ROS1介导的DNA去甲基化途径拮抗RdDM途径产生的DNA甲基化。分析表明约1/4的RdDM途径靶位点与ROS1靶位点重合。本研究鉴定到一个新蛋白DRB7.2，它突变后导致基因组3863个位点发生超甲基化，其中有1456个位点与ros1-7的超甲基化位点重合，表明DRB7.2参与ROS1介导的DNA去甲基化途径。DRB7.2含有一个双链RNA结合结构域，drb7.2突变体中Pol IV 24-nt siRNA含量明显增加，表明DRB7.2在体内结合众多源自Pol IV 转录位点的siRNA前体。DRB7.2与MBD7有蛋白相互作用，推测DRB7.2-Pol IV siRNA前体复合物引导IDM1复合体准确结合到靶作用位点，乙酰化组蛋白，从而招募ROS1到达此位点去除甲基化。本研究将进一步通过IP-seq、ChIP-seq等技术深入解析DRB7.2如何参与ROS1介导的DNA去甲基化途径。

ROS1-mediated DNA demethylation pathway plays important roles in antagonizing DNA methylation generated by RNA-directed DNA methylation (RdDM) pathway. Our analysis revealed that approximately one fourth of RdDM target loci overlap with ROS1 target loci. In this study, we identified a novel protein DRB7.2 through the 2×35S:LUC genetic screening system. Mutation of DRB7.2 leads to 3863 hypermethylated loci in drb7.2-2 mutant, and 1456 out of such hypermethylated loci overlap with the hypermethylated loci in ros1-7 mutant, suggesting that DRB7.2 participates in the ROS1-mediated DNA demethylation pathway. DRB7.2 possesses a dsRNA binding motif (dsRBM) and is able to bind dsRNA precursor in vivo. In the drb7.2-2 mutant, the abundance of Pol IV 24-nt siRNA is dramatically increased, indicating that DRB7.2 binds various species of Pol IV siRNA precursors to form DRB7.2-Pol IV siRNA precursor complex. DRB7.2 was found to directly interact with MBD7, implying that DRB7.2-Pol IV siRNA precursor complex may accurately guide IDM1-IDM2-IDM3-HDP1/2-MBD7 complex (i.e. IDM1 complex) to target loci through protein-protein interaction. Subsequently, the IDM1 complex acetylates histone H3K18 and K23 of the target loci, which in the end recruits ROS1 to such loci for DNA demethylation in an as yet unknown manner. To test this hypothesis, we are going to conduct more investigations into the mechanisms of how DRB7.2 is involved in ROS1-mediated DNA demethylation pathway by using IP-seq, ChIP-seq and other techniques.