The novel pathogen-responsive glycosyltransferase UGT73C7 mediates the redirection of phenylpropanoid metabolism and promotes SNC1-dependent Arabidopsis immunity
The novel pathogen-responsive glycosyltransferase UGT73C7 mediates the redirection of phenylpropanoid metabolism and promotes SNC1-dependent Arabidopsis immunity
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DOI：
10.1111/tpj.15280
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发表时间：
2021-05-04
期刊：
影响因子：
7.2
通讯作者：
Hou, Bing-Kai
中科院分区：
文献类型：
--
作者：
Huang, Xu-Xu;Wang, Yong;Hou, Bing-Kai
最近的研究表明，全球代谢重编程是植物先天免疫中常见的事件；然而，相关的分子机制在很大程度上仍不清楚。在这里，我们鉴定了病原菌诱导的糖基转移酶UGT73C7，它通过介导苯丙烷途径的重定向在拟南芥的抗病中发挥关键作用。UGT73C7功能缺失导致对紫丁香假单胞菌的抗性显著降低。番茄DC3000，而UGT73C7的结构性过表达导致了增强的防御反应。UGT73C7激活的免疫依赖于Toll/IL-1受体类型NLR基因SNC1的上调表达。此外，体外和体内实验表明，UGT73C7可以糖基化苯丙烷途径的上游代谢物对香豆酸和阿魏酸。导致UGT73C7酶活性丧失的突变导致SNC1表达失败。此外，UGT73C7的糖基化活性导致苯丙烷类代谢通量重定向到羟基肉桂酸和香豆素的生物合成。苯丙烷途径的中断抑制了UGT73C7促进的SNC1的表达和免疫反应。本研究不仅证实UGT73C7是病原菌攻击时调节苯丙素代谢的重要调节因子，而且还提供了苯丙素代谢与NLR基因之间的联系。
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.