系统获得性抵抗
水杨酸
哌啶酸
半胱氨酸
转录因子
信号转导
基因
化学
NADPH氧化酶
氧化酶试验
细胞生物学
生物
生物化学
酶
氨基酸
拟南芥
突变体
作者
Lijun Cao,Heejin Yoo,Tianyuan Chen,Musoki Mwimba,Xing Zhang,Xinnian Dong
标识
DOI:10.1101/2023.07.27.550865
摘要
Abstract In plants, a local infection can lead to systemic acquired resistance (SAR) through increased production of salicylic acid (SA). For 30 years, the identity of the mobile signal and its direct transduction mechanism for systemic SA synthesis in initiating SAR have been hotly debated. We found that, upon pathogen challenge, the cysteine residue of transcription factor CHE undergoes sulfenylation in systemic tissues, enhancing its binding to the promoter of SA-synthesis gene, ICS1 , and increasing SA production. This occurs independently of previously reported pipecolic acid (Pip) signal. Instead, H 2 O 2 produced by NADPH oxidase, RBOHD, is the mobile signal that sulfenylates CHE in a concentration-dependent manner. This modification serves as a molecular switch that activates CHE-mediated SA-increase and subsequent Pip-accumulation in systemic tissues to synergistically induce SAR. One Sentence Summary RBOHD-generated H 2 O 2 sulfenylates transcription factor CHE to establish systemic acquired resistance in plants.
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