Transcriptomic and physiological analyses reveal the molecular mechanisms underlying resistance to Cercospora beticola Sacc. (Cercospora leaf spot) in sugar beet.

In this study, the resistance of 54 Beta vulgaris L. (sugar beet) varieties to Cercospora beticola Sacc. (Cercospora leaf spot). High-resistance varieties outperform medium-resistance varieties and highly susceptible varieties in yield, sugar content, and sugar production. Integrated physiological and transcriptomic data indicate that the differences in brown spot disease resistance among sugar beet varieties are mainly related manly to a reduced ability in their own defense responses. In disease-susceptible varieties, the low expression of key upstream signaling genes, the calcium-binding proteins CMLs and the protein kinase OXI1, together with the high expression of the core signaling gene MPK, results in a decrease in the efficiency of early immune signal transduction. This defect disrupts the function of the hormone defense network, specifically manifested as low expression of the JAZ gene in the jasmonic acid biosynthesis pathway and reduced JA content, along with delayed accumulation of salicylic acid in susceptible varieties. The low expression of the cell wall-remodeling gene TCH4 in susceptible varieties may weaken the physical barrier function of the cell wall. Downregulation of the ROS burst gene RBOH coupled with an insufficiently sustained ROS burst, despite elevated NADPH oxidase content levels. The low expression of the disease resistance protein-encoding gene RPS2 limits the activation of specific immunity. Therefore, the weakened resistance of sugar beet varieties to disease may result from a combination of limited efficiency in upstream signal perception and transmission, dysfunction in the hormone defense network, and reduced efficiency in downstream defense execution. This study provides a theoretical basis for elucidating the resistance mechanisms of sugar beet to leaf spot disease.