P-121 - Effector gene silencing coordinated by histone methylation and small RNAs enhances host adaptation in Phytophthora sojae

Pathogens employ epigenetic mechanisms to evade host recognition and enhance adaptability, posing significant challenges to sustainable disease control. Histone H3 lysine 27 trimethylation (H3K27me3) and small RNA (sRNA)-mediated gene silencing are two classical pathways regulating effector gene expression. However, their co-regulatory interactions remain poorly explored. Here, we investigated the coordinated roles of H3K27me3 and sRNAs in silencing avirulence (Avr) effector genes in Phytophthora sojae. CRISPR/Cas9 mediated disruption of PsSu(z)12, a key component of the H3K27me3 methyltransferase complex, led to the loss of both H3K27me3 and sRNA-mediated repression at multiple RxLR effector loci, including Avr1b and Avr3a. Differential complementation effects at these loci, combined with integrative analyses of ChIP-seq, RNA-seq, and sRNA-seq data revealed a strong locus-specific correlation between H3K27me3 and sRNAs. Notably, most H3K27me3-regulated RxLR effectors are also co-regulated by sRNAs. Our findings highlight PsSu(z)12 as a critical coordinator of H3K27me3 and sRNA-mediated silencing, underscoring a synchronized epigenetic strategy exploited by P. sojae to reprogram transcription under the selection pressure of resistance genes (R-gene), enabling effector gene recycling and immune evasion.