Fulton Melody D, Zhang Jing, He Maomao, Ho Meng-Chiao, Zheng Y George
Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, The University of Georgia , Athens, Georgia 30602, United States.
Institute of Biological Chemistry, Academia Sinica , Taipei 115, Taiwan.
Biochemistry. 2017 Jul 18;56(28):3539-3548. doi: 10.1021/acs.biochem.7b00450. Epub 2017 Jul 7.
Chemical modifications of the DNA and nucleosomal histones tightly control the gene transcription program in eukaryotic cells. The "histone code" hypothesis proposes that the frequency, combination, and location of post-translational modifications (PTMs) of the core histones compose a complex network of epigenetic regulation. Currently, there are at least 23 different types and >450 histone PTMs that have been discovered, and the PTMs of lysine and arginine residues account for a crucial part of the histone code. Although significant progress has been achieved in recent years, the molecular basis for the histone code is far from being fully understood. In this study, we investigated how naturally occurring N-terminal acetylation and PTMs of histone H4 lysine-5 (H4K5) affect arginine-3 methylation catalyzed by both type I and type II PRMTs at the biochemical level. Our studies found that acylations of H4K5 resulted in decreased levels of arginine methylation by PRMT1, PRMT3, and PRMT8. In contrast, PRMT5 exhibits an increased rate of arginine methylation upon H4K5 acetylation, propionylation, and crotonylation, but not upon H4K5 methylation, butyrylation, or 2-hydroxyisobutyrylation. Methylation of H4K5 did not affect arginine methylation by PRMT1 or PRMT5. There was a small increase in the rate of arginine methylation by PRMT8. Strikingly, a marked increase in the rate of arginine methylation was observed for PRMT3. Finally, N-terminal acetylation reduced the rate of arginine methylation by PRMT3 but had little influence on PRMT1, -5, and -8 activity. These results together highlight the underlying mechanistic differences in substrate recognition among different PRMTs and pave the way for the elucidation of the complex interplay of histone modifications.
DNA和核小体组蛋白的化学修饰紧密控制着真核细胞中的基因转录程序。“组蛋白密码”假说提出,核心组蛋白翻译后修饰(PTM)的频率、组合和位置构成了一个复杂的表观遗传调控网络。目前,已发现至少23种不同类型且超过450种组蛋白PTM,赖氨酸和精氨酸残基的PTM在组蛋白密码中占关键部分。尽管近年来已取得显著进展,但组蛋白密码的分子基础仍远未完全阐明。在本研究中,我们在生化水平上研究了组蛋白H4赖氨酸-5(H4K5)天然存在的N端乙酰化和PTM如何影响I型和II型蛋白质精氨酸甲基转移酶(PRMT)催化的精氨酸-3甲基化。我们的研究发现,H4K5的酰化导致PRMT1、PRMT3和PRMT8催化的精氨酸甲基化水平降低。相反,PRMT5在H4K5乙酰化、丙酰化和巴豆酰化时精氨酸甲基化速率增加,但在H4K5甲基化、丁酰化或2-羟基异丁酰化时则不然。H4K5甲基化不影响PRMT1或PRMT5催化的精氨酸甲基化。PRMT8催化的精氨酸甲基化速率略有增加。引人注目的是,观察到PRMT3催化的精氨酸甲基化速率显著增加。最后,N端乙酰化降低了PRMT3催化的精氨酸甲基化速率,但对PRMT1、-5和-8的活性影响很小。这些结果共同突出了不同PRMT在底物识别方面潜在的机制差异,并为阐明组蛋白修饰的复杂相互作用铺平了道路。