| Literature DB >> 34910911 |
Mika Nomoto1, Michael J Skelly2, Tomotaka Itaya3, Tsuyoshi Mori3, Takamasa Suzuki4, Tomonao Matsushita5, Mutsutomo Tokizawa6, Keiko Kuwata7, Hitoshi Mori8, Yoshiharu Y Yamamoto6, Tetsuya Higashiyama9, Hironaka Tsukagoshi10, Steven H Spoel11, Yasuomi Tada12.
Abstract
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.Entities:
Keywords: MED25; MYC2; NPR1; Pseudomonas syringae; biotroph; coronatine; jasmonic acid; necrotroph; plant immunity; salicylic acid
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Year: 2021 PMID: 34910911 DOI: 10.1016/j.celrep.2021.110125
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423