Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec H3G 1Y6, Canada.
J Biol Chem. 2012 Jun 1;287(23):19040-7. doi: 10.1074/jbc.M112.356253. Epub 2012 Apr 13.
The methylation of histone H3 at lysine 4 (H3K4me) is critical for the formation of transcriptionally active chromatin in eukaryotes. In yeast, Drosophila, and some human cell lines, H3K4me is globally stimulated by the monoubiquitylation of histone H2B (H2Bub1), another histone modification associated with transcription. The mechanism of this "trans-histone" modification pathway remains uncertain, and studies carried out in different experimental systems have suggested that H2Bub1 could either influence the subunit composition of methyltransferase complexes or directly stimulate methyltransferase activity. We have reconstituted this pathway in vitro using the native H3K4-specific methyltransferase complex Set1C purified from the fission yeast Schizosaccharomyces pombe and chromatin substrates that contain semisynthetic H2Bub1. We found that the activity of S. pombe Set1C toward nucleosomal histone H3 is directly enhanced by H2Bub1 in vitro. Importantly, Set1C purified from cells lacking H2Bub1 retained activity on free histone substrates, suggesting that Set1C remains intact in the absence of H2Bub1. Chromatin immunoprecipitation assays revealed a defect in recruitment of intact Set1C to transcribed chromatin in H2Bub1-deficient mutants. Our data argue that trans-histone crosstalk in S. pombe involves direct enhancement of Set1C methyltransferase activity by H2Bub1 and suggest that this represents a conserved aspect of H2Bub1-H3K4me crosstalk in eukaryotes.
组蛋白 H3 赖氨酸 4 位的甲基化(H3K4me)对于真核生物转录活性染色质的形成至关重要。在酵母、果蝇和一些人类细胞系中,组蛋白 H2B 的单泛素化(H2Bub1)全局刺激 H3K4me,H2Bub1 是另一种与转录相关的组蛋白修饰。这种“跨组蛋白”修饰途径的机制仍不确定,并且在不同实验系统中进行的研究表明,H2Bub1 可以影响甲基转移酶复合物的亚基组成,或者直接刺激甲基转移酶活性。我们使用从裂殖酵母 Schizosaccharomyces pombe 中纯化的天然 H3K4 特异性甲基转移酶复合物 Set1C 和包含半合成 H2Bub1 的染色质底物在体外重新构建了这条途径。我们发现,H2Bub1 在体外直接增强 S. pombe Set1C 对核小体组蛋白 H3 的活性。重要的是,从缺乏 H2Bub1 的细胞中纯化的 Set1C 在游离组蛋白底物上保留活性,表明在没有 H2Bub1 的情况下 Set1C 保持完整。染色质免疫沉淀测定显示,在 H2Bub1 缺陷突变体中,完整的 Set1C 向转录染色质的募集存在缺陷。我们的数据表明,裂殖酵母中的跨组蛋白串扰涉及 H2Bub1 对 Set1C 甲基转移酶活性的直接增强,并表明这代表了真核生物中 H2Bub1-H3K4me 串扰的一个保守方面。