<scp>P</scp> op <scp>MYB</scp> 4 orchestrates disease resistance through <scp>H</scp> 3 <scp>K</scp> 36me3‐mediated epigenetic activation of <i>PopGSTU7</i> in poplars

Pathogens significantly impair plant growth and developmental processes. Emerging evidence has highlighted the pivotal roles of MYB transcription factors (TFs) and histone H3K36me3 transferase in orchestrating regulatory networks that govern plant defense responses against pathogen stress. However, the potential for synergistic interactions among these genes in woody plants, particularly within poplar subjected to biotic stress, remains largely unexplored. Functional analysis showed that PopMYB4 overexpression (OE) reduced pathogen tolerance, whereas RNA interference (RNAi)-mediated suppression enhanced host resistance to pathogens. This phenotypic change was linked to modified reactive oxygen species (ROS) dynamics and the coordinated regulation of defense genes, notably PopGSTU7. Y1H, EMSA, and dual-luciferase assays indicated that PopMYB4 directly binds to the PopGSTU7 promoter and represses its transcription. We further established that PopSDG36 physically interacts with PopMYB4, thereby alleviating PopMYB4's inhibitory effects on PopGSTU7 expression. Functional analysis using overexpression demonstrated that PopSDG36 positively regulates resistance to Colletotrichum gloeosporioides in poplars. Moreover, the PopSDG36 transgenic plants led to increased H3K36me3 levels at PopGSTU7, thus increasing PopGSTU7 expression. The PopMYB4-PopSDG36 represents a dual-function regulatory hub in poplars, integrating transcriptional regulation and H3K36me3-mediated epigenetic regulation to fine-tune immune signaling networks, thereby providing mechanistic insights into plant-pathogen coevolution.