In plants, a local infection can lead to systemic acquired resistance (SAR) through increased production of salicylic acid (SA). For many years, the identity of the mobile signal and its direct transduction mechanism for systemic SA synthesis in initiating SAR have been debated. We found that in Arabidopsis thaliana , after a local infection, the conserved cysteine residue of the transcription factor CCA1 HIKING EXPEDITION (CHE) undergoes sulfenylation in systemic tissues, which enhances its binding to the promoter of the SA-synthesis gene ISOCHORISMATE SYNTHASE1 ( ICS1 ) and increases SA production. Furthermore, hydrogen peroxide (H 2 O 2 ) produced through NADPH oxidases is the mobile signal that sulfenylates CHE in a concentration-dependent manner. Accumulation of SA and the previously reported signal molecules, such as N -hydroxypipecolic acid (NHP), then form a signal amplification loop to establish SAR.

中文翻译：

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H 2 O 2 次磺酰化 CHE，将局部感染与全身获得性耐药的建立联系起来


在植物中，局部感染可通过增加水杨酸 （SA） 的产生导致全身获得性耐药 （SAR）。多年来，移动信号的身份及其在启动 SAR 中全身性 SA 合成的直接转导机制一直存在争议。我们发现，在拟南芥中，局部感染后，转录因子 CCA1 HIKING EXPEDITION （CHE） 的保守半胱氨酸残基在内吸组织中发生亚磺酰化，这增强了它与 SA 合成基因异端SYNTHASE1 （ICS1） 启动子的结合并增加了 SA 的产生。此外，通过 NADPH 氧化酶产生的过氧化氢 （H 2 O 2 ） 是以浓度依赖性方式磺酰化 CHE 的移动信号。SA 和先前报道的信号分子（如 N-羟基哌啶酸 （NHP））的积累然后形成信号放大环以建立 SAR。