Barley MLA Immune Receptors Directly Interfere with Antagonistically Acting Transcription Factors to Initiate Disease Resistance Signaling
Barley MLA Immune Receptors Directly Interfere with Antagonistically Acting Transcription Factors to Initiate Disease Resistance Signaling
复制标题
大麦 MLA 免疫受体直接干扰拮抗作用的转录因子以启动抗病信号
DOI：
10.1105/tpc.113.109942
复制
发表时间：
2013-03-01
期刊：
影响因子：
11.6
通讯作者：
Shen, Qian-Hua
中科院分区：
文献类型：
--
作者：
Chang, Cheng;Yu, Deshui;Shen, Qian-Hua
植物和动物的核苷酸结合域和富含亮氨酸重复序列（NLR）的蛋白介导宿主细胞内的病原体感知，并引发针对微生物病原体的先天免疫反应。大麦（Hordeum vulgare）霉A （MLA）基因座编码介导对白粉病病原菌蓝灰菌（Blumeria graminis）抗性的卷曲卷曲（CC）型NLRs。在这里，我们报告了MLA与两个拮抗转录因子MYB6和WRKY1之间的直接相互作用。MLA的n端CC信号域与MYB6相互作用，刺激其DNA结合活性。MYB6在基础和mla介导的对禾本科芽孢杆菌的免疫应答中起积极调节作用。MYB6 DNA结合被WRKY1阻遏因子直接拮抗，而WRKY1阻遏因子反过来又与MLA CC结构域相互作用。激活形式的全长MLA10受体是释放MYB6激活因子从WRKY1抑制和刺激MYB6依赖基因表达所必需的。这表明，虽然在静止免疫受体存在的情况下，MYB6被WRKY1抑制因子隔离，但在先天免疫应答的转录重编程过程中，MYB6作为MLA活性状态的直接和积极的激活后信号传导成分。
The nucleotide binding domain and Leucine-rich repeat (NLR)-containing proteins in plants and animals mediate pathogen sensing inside host cells and mount innate immune responses against microbial pathogens. The barley (Hordeum vulgare) mildew A (MLA) locus encodes coiled-coil (CC)-type NLRs mediating disease resistance against the powdery mildew pathogen Blumeria graminis. Here, we report direct interactions between MLA and two antagonistically acting transcription factors, MYB6 and WRKY1. The N-terminal CC signaling domain of MLA interacts with MYB6 to stimulate its DNA binding activity. MYB6 functions as a positive regulator of basal and MLA-mediated immunity responses to B. graminis. MYB6 DNA binding is antagonized by direct association with WRKY1 repressor, which in turn also interacts with the MLA CC domain. The activated form of full-length MLA10 receptor is needed to release MYB6 activator from WRKY1 repression and to stimulate MYB6-dependent gene expression. This implies that, while sequestered by the WRKY1 repressor in the presence of the resting immune receptor, MYB6 acts as an immediate and positive postactivation signaling component of the active state of MLA during transcriptional reprogramming for innate immune responses.