The Key Laboratory of Plant Development and Environmental Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao, 266237, China.
Center for Genomics and Biotechnology, Haixia Institute of Science and Technology, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Plant J. 2021 Jul;107(1):149-165. doi: 10.1111/tpj.15280. Epub 2021 May 4.
Recent studies have shown that global metabolic reprogramming is a common event in plant innate immunity; however, the relevant molecular mechanisms remain largely unknown. Here, we identified a pathogen-induced glycosyltransferase, UGT73C7, that plays a critical role in Arabidopsis disease resistance through mediating redirection of the phenylpropanoid pathway. Loss of UGT73C7 function resulted in significantly decreased resistance to Pseudomonas syringae pv. tomato DC3000, whereas constitutive overexpression of UGT73C7 led to an enhanced defense response. UGT73C7-activated immunity was demonstrated to be dependent on the upregulated expression of SNC1, a Toll/interleukin 1 receptor-type NLR gene. Furthermore, in vitro and in vivo assays indicated that UGT73C7 could glycosylate p-coumaric acid and ferulic acid, the upstream metabolites in the phenylpropanoid pathway. Mutations that lead to the loss of UGT73C7 enzyme activities resulted in the failure to induce SNC1 expression. Moreover, glycosylation activity of UGT73C7 resulted in the redirection of phenylpropanoid metabolic flux to biosynthesis of hydroxycinnamic acids and coumarins. The disruption of the phenylpropanoid pathway suppressed UGT73C7-promoted SNC1 expression and the immune response. This study not only identified UGT73C7 as an important regulator that adjusts phenylpropanoid metabolism upon pathogen challenge, but also provided a link between phenylpropanoid metabolism and an NLR gene.
最近的研究表明，全球代谢重编程是植物先天免疫中的一个常见事件；然而，相关的分子机制在很大程度上仍然未知。在这里，我们鉴定了一个病原体诱导的糖基转移酶 UGT73C7，它通过介导苯丙烷途径的重定向，在拟南芥疾病抗性中发挥关键作用。UGT73C7 功能丧失导致对丁香假单胞菌 pv 的抗性显著降低。番茄 DC3000，而 UGT73C7 的组成型过表达导致防御反应增强。UGT73C7 激活的免疫被证明依赖于 SNC1 的上调表达，SNC1 是 Toll/白细胞介素 1 受体型 NLR 基因。此外，体外和体内试验表明，UGT73C7 可以糖基化 p-香豆酸和阿魏酸，苯丙烷途径的上游代谢物。导致 UGT73C7 酶活性丧失的突变导致 SNC1 表达的诱导失败。此外，UGT73C7 的糖基化活性导致苯丙烷代谢通量向羟基肉桂酸和香豆素生物合成的重定向。苯丙烷途径的中断抑制了 UGT73C7 促进的 SNC1 表达和免疫反应。这项研究不仅鉴定了 UGT73C7 作为一个重要的调节剂，在病原体挑战时调整苯丙烷代谢，而且还提供了苯丙烷代谢和 NLR 基因之间的联系。
