H2O2 sulfenylates CHE, linking local infection to the establishment of systemic acquired resistance

• 成果类型: Article
• 署名作者: Cao, Lijun; Karapetyan, Sargis; Yoo, Heejin; Chen, Tianyuan; Mwimba, Musoki; Zhang, Xing; Dong, Xinnian
• 署名单位: Duke University; Duke University; Howard Hughes Medical Institute; Utah System of Higher Education; University of Utah
• 刊物名称: SCIENCE
• ISSN/ISSBN: 0036-13432
• DOI: 10.1126/science.adj7249
• 发表日期: 2024-09-13
• 页码: 1211-1217
• 关键词: n-hydroxypipecolic acid; hydroxy-pipecolic acid; salicylic-acid; disease resistance; abiotic stress; cell-death; signal; biosynthesis; isochorismate; induction

摘要

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 (H2O2) 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.