背景回顾：It is well-known that plants activate defense responses at the cost of growth. 

提出问题：However, the underlying molecular mechanisms are not well-understood. 

主要发现：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. 

结果1-蛋白互作：We found that the SA receptor NPR1 interacts with the GA receptor GID1. 

结果2-生化证据：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, the negative regulators of GA signaling. 

结果3-遗传实验：Genetic analysis suggested that NPR1, GID1, and DELLA are all required for the SA-mediated growth inhibition. 

结论：Our study not only uncovered a novel regulatory mechanism of growth-defense tradeoff but also revealed the interaction of hormone receptors as a new mode of hormone crosstalk.

A proposed model for SA to repress GA signaling.

众所周知，植物激活防御响应需要付出生长减缓的代价。但是，该现象潜在的分子机制还不清楚。水杨酸（SA）和赤霉素（GA）分别促进植物的防御响应和生长。本文中，作者发现SA抑制GA信号转导，从而抑制植物生长。作者发现SA受体NPR1与GA受体GID1互作。进一步的生化实验发现NPR1作为泛素E3连接酶的接头发挥功能，促进GID1蛋白的多泛素化和降解，从而增强DELLA蛋白的稳定性，负调控GA信号转导。遗传分析显示NPR1、GID1和DELLA对于SA介导的生长抑制都是必须的。本文的研究不仅揭示了植物生长与防御平衡的分子调控机制，同时也表明植物激素受体间的相互作用是植物激素间交联的新模式。

** 严顺平 **