The occurrence of plant disease is determined by interactions among host, pathogen, and environment. Air humidity shapes various aspects of plant physiology and high humidity has long been known to promote numerous phyllosphere diseases. However, the molecular basis of how high humidity interferes with plant immunity to favor disease has remained elusive. Here we show that high humidity is associated with an “immuno-compromised” status in Arabidopsis plants. Furthermore, accumulation and signaling of salicylic acid (SA), an important defense hormone, are significantly inhibited under high humidity. NPR1, an SA receptor and central transcriptional co-activator of SA-responsive genes, is less ubiquitinated and displays a lower promoter binding affinity under high humidity. The cellular ubiquitination machinery, particularly the Cullin 3-based E3 ubiquitin ligase mediating NPR1 protein ubiquitination, is downregulated under high humidity. Importantly, under low humidity the Cullin 3a/b mutant plants phenocopy the low SA gene expression and disease susceptibility that is normally observed under high humidity. Our study uncovers a mechanism by which high humidity dampens a major plant defense pathway and provides new insights into the long-observed air humidity influence on diseases.

中文翻译：

---

高空气湿度会抑制水杨酸途径和 NPR1 促进植物病害的功能

植物病害的发生是由寄主、病原体和环境之间的相互作用决定的。空气湿度影响植物生理学的各个方面，长期以来人们都知道高湿度会促进多种叶际疾病。然而，高湿度如何干扰植物免疫力从而促进疾病的分子基础仍然难以捉摸。在这里，我们表明高湿度与拟南芥植物的“免疫受损”状态有关。此外，水杨酸（SA）这种重要的防御激素的积累和信号传导在高湿度下会受到显着抑制。NPR1 是一种 SA 受体和 SA 响应基因的中央转录共激活因子，其泛素化程度较低，在高湿度下显示出较低的启动子结合亲和力。细胞泛素化机制，特别是介导 NPR1 蛋白泛素化的基于 Cullin 3 的 E3 泛素连接酶，在高湿度下下调。重要的是，在低湿度下，Cullin 3a/b突变体植物表现出通常在高湿度下观察到的低 SA 基因表达和疾病易感性。我们的研究揭示了高湿度抑制主要植物防御途径的机制，并为长期观察到的空气湿度对疾病的影响提供了新的见解。