The Arabidopsis active demethylase ROS1 cis-regulates defence genes by erasing DNA methylation at promoter-regulatory regions.
The Arabidopsis active demethylase ROS1 cis-regulates defence genes by erasing DNA methylation at promoter-regulatory regions.
复制标题
DOI：
10.7554/elife.62994
复制
发表时间：
2021-01-20
期刊：
影响因子：
7.7
通讯作者：
Navarro L
中科院分区：
文献类型：
--
作者：
Halter T;Wang J;Amesefe D;Lastrucci E;Charvin M;Singla Rastogi M;Navarro L
主动DNA去甲基化已成为植物和哺乳动物免疫的重要调节过程。然而，关于主动去甲基化控制转录免疫重编程和抗病性的机制知之甚少。在这里，我们首先表明，拟南芥活性脱甲基酶ROS1通过拮抗RNA指导的DNA甲基化（RdDM）促进对假单胞菌的基础抗性。此外，我们证明，ROS1有利于鞭毛蛋白触发的抗病基因RMG 1的诱导限制RdDM在3'边界的转座因子（TE）衍生的重复嵌入其启动子。我们进一步确定了鞭毛蛋白响应ROS1推定的主要目标，并表明在启动子的子集，ROS1擦除甲基化在离散区域表现出WRKY转录因子（TF）的结合。特别是，我们证明了ROS1去除了孤儿免疫受体RLP43启动子的甲基化，以确保WRKY TF的DNA结合。最后，我们表明，ROS1指导的RMG 1和RLP43启动子的去甲基化是这些基因的鞭毛蛋白反应和基础抗性的原因。总的来说，这些发现大大推进了我们对活性脱甲基酶如何塑造转录免疫重编程以实现抗菌药物耐药性的理解。
Active DNA demethylation has emerged as an important regulatory process of plant and mammalian immunity. However, very little is known about the mechanisms by which active demethylation controls transcriptional immune reprogramming and disease resistance. Here, we first show that the Arabidopsis active demethylase ROS1 promotes basal resistance towards Pseudomonas syringae by antagonizing RNA-directed DNA methylation (RdDM). Furthermore, we demonstrate that ROS1 facilitates the flagellin-triggered induction of the disease resistance gene RMG1 by limiting RdDM at the 3' boundary of a transposable element (TE)-derived repeat embedded in its promoter. We further identify flagellin-responsive ROS1 putative primary targets and show that at a subset of promoters, ROS1 erases methylation at discrete regions exhibiting WRKY transcription factors (TFs) binding. In particular, we demonstrate that ROS1 removes methylation at the orphan immune receptor RLP43 promoter, to ensure DNA binding of WRKY TFs. Finally, we show that ROS1-directed demethylation of RMG1 and RLP43 promoters is causal for both flagellin responsiveness of these genes and for basal resistance. Overall, these findings significantly advance our understanding of how active demethylases shape transcriptional immune reprogramming to enable antibacterial resistance.