美国杜克大学Xinnian Dong小组揭示了水杨酸参与中枢代谢调节因子SnRK1和TOR，通过NPR1的差异磷酸化来控制免疫。相关论文于2026年9月30日发表于国际顶尖学术期刊《细胞》杂志上。

免疫需要在对抗感染与维持代谢功能之间保持微妙的平衡。然而，免疫反应与细胞代谢如何协调的机制仍很大程度上未知。在此，研究人员表明，NPR1——水杨酸介导防御反应的核心植物免疫调控因子——受涉及两个主要营养感知激酶的翻译后修饰级联调控。在缺乏病原体挑战时，雷帕霉素靶标通过磷酸化Ser-55/59抑制NPR1。在防御反应期间，升高的水杨酸降低糖磷酸水平并增强SNF1相关蛋白激酶1活性，后者进而抑制TOR信号并在Ser-557位点磷酸化NPR1，这一修饰是后续翻译后修饰和NPR1激活所必需的。总之，研究人员的发现确定水杨酸是通过调节中央代谢调控因子SnRK1和TOR来协调病原体挑战下生长与免疫的协调因子，这两个调控因子通过差异磷酸化拮抗性地控制NPR1免疫活性。

附：英文原文

Title: Salicylic acid engages central metabolic regulators SnRK1 and TOR to govern immunity by differential phosphorylation of NPR1

Author: Yixuan Chen, John Withers, Yulin Sun, Tianyuan Chen, Sargis Karapetyan, Jan Draken, Yezi Xiang, Yuzhe Yuan, Yang He, Wolfgang Drge-Laser, Jing-Ke Weng, Xinnian Dong

Issue&Volume: 2026-09-30

Abstract: Immunity requires a delicate balance between combating infection and preserving metabolic functions. However, the mechanisms by which immune responses are coordinated with cellular metabolism remain largely unknown. Here, we show that NONEXPRESSER OF PR GENES 1 (NPR1), the central plant immune regulator of salicylic acid (SA)-mediated defense responses, is controlled by a cascade of post-translational modifications (PTMs) involving two master nutrient-sensing kinases. In the absence of pathogen challenge, TARGET OF RAPAMYCIN (TOR) inhibits NPR1 through phosphorylation at Ser-55/59. During defense responses, elevated SA reduces sugar phosphate levels and enhances SNF1-RELATED PROTEIN KINASE 1 (SnRK1) activity, which in turn inhibits TOR signaling and phosphorylates NPR1 at Ser-557, a modification required for subsequent PTMs and NPR1 activation. Together, our findings identify SA as a coordinator of growth and immunity in response to pathogen challenge by modulating the central metabolic regulators SnRK1 and TOR, which antagonistically control NPR1 immune activity through differential phosphorylation.

DOI: 10.1016/j.cell.2026.09.011

Source: https://www.cell.com/cell/abstract/S0092-8674(26)01080-9