The key pathogenic factor GcSP2 of Geotrichum citri-aurantii plays an important role in disrupting citrus metabolism and immunity

Abstract

The pathogen Geotrichum citri-aurantii (G. citri-aurantii) causes postharvest sour rot disease in citrus fruits worldwide, severely impacting citrus economic value. However, the pathogenic mechanisms of this fungus remain inadequately understood. Here, we identified 15 candidate effector proteins from G. citri-aurantii genome, of which five were highly expressed during infection and were capable of suppressing BAX-induced cell death, indicating their role in inhibiting plant immunity. Gene expression analysis showed that these five effector proteins primarily induced the upregulation of pattern-triggered immunity (PTI)-related gene expression. Diaminobenzidine (DAB) staining results indicated that only GcSP2 triggered reactive oxygen species (ROS) burst. Notably, GcSP2 contains a known carbohydrate-binding module 1 (CBM1) domain and exhibits low overall conservation. Gene knockout experiments revealed that the absence of GcSP2 delayed disease onset by 1–2 days and significantly reduced lesion size, establishing it as a key pathogenic factor. Assessments of total phenols, flavonoids, and pathogenesis-related protein expression indicated that GcSP2 significantly affects citrus metabolism at 72 hours post-infection.