State Key Laboratory of Crop Stress Biology for Arid Areas, College of Plant Protection, Northwest A&F University, Yangling, Shaanxi 712100, China; Pioneering Innovation Center for Wheat Stress Tolerance Improvement, State Key Laboratory of Crop Stress Biology for Arid Areas, Northwest A&F University, Yangling, Shaanxi 712100, China; State Key Laboratory of Crop Stress Biology for Arid Areas, College of Life Science, Northwest A&F University, Yangling, Shaanxi 712100, China.
State Key Laboratory of Crop Stress Biology for Arid Areas, College of Plant Protection, Northwest A&F University, Yangling, Shaanxi 712100, China; Pioneering Innovation Center for Wheat Stress Tolerance Improvement, State Key Laboratory of Crop Stress Biology for Arid Areas, Northwest A&F University, Yangling, Shaanxi 712100, China.
Cell. 2022 Aug 4;185(16):2961-2974.e19. doi: 10.1016/j.cell.2022.06.027. Epub 2022 Jul 14.
Wheat crops are frequently devastated by pandemic stripe rust caused by Puccinia striiformis f. sp. tritici (Pst). Here, we identify and characterize a wheat receptor-like cytoplasmic kinase gene, TaPsIPK1, that confers susceptibility to this pathogen. PsSpg1, a secreted fungal effector vital for Pst virulence, can bind TaPsIPK1, enhance its kinase activity, and promote its nuclear localization, where it phosphorylates the transcription factor TaCBF1d for gene regulation. The phosphorylation of TaCBF1d switches its transcriptional activity on the downstream genes. CRISPR-Cas9 inactivation of TaPsIPK1 in wheat confers broad-spectrum resistance against Pst without impacting important agronomic traits in two years of field tests. The disruption of TaPsIPK1 leads to immune priming without constitutive activation of defense responses. Taken together, TaPsIPK1 is a susceptibility gene known to be targeted by rust effectors, and it has great potential for developing durable resistance against rust by genetic modifications.
小麦作物经常受到由条形柄锈菌引起的流行性条锈病的严重破坏。在这里,我们鉴定并表征了一个小麦类受体胞质激酶基因 TaPsIPK1,该基因赋予了小麦对这种病原体的易感性。PsSpg1 是一种对 Pst 毒力至关重要的分泌真菌效应物,能够与 TaPsIPK1 结合,增强其激酶活性,并促进其核定位,在核定位中,它使转录因子 TaCBF1d 磷酸化以进行基因调控。TaCBF1d 的磷酸化改变了其对下游基因的转录活性。在两年的田间试验中,利用 CRISPR-Cas9 技术使 TaPsIPK1 在小麦中失活,赋予了广谱抗条形柄锈病的能力,而不影响重要的农艺性状。TaPsIPK1 的破坏导致免疫启动而不导致防御反应的组成性激活。总之,TaPsIPK1 是一个已知被锈病效应物靶向的感病基因,通过遗传修饰具有开发持久抗锈病能力的巨大潜力。