在早期发育过程中，表观遗传图谱在胚胎发育过程中有着非常动态的变化。之前的研究表明TGF-β超家族信号通路可以与表观遗传图谱crosstalk从而调控有时空特异性的早期决定分化因子的表达。鉴于目前还没有针对BMP信号通路中特异的染色质解码蛋白的研究，我们以小鼠胚胎干细胞为研究对象，通过Smad1亲和层析结合质谱分析技术，鉴定出了一系列与Smad1互作的染色质相关蛋白。初步研究鉴定了一个与Smad1互作的新型甲基化DNA解码蛋白Hint37，它会影响经典BMP信号通路靶基因的表达，缺失Hint37基因的小鼠胚胎干细胞表现出多个细胞命运谱系分化能力的缺陷。这意味着Hint37可以在表观遗传水平调控BMP信号通路。.我们的研究将致力于解析Hint37如何在表观遗传水平调节BMP信号通路，特别是BMP信号通路如何识别DNA甲基化修饰而影响胚胎早期发育。

During embryonic development, dynamic changes of epigenetic landscape are tightly associated with cell differentiation of different lineages. Our previous work has demonstrated that TGF-β signaling crosstalks with epigenetic landscape through a chromatin reader Trim33 and thereby regulates expression of master differentiation regulators. However, little is known about the crosstalk between BMP signaling and cell epigenetic landscape. Toward this end, we utilized Smad1, a key player of BMP signaling, as bait to identify its interacting partners through affinity purification followed by mass spectrometry analysis. The preliminary results revealed several Smad1-interacting candidates that function as chromatin readers. One of the candidates, which we named Hint37, is functionally linked to transcriptional up regulation of BMP responsive genes Id1/2/3. Using mouse embryonic stem cells and Hint37 knock out mouse model, I propose to investigate how the chromatin reader Hint37 mediated epigenetic regulation of BMP signaling during embryonic development, and to decipher the molecular mechanism by which Hint37 regulates expression of its target genes.