State Key Laboratory of Crop Stress Biology for Arid Areas and NWAFU-Purdue Joint Research Center, College of Plant Protection, Northwest A&F University, 712100, Yangling, Shaanxi, China.
Department of Botany and Plant Pathology, Purdue University, West Lafayette, IN, 47907, USA.
Nat Commun. 2020 Sep 1;11(1):4382. doi: 10.1038/s41467-020-18240-y.
Fusarium graminearum is a causal agent of Fusarium head blight (FHB) and a deoxynivalenol (DON) producer. In this study, OSP24 is identified as an important virulence factor in systematic characterization of the 50 orphan secreted protein (OSP) genes of F. graminearum. Although dispensable for growth and initial penetration, OSP24 is important for infectious growth in wheat rachis tissues. OSP24 is specifically expressed during pathogenesis and its transient expression suppresses BAX- or INF1-induced cell death. Osp24 is translocated into plant cells and two of its 8 cysteine-residues are required for its function. Wheat SNF1-related kinase TaSnRK1α is identified as an Osp24-interacting protein and shows to be important for FHB resistance in TaSnRK1α-overexpressing or silencing transgenic plants. Osp24 accelerates the degradation of TaSnRK1α by facilitating its association with the ubiquitin-26S proteasome. Interestingly, TaSnRK1α also interacts with TaFROG, an orphan wheat protein induced by DON. TaFROG competes against Osp24 for binding with the same region of TaSnRKα and protects it from degradation. Overexpression of TaFROG stabilizes TaSnRK1α and increases FHB resistance. Taken together, Osp24 functions as a cytoplasmic effector by competing against TaFROG for binding with TaSnRK1α, demonstrating the counteracting roles of orphan proteins of both host and fungal pathogens during their interactions.
镰刀菌禾谷孢是赤霉病（FHB）和脱氧雪腐镰刀菌烯醇（DON）的致病因子。在这项研究中，OSP24 被鉴定为系统表征禾谷镰刀菌 50 个孤儿分泌蛋白（OSP）基因的一个重要毒力因子。尽管 OSP24 对于生长和初始穿透不是必需的，但它对于在小麦穗轴组织中的感染性生长是重要的。OSP24 在发病机制中特异性表达，其瞬时表达抑制 BAX 或 INF1 诱导的细胞死亡。Osp24 易位到植物细胞中，其 8 个半胱氨酸残基中的两个是其功能所必需的。小麦 SNF1 相关激酶 TaSnRK1α 被鉴定为 Osp24 的互作蛋白，并且在 TaSnRK1α 过表达或沉默转基因植物中显示对 FHB 抗性很重要。Osp24 通过促进其与泛素-26S 蛋白酶体的关联来加速 TaSnRK1α 的降解。有趣的是，TaSnRK1α 还与 TaFROG 相互作用，后者是 DON 诱导的孤儿小麦蛋白。TaFROG 与 TaSnRKα 的相同区域竞争与 Osp24 的结合，并保护其免受降解。TaFROG 的过表达稳定了 TaSnRK1α 并增加了 FHB 抗性。总之，Osp24 通过与 TaFROG 竞争结合 TaSnRK1α 作为细胞质效应物发挥作用，证明了宿主和真菌病原体的孤儿蛋白在它们相互作用过程中发挥拮抗作用。
