Hubei Hongshan Laboratory, Wuhan 430070, China; College of Life Science and Technology, Huazhong Agricultural University, Wuhan 430070, China; Shenzhen Institute of Nutrition and Health, Huazhong Agricultural University, Shenzhen 518000, China; Shenzhen Branch, Guangdong Laboratory for Lingnan Modern Agriculture, Shenzhen 518000, China; Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences, Shenzhen 518000, China.
Hubei Hongshan Laboratory, Wuhan 430070, China; College of Life Science and Technology, Huazhong Agricultural University, Wuhan 430070, China; Shenzhen Institute of Nutrition and Health, Huazhong Agricultural University, Shenzhen 518000, China; Shenzhen Branch, Guangdong Laboratory for Lingnan Modern Agriculture, Shenzhen 518000, China; Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences, Shenzhen 518000, China.
Mol Plant. 2022 Nov 7;15(11):1759-1771. doi: 10.1016/j.molp.2022.10.001. Epub 2022 Oct 4.
It is well known that plants activate defense responses at the cost of growth. However, the underlying molecular mechanisms are not well understood. The phytohormones salicylic acid (SA) and gibberellin (GA) promote defense response and growth, respectively. Here we show that SA inhibits GA signaling to repress plant growth. We found that the SA receptor NPR1 interacts with the GA receptor GID1. Further biochemical studies revealed that NPR1 functions as an adaptor of ubiquitin E3 ligase to promote the polyubiquitination and degradation of GID1, which enhances the stability of DELLA proteins, the negative regulators of GA signaling. Genetic analysis suggested that NPR1, GID1, and DELLA proteins are all required for the SA-mediated growth inhibition. Collectively, our study not only uncovers a novel regulatory mechanism of growth-defense trade-off but also reveals the interaction of hormone receptors as a new mode of hormonal crosstalk.
众所周知，植物会以牺牲生长为代价激活防御反应。然而，其潜在的分子机制尚不清楚。植物激素水杨酸（SA）和赤霉素（GA）分别促进防御反应和生长。在这里，我们表明 SA 抑制 GA 信号转导以抑制植物生长。我们发现 SA 受体 NPR1 与 GA 受体 GID1 相互作用。进一步的生化研究表明，NPR1 作为泛素 E3 连接酶的接头发挥作用，促进 GID1 的多泛素化和降解，从而增强 GA 信号转导的负调节剂 DELLA 蛋白的稳定性。遗传分析表明，NPR1、GID1 和 DELLA 蛋白均是 SA 介导的生长抑制所必需的。总之，我们的研究不仅揭示了生长-防御权衡的新调控机制，还揭示了激素受体的相互作用是激素串扰的一种新模式。
