Comparative transcriptome analysis revealed the molecular response mechanism of sugar beet (Beta vulgaris L.) against...

Cercospora leaf spot (CLS), caused by the hemibiotrophic fungus Cercospora beticola (C. beticola), critically threatens global sugar beet production through defoliation and chlorosis, reducing root yields by ≤50 % and impairing sucrose crystallization. As fungicide resistance escalates in C. beticola populations, developing genetically resistant sugar beet becomes imperative. We dissected CLS resistance mechanisms via comparative transcriptomics of resistant (81GM241) and susceptible (KWS6661) genotypes across four infection stages (0-30 dpi). Resistant plants deployed a triphasic defense strategy: During early infection (10 dpi), rapid activation of phenylpropanoid biosynthesis, fatty acid elongation, and glutathione metabolism established dual barriers of lignin-mediated cell wall fortification and ROS scavenging. By mid-infection (20 dpi), pathogen recognition receptors triggered MAPK-WRKY cascades that amplified jasmonate-mediated defenses while mobilizing flavonoid antimicrobials. In late infection (30 dpi), systemic downregulation of photosynthetic antenna proteins redirected resources to tryptophan-derived phytoalexins, sustaining defense without growth penalties. Crucially, resistant plants proactively anticipated stress through coordinated calcium signaling (CDPK), pectin methylesterase-driven cell wall remodeling, and antioxidant activation before pathogen proliferation. In contrast, susceptible plants exhibited delayed ROS detoxification and impaired signal transduction. This phased defense architecture-initiating with pathogen recognition and transient oxidative bursts, progressing through sustained immune activation, and culminating in metabolic optimization-provides a molecular framework for breeding resistant varieties by stacking phase-specific defense regulators.