Suppression of MYC transcription activators by the immune cofactor NPR1 fine-tunes plant immune responses
Suppression of MYC transcription activators by the immune cofactor NPR1 fine-tunes plant immune responses
复制标题
DOI：
10.1016/j.celrep.2021.110125
复制
发表时间：
2021-12-14
期刊：
影响因子：
8.8
通讯作者：
Tada, Yasuomi
中科院分区：
文献类型：
--
作者：
Nomoto, Mika;Skelly, Michael J.;Tada, Yasuomi
植物调整免疫反应，以抵御不同生活方式的病原体。在这个过程中，免疫激素水杨酸（SA）和茉莉酸（JA）之间的拮抗作用优化了针对攻击者的转录特征。拮抗作用由转录辅因子NPR 1控制。NPR1在激活SA应答基因中不可或缺的作用已被充分理解，但它如何作为JA应答基因的阻遏物发挥作用仍不清楚。在这里，我们证明SA诱导的NPR1被招募到JA响应启动子区域，该区域被由MYC2激活剂和MED25介体亚基组成的JA诱导的转录复合物共同占据。在SA存在下，NPR 1与JA诱导的MYC 2物理结合，并通过破坏其与MED25的相互作用来抑制转录激活。重要的是，NPR1介导的MYC2抑制是抑制病原体毒力的主要免疫机制。因此，NPR 1不仅通过激活SA应答基因，而且通过充当JA应答MYC 2的辅阻遏物来协调免疫转录组。
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.