N6-甲基腺嘌呤（m6A）和可选择性多聚腺苷酸化（APA）在基因表达调控上扮演重要功能，近来研究表明m6A与APA调控密切相关，但是具体的调控机制仍不清楚。我们前期已证明m6A识别蛋白YTHDC1可以调控APA，YTHDC1与3'末端加工核心蛋白FIP1L1存在直接作用，并且发现YTHDC1与FIP1L1的互作方式具有明显“相分离”的特征。据此，我们推测m6A识别蛋白YTHDC1可能与FIP1L1以“相分离”互作的模式调控APA。本项目欲通过基因编辑、体外蛋白表达与纯化、超分辨显成像、APA与iCLIP高通量测序等技术研究YTHDC1与FIP1L1”相分离“互作调控APA的规律，鉴定“相分离”相互作用的关键位点，明确两者”相分离“调控APA的分子机制。本项目首次从“相分离”的角度解析转录终止调控的机制，为研究APA的分子机制提供了全新的方向。

Both N6-methyl adenine (m6A) and APA play an important role in gene expression regulation, and recent studies have shown that m6A is closely related to APA regulation, but the specific regulatory mechanism is still obscure. We have previously proved that m6A reader YTHDC1 can regulate APA, YTHDC1 interacts directly with 3 'end processing factor FIP1L1 in a way of phase separation. We speculate that m6A reader YTHDC1 and FIP1L1 may regulate APA in a phase separation mode. Applied with gene editing, in vitro protein expression and purification, super-resolution imaging, high-throughput sequencing of APA and iCLIP, this project aims to analyze the role of phase separation between YTHDC1 and FIP1L1 on regulation of APA, identification the key interacting sites, and clarify the molecular mechanism of phase separation regulating APA. This is the first project studies the mechanism of transcription termination from the angle of phase separation, which shed a light on novel direction for studying the molecular mechanism of APA.