Cold stress affects plant immune responses, and this process may involve the salicylic acid (SA) signaling pathway. However, the underlying mechanism by which low temperature signals coordinate with SA signaling to regulate plant immunity remains unclear. Here, we found that low temperatures enhanced the disease resistance of Arabidopsis thaliana against Pseudomonas syringae pv. tomato (Pst) DC3000. This process required INDUCER OF CBF EXPRESSION 1 (ICE1), the core transcription factor in cold-signal cascades. ICE1 physically interacted with NON-EXPRESSER OF PR GENES 1 (NPR1), the master regulator of the SA signaling pathway. Enrichment of ICE1 on the PATHOGENESIS-RELATED GENE 1 (PR1) promoter and its ability to transcriptionally activate PR1 were enhanced by NPR1. Further analyses revealed that cold stress signals cooperate with SA signals to facilitate plant immunity against pathogen attack in an ICE1-dependent manner. Cold treatment promoted interactions of NPR1 and TGACG-BINDING FACTOR 3 (TGA3) with ICE1, and increased the ability of the ICE1–TGA3 complex to transcriptionally activate PR1. Together, our results characterize a critical role of ICE1 as an indispensable regulatory node linking low temperature-activated and SA-regulated immunity. Understanding this crucial role of ICE1 in coordinating multiple signals associated with immunity broadens our understanding of plant–pathogen interactions.

中文翻译：

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CBF表达诱导剂1通过直接激活水杨酸信号传导促进冷增强免疫力

冷胁迫影响植物免疫反应，这一过程可能涉及水杨酸（SA）信号通路。然而，低温信号与SA信号协调调节植物免疫的潜在机制仍不清楚。在这里，我们发现低温增强了拟南芥对丁香假单胞菌的抗病性。番茄（太平洋标准时间）DC3000。这个过程需要 CBF 表达诱导剂 1 (ICE1)，它是冷信号级联中的核心转录因子。 ICE1 与 SA 信号通路的主要调节因子 PR 基因 1 的非表达蛋白 (NPR1) 发生物理相互作用。 NPR1 增强了 ICE1 在发病相关基因 1 (PR1) 启动子上的富集及其转录激活 PR1 的能力。进一步的分析表明，冷胁迫信号与SA信号协同作用，以ICE1依赖性方式促进植物抵抗病原体攻击的免疫力。冷处理促进了 NPR1 和 TGACG 结合因子 3 (TGA3) 与 ICE1 的相互作用，并增加了 ICE1-TGA3 复合物转录激活 PR1 的能力。总之，我们的结果表明 ICE1 作为连接低温激活和 SA 调节免疫的不可或缺的调节节点的关键作用。了解 ICE1 在协调与免疫相关的多个信号中的关键作用可以拓宽我们对植物与病原体相互作用的理解。