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活性 DNA 去甲基化调控拟南芥中模式触发免疫的起始。

Active DNA demethylation regulates MAMP-triggered immune priming in Arabidopsis.

机构信息

State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei 430070, China; The Provincial Key Lab of Plant Pathology of Hubei Province, College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, Hubei 430070, China; Hubei Hongshan Laboratory, Wuhan, Hubei 430070, China.

State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei 430070, China; The Provincial Key Lab of Plant Pathology of Hubei Province, College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, Hubei 430070, China.

出版信息

J Genet Genomics. 2022 Aug;49(8):796-809. doi: 10.1016/j.jgg.2022.02.021. Epub 2022 Mar 12.

DOI:10.1016/j.jgg.2022.02.021
PMID:35288370
Abstract

Plants recognize microbe-associated molecular patterns (MAMPs) to activate immune responses and defense priming to defend against pathogen infections. Transcriptional regulation of gene expression is crucial for plant immunity and is mediated by multiple factors, including DNA methylation. However, it remains unknown whether and how DNA demethylation contributes to immune responses in MAMP-triggered immunity. Here, we report that active DNA demethylation is required for MAMP-triggered immunity to bacterial pathogens. The rdd-2 triple mutant carrying mutations in ROS1, DML2, and DML3 that encode DNA glycosylases, which are key DNA demethylation enzymes, exhibits compromised immune responses triggered by the MAMPs flg22 and elf18. Genome-wide methylome analysis reveals that flg22 induces rapid and specific DNA demethylation in an RDD-dependent manner. The expression levels of salicylic acid signaling-related and phytoalexin biosynthesis-related genes are tightly associated with the flg22-induced promoter demethylation. The compromised accumulation of priming compounds and antimicrobial metabolites ultimately leads to a defense priming defect in the rdd-2 mutant. Our results reveal the critical role of active DNA demethylation in the MAMP-triggered immune response and provide unique insight into the molecular mechanism of flg22-modulated DNA demethylation.

摘要

植物通过识别微生物相关分子模式(MAMPs)来激活免疫反应和防御前馈,以抵御病原体感染。基因表达的转录调控对于植物免疫至关重要,它受到多种因素的介导,包括 DNA 甲基化。然而,目前尚不清楚 DNA 去甲基化是否以及如何参与 MAMP 触发的免疫反应。在这里,我们报告称,活性 DNA 去甲基化是 MAMP 触发细菌病原体免疫反应所必需的。携带编码 DNA 糖苷酶的 ROS1、DML2 和 DML3 突变的 rdd-2 三重突变体,其突变体是关键的 DNA 去甲基化酶,表现出对 MAMPs flg22 和 elf18 触发的免疫反应受损。全基因组甲基组分析表明,flg22 以 RDD 依赖的方式诱导快速和特异性的 DNA 去甲基化。水杨酸信号相关和植物抗毒素生物合成相关基因的表达水平与 flg22 诱导的启动子去甲基化密切相关。引发化合物和抗菌代谢物积累的缺陷最终导致 rdd-2 突变体的防御前馈缺陷。我们的研究结果揭示了活性 DNA 去甲基化在 MAMP 触发免疫反应中的关键作用,并为 flg22 调节的 DNA 去甲基化的分子机制提供了独特的见解。

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