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

Cell Reports

Michael J. Skelly¹  Mutsutomo Tokizawa²  Yasuomi Tada³  Steven H. Spoel⁴  Takamasa Suzuki⁴  Tsuyoshi Mori⁴  Mika Nomoto⁴  Hironaka Tsukagoshi⁵  Hitoshi Mori⁵  Tetsuya Higashiyama⁶  Keiko Kuwata⁷  Tomotaka Itaya⁸  Yoshiharu Y. Yamamoto⁹  Tomonao Matsushita^1,10 

[1] Center for Gene Research, Nagoya University, Chikusa, Nagoya, Aichi 464-8602, Japan;College of Bioscience and Biotechnology, Chubu University, Aichi 487-8501, Japan;JST ERATO Higashiyama Live-Holonics Project, Nagoya University, Chikusa, Nagoya, Aichi 464-8602, Japan;Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa, Nagoya, Aichi 464-8602, Japan;Faculty of Applied Biological Sciences, Gifu University, Gifu 501-1193, Japan;Graduate School of Agriculture, Nagoya University, Chikusa, Nagoya, Aichi 464-8601, Japan;Graduate School of Science, Kyoto University, Sakyo, Kyoto 606-8502, Japan;Institute of Molecular Plant Sciences, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3BF, UK;Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University, Chikusa, Nagoya, Aichi 464-8602, Japan;JST ERATO Higashiyama Live-Holonics Project, Nagoya University, Chikusa, Nagoya, Aichi 464-8602, Japan;

关键词: plant immunity;    salicylic acid;    jasmonic acid;    coronatine;    biotroph;    necrotroph;   

DOI  :  

来源: DOAJ

【 摘 要 】

Summary: 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.

【 授权许可】

Unknown