转录因子PsERF117通过激活PR10.18调控杨树锈病抗性机制

Abstract

Biotic stresses can induce disease when plant immune systems are compromised. Numerous resistance genes are triggered by pathogen effectors, forming plant immunity cascades that protect plants from damage. However, the resistance genes and defense signaling pathways of poplars against the rust fungus Melampsora spp. are unclear. Melampsora larici-populina race C2 was inoculated on race-compatible ( Populus purdomii ) and race-incompatible ( Populus szechuanica ) poplar species, respectively, for transcriptome analysis. Expression patterns of defense-related genes were determined, followed by weighted gene co-expression network analysis (WGCNA) to extract key defense modules. Thirteen gene families associated with defense mechanisms were identified along with members from 17 pathogenesis-related gene families. WGCNA identified regulatory networks that involve ERF and WRKY transcription factors. Among them, PsERF117 can bind to the GCC-box in the PsPR10.18 promoter region to activate expression. Reduced PR10.18 expression potentially impairs RNase activity, thereby decreasing rust resistance. Knocking out PsERF117 in race-incompatible P. szechuanica weakened the hypersensitive response and reduced reactive oxygen species production, while overexpressing PsERF117 in rust-compatible poplar enhanced resistance to M. magnusiana . PsERF117 can also enhance poplar resistance by upregulating other defense-related genes. PsERF117 confers resistance to rust fungus in poplar through multiple regulatory pathways, establishing a potential candidate for resistance breeding programs.