Zheng Peijing, Yuan Pu, Fang Nannan, Ma Xiaoxuan, Jiang Lihua, Zeng Qingdong, Han Dejun, Kang Zhensheng, Liu Jie
State Key Laboratory for Crop Stress Resistance and High-Efficiency Production and College of Life Sciences, Northwest A&F University, Yangling 712100, Shaanxi, China.
State Key Laboratory for Crop Stress Resistance and High-Efficiency Production and College of Plant Protection, Northwest A&F University, Yangling 712100, Shaanxi, China.
Sci Adv. 2025 Jul 11;11(28):eadv1760. doi: 10.1126/sciadv.adv1760.
Biotrophic pathogens rely on host plants for carbon acquisition, making plant sugar transporters, such as Sugars Will Eventually be Exported Transporters (SWEETs), key targets in sugar competition between plants and pathogens. In this study, we identified as a f. sp. ()-induced, secretory vesicle-localized SWEET family member that facilitates hexose and sucrose translocation in wheat. Knockout of led to enhanced wheat resistance to , while overexpressing promoted susceptibility to stripe rust and sugar accumulation in wheat leaves. In addition, wheat transcription factor TaMYB50 contributed to stripe rust resistance by suppressing expression through binding directly to the TA-box motif in the promoter region. Furthermore, we found that effector protein Pst15882, required for infection and pathogenicity, interacted with TaMYB50 to prevent this repression, thus revealing a distinctive regulation strategy by to exploit host sugars for fungal invasion.
活体营养型病原菌依赖寄主植物获取碳源，这使得植物糖转运蛋白，如蔗糖最终输出转运蛋白（SWEETs），成为植物与病原菌之间糖竞争的关键靶点。在本研究中，我们鉴定出一个条锈菌诱导的、定位于分泌囊泡的SWEET家族成员，它促进小麦中己糖和蔗糖的转运。该基因敲除导致小麦对条锈菌的抗性增强，而过量表达则促进小麦对条锈病的易感性及叶片中糖分积累。此外，小麦转录因子TaMYB50通过直接结合启动子区域的TA-box基序抑制该基因的表达，从而有助于小麦抗条锈病。此外，我们发现条锈菌侵染和致病所需的效应蛋白Pst15882与TaMYB50相互作用以阻止这种抑制作用，从而揭示了条锈菌利用寄主糖分进行真菌侵染的独特调控策略。
