PDF(Pubmed)
Abstract：
Plant intracellular nucleotide-binding domain, leucine-rich repeat-containing receptors (NLRs) activate a robust immune response upon detection of pathogen effectors. How NLRs induce downstream immune defense genes remains poorly understood. The Mediator complex plays a central role in transducing signals from gene-specific transcription factors to the transcription machinery for gene transcription/activation. In this study, we demonstrate that MED10b and MED7 of the Mediator complex mediate jasmonate-dependent transcription repression, and coiled-coil NLRs (CNLs) in Solanaceae modulate MED10b/MED7 to activate immunity. Using the tomato CNL Sw-5b, which confers resistance to tospovirus, as a model, we found that the CC domain of Sw-5b directly interacts with MED10b. Knockout/down of MED10b and other subunits including MED7 of the middle module of Mediator activates plant defense against tospovirus. MED10b was found to directly interact with MED7, and MED7 directly interacts with JAZ proteins, which function as transcriptional repressors of jasmonic acid (JA) signaling. MED10b-MED7-JAZ together can strongly repress the expression of JA-responsive genes. The activated Sw-5b CC interferes with the interaction between MED10b and MED7, leading to the activation of JA-dependent defense signaling against tospovirus. Furthermore, we found that CC domains of various other CNLs including helper NLR NRCs from Solanaceae modulate MED10b/MED7 to activate defense against different pathogens. Together, our findings reveal that MED10b/MED7 serve as a previously unknown repressor of jasmonate-dependent transcription repression and are modulated by diverse CNLs in Solanaceae to activate the JA-specific defense pathways.
摘要：
植物细胞内核苷酸结合域，富含亮氨酸的含重复序列的受体（NLR）在检测到病原体效应物时激活强大的免疫反应。NLR如何诱导下游免疫防御基因仍然知之甚少。介体复合物在将信号从基因特异性转录因子传导到基因转录/激活的转录机制中起着核心作用。在这项研究中,我们证明介体复合物的MED10b和MED7介导茉莉酸依赖性转录抑制，茄科植物中的卷曲螺旋NLR（CNL）调节MED10b/MED7以激活免疫。使用番茄CNLSw-5b，赋予病毒抗性，作为一个模型，我们发现Sw-5b的CC域与MED10b直接相互作用。敲除/降低MED10b和其他亚基，包括Mediator中间模块的MED7，可激活植物对topspovirus的防御。发现MED10b与MED7直接相互作用，MED7与JAZ蛋白直接相互作用，其作为茉莉酸（JA）信号的转录阻遏物。MED10b-MED7-JAZ一起可以强烈抑制JA应答基因的表达。激活的Sw-5bCC干扰MED10b和MED7之间的相互作用，导致激活JA依赖的针对tspovirus的防御信号。此外，我们发现，包括来自茄科的辅助NLRNRC在内的各种其他CNL的CC结构域调节MED10b/MED7以激活对不同病原体的防御。一起,我们的发现表明，MED10b/MED7是茉莉酸依赖性转录抑制的先前未知的阻遏物，并受到茄科中多种CNL的调节，以激活JA特异性防御途径。
