Project description:Larch (Larix spp.), a key species in China's reforestation efforts, faces increasing threats from shoot blight caused by Neofusicoccum laricinum. This study characterized the biological traits, virulence mechanisms, and host interactions of this pathogen to inform disease management. Twenty-five N. laricinum strains were isolated from six regions in Northeast China and identified through morphological and molecular analysis. Comprehensive growth assessments revealed optimal development at 18°C and pH 9-11, with significant strain-specific variation in virulence (lesions 18.4-38.8 mm). Pathogenicity assays revealed that the hypervirulent TM02 strain exhibited early and robust production of cell wall-degrading enzymes，such as pectin methylgalacturonase (PMG, 208.9 U/mg) and polygalacturonase (PG, 54.9 U/mg), correlated with its aggressive infection phenotype. Biochemical analyses revealed that the pathogen actively disrupted host oxidative defenses, with superoxide dismutase (SOD) activity peaking at 3 dpi (456.7 U/g·min-1) before decreasing to 0.8× control levels by 7 dpi, whereas peroxidase (POD) activity exhibited a transient 4.6-fold increase followed by rapid suppression. Transcriptome analysis revealed generally downregulation of defense genes, mainly cellulose synthase (21/25 genes) and peroxidase (38/45 genes), with –10.5-fold inhibition of Ces-g8671 and an –11.4-fold reduction in Pod-g18614 expression, indicating that pathogens can simultaneously damage larch cell wall synthesis and the ROS scavenging defense system. These findings establish N. laricinum’s sophisticated two-phase infection strategy: initial physical breach of cell walls facilitated by CWDEs, followed by systematic suppression of host antioxidant defenses. This study identifies specific molecular targets for developing intervention strategies and provides critical insights into host‒pathogen dynamics in larch plantations under climate change scenarios.
