Suppression of MYC transcription activators by the immune cofactor NPR1 fine-tunes plant immune responses

• Published in: Cell reports (Cambridge) 2021-12, Vol.37 (11), p.110125-110125, Article 110125
• Main Authors: Nomoto, Mika, Skelly, Michael J., Itaya, Tomotaka, Mori, Tsuyoshi, Suzuki, Takamasa, Matsushita, Tomonao, Tokizawa, Mutsutomo, Kuwata, Keiko, Mori, Hitoshi, Yamamoto, Yoshiharu Y., Higashiyama, Tetsuya, Tsukagoshi, Hironaka, Spoel, Steven H., Tada, Yasuomi
• Format: Article
• Language: English
• Subjects: Amino Acids - toxicity; Anti-Infective Agents; Arabidopsis - drug effects; Arabidopsis - growth & development; Arabidopsis - immunology; Arabidopsis - metabolism; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; biotroph; Co-Repressor Proteins; coronatine; Cyclopentanes - pharmacology; Gene Expression Regulation, Plant - drug effects; Indenes - toxicity; jasmonic acid; MED25; MYC2; necrotroph; NPR1; Oxylipins - pharmacology; Plant Diseases - immunology; Plant Diseases - microbiology; Plant Growth Regulators - pharmacology; Plant Immunity; Proto-Oncogene Proteins c-myc - antagonists & inhibitors; Pseudomonas syringae; Pseudomonas syringae - chemistry; salicylic acid; Salicylic Acid - pharmacology; Signal Transduction
• ISSN: 2211-1247; 2211-1247
• DOI: 10.1016/j.celrep.2021.110125

Plants tailor immune responses to defend against pathogens with different lifestyles. In this process, antagonism between the immune hormones salicylic acid (SA) and jasmonic acid (JA) optimizes transcriptional signatures specifically to the attacker encountered. Antagonism is controlled by the transcription cofactor NPR1. The indispensable role of NPR1 in activating SA-responsive genes is well understood, but how it functions as a repressor of JA-responsive genes remains unclear. Here, we demonstrate that SA-induced NPR1 is recruited to JA-responsive promoter regions that are co-occupied by a JA-induced transcription complex consisting of the MYC2 activator and MED25 Mediator subunit. In the presence of SA, NPR1 physically associates with JA-induced MYC2 and inhibits transcriptional activation by disrupting its interaction with MED25. Importantly, NPR1-mediated inhibition of MYC2 is a major immune mechanism for suppressing pathogen virulence. Thus, NPR1 orchestrates the immune transcriptome not only by activating SA-responsive genes but also by acting as a corepressor of JA-responsive MYC2. [Display omitted] •NPR1 physically interacts with JA-induced MYC2 and its homologs•NPR1 is distributed to the JA-responsive promoters occupied by MYC2 and MED25•NPR1 dissociates the MYC2-MED25 interaction to repress JA-responsive gene expression•NPR1 suppresses MYC-mediated susceptibility of virulent Pseudomonas syringae Nomoto et al. demonstrate the mechanistic details of crosstalk signaling between the phytohormones salicylic acid (SA) and jasmonic acid (JA). The SA-induced immune cofactor NPR1 directly inhibits JA-induced MYC activators, suppressing the virulent effect of the phytotoxin coronatine (COR) secreted from Pseudomonas syringae.