免疫反应能增强植物的抗病性，但会抑制植物的生长，即存在免疫与生长的权衡（tradeoff）。植物激素水杨酸和赤霉素分别在免疫反应和生长中发挥重要作用。目前尚不清楚水杨酸能否以及如何通过调控赤霉素信号通路来抑制植物的生长。水杨酸的受体NPR1是一个潜在的E3泛素连接酶，但是其泛素化底物一直没有被发现。在前期的研究中，我们发现NPR1能与赤霉素受体GID1相互作用。这为我们研究水杨酸和赤霉素的相互关系提供了很好的切入点。本项目将结合生物化学、遗传学、转录组学等多种手段研究水杨酸和NPR1通过促进GID1的泛素化和降解来抑制赤霉素信号通路的分子机理。本研究不仅将揭示免疫反应抑制生长的新机制(通过抑制赤霉素信号通路)和激素交互调控的新机制(通过受体与受体之间的相互作用)，而且将发现NPR1的第一个底物(GID1)，具有重要的科学意义。

Mechanistic study on how salicylic acid inhibits gibberellin signaling pathway.The immune response promotes plant disease resistance but inhibits plant growth, indicating the presence of immunity-growth tradeoff. The plant hormones salicylic acid and gibberellin play vital roles in immunity and growth, respectively. However, it remains unclear whether and how salicylic acid regulates gibberellin signaling to inhibit plant growth. The SA receptor NPR1 is a potential E3 ubiquitin ligase. But its ubiquitination substrates have not been identified. In previous studies, we found that NPR1 interacts with the gibberellin receptor GID1 and promotes GID1 degradation, providing a good starting point to study the relationship between salicylic acid and gibberellin. In this proposal, we will study the molecular mechanisms by which salicylic acid and NPR1 inhibit gibberellin signaling by promoting ubiquitination and degradation of GID1 using integrated approaches of biochemistry, genetics and transcriptomics. This study not only will uncover the new mechanism of growth inhibition caused by immune responses (through inhibition of gibberellin signaling) and the new mechanism of hormone crosstalk (through receptors interactions), but also will discover the first NPR1 substrate (GID1), which has important scientific significance.