Wheat stripe rust, due to infection by Puccinia striiformis f. sp. tritici (Pst), is a devastating disease that causes significant global grain yield losses. Yr36, which encodes Wheat Kinase START1 (WKS1), is an effective high-temperature adult-plant resistance gene and confers resistance to a broad spectrum of Pst races. We previously showed that WKS1 phosphorylates the thylakoid ascorbate peroxidase protein and reduces its ability to detoxify peroxides, which may contribute to the accumulation of reactive oxygen species (ROS). WKS1-mediated Pst resistance is accompanied by leaf chlorosis in Pst-infected regions, but the underlying mechanisms remain elusive. Here, we show that WKS1 interacts with and phosphorylates PsbO, an extrinsic member of photosystem II (PSII), to reduce photosynthesis, regulate leaf chlorosis, and confer Pst resistance. A point mutation in PsbO-A1 or reduction in its transcript levels by RNA interference resulted in chlorosis and reduced Pst sporulation. Biochemical analyses revealed that WKS1 phosphorylates PsbO at two conserved amino acids involved in physical interactions with PSII and reduces the binding affinity of PsbO with PSII. Presumably, phosphorylated PsbO proteins dissociate from the PSII complex and then undergo rapid degradation by cysteine and aspartic proteases. Taken together, these results demonstrate that perturbations of wheat PsbO by point mutation or phosphorylation by WKS1 reduce the rate of photosynthesis and delay the growth of Pst pathogen before the induction of ROS.

小麦条锈病，由于被条锈菌感染。sp。Tritici（Pst）是一种破坏性疾病，导致全球粮食单产大幅下降。Yr36，其编码小麦激酶START1（WKS1），是广谱的有效的高温成株抗性基因和赋予抗性的Pst种族。我们以前显示WKS1磷酸化类囊体抗坏血酸过氧化物酶蛋白，并降低其对过氧化物进行解毒的能力，这可能有助于活性氧（ROS）的积累。WKS1介导的Pst阻力伴随着叶萎黄的Pst感染区域，但潜在的机制仍然难以捉摸。在这里，我们表明WKS1与光系统II（PSII）的外在成员PsbO相互作用并使其磷酸化，以减少光合作用，调节叶绿化和赋予 Pst抗性。PsbO - A1的点突变或RNA干扰导致转录水平降低导致萎黄和Pst降低。孢子形成。生化分析表明，WKS1在与PSII物理相互作用中涉及的两个保守氨基酸上使PsbO磷酸化，并降低了PsbO与PSII的结合亲和力。据推测，磷酸化的PsbO蛋白从PSII复合物中解离，然后被半胱氨酸和天冬氨酸蛋白酶迅速降解。综上所述，这些结果表明，通过点突变或WKS1磷酸化对小麦PsbO的干扰降低了光合作用的速率，并延迟了ROS诱导前Pst病原体的生长。