the systemic tissues. Here, we show that RSI1 negatively regulates the expression of miR159b, which in turn regulates the expression of a set of genes that control SAR development. RSI1 physically associates and contributes to SAR-associated demethylation of H3K4me2 and H3K4me3 at the MIR159B locus. Overexpression of miR159b suppresses SAR development, whereas SAR is exaggerated in mir159ab double mutants and target mimic expressing STTM159 lines. Through bioinformatics and expression analysis, we identified several targets of miR159, among which SDG14, RD19A, MYB65, MYB33, MYB120, TPST, TIE4, CSD3, and PPDK positively regulate SAR development, whereas MYB97 and MYB104 negatively regulate it. Altogether, our work identified a functional network of genes that activate and fine-tune SAR development in Arabidopsis thaliana.