Bode Daniel, Yu Lu, Tate Peri, Pardo Mercedes, Choudhary Jyoti
From the ‡Proteomic Mass Spectrometry, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK;
§Stem Cell Engineering, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK.
Mol Cell Proteomics. 2016 Mar;15(3):878-91. doi: 10.1074/mcp.M115.053207. Epub 2015 Dec 29.
Pluripotency and self-renewal, the defining properties of embryonic stem cells, are brought about by transcriptional programs involving an intricate network of transcription factors and chromatin remodeling complexes. The Nucleosome Remodeling and Deacetylase (NuRD) complex plays a crucial and dynamic role in the regulation of stemness and differentiation. Several NuRD-associated factors have been reported but how they are organized has not been investigated in detail. Here, we have combined affinity purification and blue native polyacrylamide gel electrophoresis followed by protein identification by mass spectrometry and protein correlation profiling to characterize the topology of the NuRD complex. Our data show that in mouse embryonic stem cells the NuRD complex is present as two distinct assemblies of differing topology with different binding partners. Cell cycle regulator Cdk2ap1 and transcription factor Sall4 associate only with the higher mass NuRD assembly. We further establish that only isoform Sall4a, and not Sall4b, associates with NuRD. By contrast, Suz12, a component of the PRC2 Polycomb repressor complex, associates with the lower mass entity. In addition, we identify and validate a novel NuRD-associated protein, Wdr5, a regulatory subunit of the MLL histone methyltransferase complex, which associates with both NuRD entities. Bioinformatic analyses of published target gene sets of these chromatin binding proteins are in agreement with these structural observations. In summary, this study provides an interesting insight into mechanistic aspects of NuRD function in stem cell biology. The relevance of our work has broader implications because of the ubiquitous nature of the NuRD complex. The strategy described here can be more broadly applicable to investigate the topology of the multiple complexes an individual protein can participate in.
多能性和自我更新是胚胎干细胞的决定性特性,它们由涉及转录因子和染色质重塑复合物复杂网络的转录程序所引发。核小体重塑与去乙酰化酶(NuRD)复合物在干性和分化的调控中发挥着关键且动态的作用。已有若干与NuRD相关的因子被报道,但它们的组织方式尚未得到详细研究。在此,我们将亲和纯化与蓝色非变性聚丙烯酰胺凝胶电泳相结合,随后通过质谱进行蛋白质鉴定以及蛋白质相关性分析,以表征NuRD复合物的拓扑结构。我们的数据表明,在小鼠胚胎干细胞中,NuRD复合物以两种具有不同拓扑结构且结合不同伙伴的不同组装形式存在。细胞周期调节因子Cdk2ap1和转录因子Sall4仅与较高分子量的NuRD组装体相关联。我们进一步证实,只有Sall4a亚型而非Sall4b与NuRD相关联。相比之下,PRC2多梳抑制复合物的一个组分Suz12与较低分子量的实体相关联。此外,我们鉴定并验证了一种新的与NuRD相关的蛋白质Wdr5,它是MLL组蛋白甲基转移酶复合物的一个调节亚基,与两种NuRD实体都相关联。对这些染色质结合蛋白已发表的靶基因集进行的生物信息学分析与这些结构观察结果一致。总之,本研究为干细胞生物学中NuRD功能的机制方面提供了有趣的见解。由于NuRD复合物的普遍存在,我们工作的相关性具有更广泛的意义。这里描述的策略可更广泛地应用于研究单个蛋白质可参与的多种复合物的拓扑结构。