水杨酸
诱导剂
生物
NPR1
丁香假单胞菌
转录因子
免疫
细胞生物学
系统获得性抵抗
植物对草食的防御
拟南芥
植物免疫
信号转导
生物化学
免疫系统
遗传学
基因
利钠肽
突变体
拟南芥
医学
心力衰竭
内科学
作者
Shaoqin Li,Li‐Ke He,Yongping Yang,Y. Zhang,Xiao Han,Yanru Hu,Yanjuan Jiang
出处
期刊:The Plant Cell
[Oxford University Press]
日期:2024-03-27
卷期号:36 (7): 2587-2606
被引量:3
标识
DOI:10.1093/plcell/koae096
摘要
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 DC3000. This process required INDUCER OF CBF EXPRESSION 1 (ICE1), the core transcription factor in cold-signal cascades. ICE1 physically interacted with NONEXPRESSER OF PATHOGENESIS-RELATED 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.
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