Enhancers act to regulate cell-type-specific gene expression by facilitating the transcription of target genes. In mammalian cells, active or primed enhancers are commonly marked by monomethylation of histone H3 at lysine 4 (H3K4me1) in a cell-type-specific manner. Whether and how this histone modification regulates enhancer-dependent transcription programs in mammals is unclear. In this study, we conducted SILAC mass spectrometry experiments with mononucleosomes and identified multiple H3K4me1-associated proteins, including many involved in chromatin remodeling. We demonstrate that H3K4me1 augments association of the chromatin-remodeling complex BAF to enhancers in vivo and that, in vitro, H3K4me1-marked nucleosomes are more efficiently remodeled by the BAF complex. Crystal structures of the BAF component BAF45C indicate that monomethylation, but not trimethylation, is accommodated by BAF45C's H3K4-binding site. Our results suggest that H3K4me1 has an active role at enhancers by facilitating binding of the BAF complex and possibly other chromatin regulators.

中文翻译：

---

H3K4me1相关蛋白在哺乳动物增强子上的鉴定。

增强子通过促进靶基因的转录来调节细胞类型特异性基因的表达。在哺乳动物细胞中，通常以细胞类型特异性的方式通过组氨酸H3在赖氨酸4（H3K4me1）处的单甲基化来标记活性或引发增强剂。目前尚不清楚这种组蛋白修饰是否以及如何调节哺乳动物中依赖增强子的转录程序。在这项研究中，我们使用单核小体进行了SILAC质谱实验，并鉴定了多个H3K4me1相关蛋白，包括许多参与染色质重塑的蛋白。我们证明，H3K4me1在体内增强了染色质重塑复合物BAF与增强子的结合，并且在体外，H3K4me1标记的核小体被BAF复合物更有效地重塑了。BAF组分BAF45C的晶体结构表明单甲基化，BAF45C的H3K4结合位点可容纳三甲基化，但不能三甲基化。我们的结果表明，H3K4me1通过促进BAF复合物和可能的其他染色质调节剂的结合而在增强子中发挥积极作用。