Physiological, Biochemical, and Molecular Mechanisms of Resistance of Poacynum hendersonii to Melampsora apocyni

The rust disease caused by <i>Melampsora apocyni</i> seriously affects the growth of <i>Poacynum hendersonii.</i> However, the defense mechanisms against rust infection remain unclear. This study explored the regulatory mechanisms of <i>P. hendersonii</i> in response to rust disease through combined physiological, biochemical, and transcriptomic analyses. The results showed that with the increase in disease severity, the chlorophyll content of leaves decreased significantly, while the antioxidant and phenylalanine ammonia lyase activities progressively increased. Mild infection triggered an 11.9-fold surge in salicylic acid levels and a sharp decline in abscisic acid compared to controls, as well as increased synthesis of total phenolics, total flavonoids, chlorogenic acid, cryptochlorogenic acid, isoquercetin, hyperoside, rutin, and astragalin. Transcriptome analysis showed that the "plant-pathogen interaction, plant hormone signal transduction and phenylpropanoid biosynthesis" pathways were significantly up-regulated in the mild infection stage, while "glycerophospholipid metabolism, fatty acid degradation and ABC transporters" were activated in the severe infection stage. In summary, <i>P. hendersonii</i> regulates energy metabolism and phenylpropanoid metabolism through salicylic acid signaling and promotes the accumulation of secondary metabolites and the lignification process of leaves, thereby enhancing rust resistance. Key enzyme genes (COMT, POD, CAD, F5H) and metabolites (chlorogenic acid, isoquercitrin, rutin) can be used as important targets for disease resistance breeding. Our research provides important reference for the prevention and control of <i>M. apocyni</i> in <i>P. hendersonii</i>.