StSUT2 Regulates Cell Wall Architecture and Biotic Stress Responses in Potatoes (Solanum tuberosum)

Plant sucrose transporters (SUTs) are essential membrane proteins that mediate sucrose phloem loading in source tissues and unloading in sink tissues. In addition to their role in carbohydrate partitioning, SUTs have been implicated in plant responses to both biotic and abiotic stresses. Our previous research demonstrated that silencing <i>StSUT2</i> in potatoes (<i>Solanum tuberosum</i>) affects plant growth, flowering time, and tuber yield, with transcriptomic analysis suggesting its involvement in cell wall metabolic pathways. In this study, we further investigated the effects of <i>StSUT2</i> inhibition on the cell wall structure and biotic stress response of potatoes. Transmission electron microscopy revealed that the tuber cell wall thickness of the <i>StSUT2</i> RNA interference (RNAi) line <i>RNAi-2</i> was reduced by 7.8%, and the intercellular space was increased by 214% compared with the wild-type plants. Biochemical analyses showed that <i>StSUT2</i> silencing significantly decreased cellulose, hemicellulose, and lignin contents in both the leaves and tubers, e.g., tuber cellulose reduced by up to 20.1%, while pectin levels remained unaffected, with distinct effects on source leaves and sink tubers' organs. Additionally, activities of cellulase, xyloglucan glycosyltransferase/hydrolase XTH, and polygalacturonase were elevated in RNAi lines, e.g., leaf cellulase increased by 43.3%, whereas the pectinase activity was unchanged. Pathogen inoculation assays demonstrated that <i>StSUT2</i> RNAi lines were more susceptible to <i>Ralstonia solanacearum</i> bacterial wilt and <i>Fusarium sulphureum</i> dry rot, showing larger leaf lesions, wider tuber necrotic plaques, and severe seedling wilting. These findings demonstrate that silencing <i>StSUT2</i> regulates the cell wall structure, composition, and the activity of cell wall-degrading enzymes, thereby reducing the plant's resistance to fungal and bacterial pathogens.