Key Laboratory of Ministry of Education for Genetics, Breeding and Multiple Utilization of Crops, Fujian University Key Laboratory for Plant-Microbe Interaction, Ministerial and Provincial Joint Innovation Centre for Safety Production of Cross-Strait Crops, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
State Key Laboratory for Crop Genetics and Germplasm Enhancement, JiangSu Collaborative Innovation Center for Modern Crop Production, Nanjing Agricultural University, Nanjing 210095, China.
Plant Cell. 2022 Aug 25;34(9):3425-3442. doi: 10.1093/plcell/koac164.
Plants manage the high cost of immunity activation by suppressing the expression of defense genes during normal growth and rapidly switching them on upon pathogen invasion. TGAs are key transcription factors controlling the expression of defense genes. However, how TGAs function, especially in monocot plants like rice with continuously high levels of endogenous salicylic acid (SA) remains elusive. In this study, we characterized the role of OsTGA5 as a negative regulator of rice resistance against blast fungus by transcriptionally repressing the expression of various defense-related genes. Moreover, OsTGA5 repressed PTI responses and the accumulation of endogenous SA. Importantly, we showed that the nucleus-localized casein kinase II (CK2) complex interacts with and phosphorylates OsTGA5 on Ser-32, which reduces the affinity of OsTGA5 for the JIOsPR10 promoter, thereby alleviating the repression of JIOsPR10 transcription and increasing rice resistance. Furthermore, the in vivo phosphorylation of OsTGA5 Ser-32 was enhanced by blast fungus infection. The CK2 α subunit, depending on its kinase activity, positively regulated rice defense against blast fungus. Taken together, our results provide a mechanism for the role of OsTGA5 in negatively regulating the transcription of defense-related genes in rice and the repressive switch imposed by nuclear CK2-mediated phosphorylation during blast fungus invasion.
植物通过在正常生长过程中抑制防御基因的表达，以及在受到病原体侵袭时迅速开启防御基因的表达，来控制免疫激活的高成本。TGA 是控制防御基因表达的关键转录因子。然而，TGA 如何发挥作用，特别是在像水稻这样内源水杨酸（SA）水平持续较高的单子叶植物中，仍然难以捉摸。在这项研究中，我们通过转录抑制各种防御相关基因的表达，来鉴定 OsTGA5 在水稻抵抗稻瘟病菌中的负调控作用。此外，OsTGA5 还抑制了 PTI 反应和内源 SA 的积累。重要的是，我们表明定位于细胞核的酪蛋白激酶 II（CK2）复合物与 OsTGA5 相互作用，并在 Ser-32 上磷酸化 OsTGA5，这降低了 OsTGA5 与 JIOsPR10 启动子的结合亲和力，从而减轻了 JIOsPR10 转录的抑制作用，增强了水稻的抗性。此外，稻瘟病菌感染增强了 OsTGA5 Ser-32 的体内磷酸化。CK2α亚基依赖其激酶活性正向调控水稻对稻瘟病菌的防御。综上所述，我们的研究结果提供了一种机制，解释了 OsTGA5 在负调控水稻防御相关基因转录中的作用，以及在稻瘟病菌入侵时，由核 CK2 介导的磷酸化作用所施加的抑制开关。
