SWEET是植物中一类跨膜转运糖的易化扩散蛋白家族，对调控寄主-病原菌互作中的碳素转运与分配具有重要意义。目前已鉴定出参与植物与真菌和细菌等病原菌互作中的多个关键SWEET基因。但根肿菌（原生动物）侵染造成的根瘤这一“库”组织中SWEET对介导糖供给与积累的调控机理尚无报道。本项目在获得大白菜32个SWEET基因及其表达特性、根肿菌可促进糖在根系的积累等研究基础上，拟结合接种根肿菌后大白菜SWEET表达差异、含糖量变化和前人研究基础，明确参与大白菜-根肿菌互作中的关键SWEET；在验证SWEET蛋白糖转运活性的基础上，通过体内和体外试验分析基因之间的互作关系；在获得SWEET基因的大白菜沉默转基因植株和拟南芥功能获得突变体的基础上，通过分析根肿病抗性、含糖量和其它性状，明确在大白菜-根肿菌互作中SWEET调控糖转运的分子机理，为研究根肿菌致病机理和抗根肿病的遗传改良提供理论依据。

SWEETs are a class of proteins responsible for transporting sugars across cell membranes, being crucial to regulate carbon transport and allocation in the host plants and pathogen interaction. Multiple SWEET genes have been identified to be involved in plant and microbiome interaction. However, the regulatory mechanism of SWEET-mediated sugar transport and accumulation in galls caused by Plasmodiophora brassicae infection as a ‘Sink’ is very less known. Previously, we characterized 32 SWEET family genes and their expression pattern in Chinese cabbage, and also found that P. brassicae could promote sugar accumulation in the infected roots. In this study, we propose to further define the key SWEET genes involved in the interaction between Chinese cabbage and P. brassicae based on the expression profiling of 32 SWEET genes, changes of sugars contents in Chinese cabbage after infection by P. brassicae and the SWEET activity identified by others. We also propose to analyze the interactions between SWEET genes by in vivo and in vitro experiments after validation of SWEET protein activity for sugar transport. To understand the molecular mechanism of SWEET in sugar transport regulation during the Chinese cabbage-P. bassicae interaction, the response to P. brassica, sugar content and other importent traits will be analyzed by using Chinese cabbage gene-silencing transgenic plants and Arabidopsis gain-of-function mutants of the key SWEET genes. Our results would provide new insight into pathogenesis of P. bassicae and genetic improvement of clubroot resistance.