Epigenetic regulation is a critical component of lineage determination. Adipogenesis is the process through which uncommitted stem cells or adipogenic precursor cells differentiate into adipocytes, the most abundant cell type of the adipose tissue. Studies examining chromatin modification during adipogenesis have provided further understanding of the molecular blueprint that controls the onset of adipogenic differentiation. Unlike histone acetylation, histone methylation has context dependent effects on the activity of a transcribed region of DNA, with individual or combined marks on different histone residues providing distinct signals for gene expression. Over half of the 42 histone methyltransferases identified in mammalian cells have been investigated in their role during adipogenesis, but across the large body of literature available, there is a lack of clarity over potential correlations or emerging patterns among the different players. In this review, we will summarize important findings from studies published in the past 15 years that have investigated the role of histone methyltransferases during adipogenesis, including both protein arginine methyltransferases (PRMTs) and lysine methyltransferases (KMTs). We further reveal that PRMT1/4/5, H3K4 KMTs (MLL1, MLL3, MLL4, SMYD2 and SET7/9) and H3K27 KMTs (EZH2) all play positive roles during adipogenesis, while PRMT6/7 and H3K9 KMTs (G9a, SUV39H1, SUV39H2, and SETDB1) play negative roles during adipogenesis.

中文翻译：

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组蛋白甲基转移酶调节脂肪生成

表观遗传调控是谱系决定的关键组成部分。脂肪生成是未定型干细胞或脂肪形成前体细胞分化为脂肪细胞（脂肪组织中最丰富的细胞类型）的过程。检查脂肪形成过程中染色质修饰的研究进一步了解了控制脂肪形成分化开始的分子蓝图。与组蛋白乙酰化不同，组蛋白甲基化对 DNA 转录区域的活性具有上下文依赖性影响，不同组蛋白残基上的单独或组合标记为基因表达提供不同的信号。在哺乳动物细胞中鉴定的 42 种组蛋白甲基转移酶中，有一半以上已对其在脂肪形成过程中的作用进行了研究，但在现有的大量文献中，不同参与者之间的潜在相关性或新出现的模式缺乏明确性。在这篇综述中，我们将总结过去 15 年发表的研究的重要发现，这些研究调查了组蛋白甲基转移酶在脂肪形成过程中的作用，包括蛋白质精氨酸甲基转移酶 (PRMT) 和赖氨酸甲基转移酶 (KMT)。我们进一步发现，PRMT1/4/5、H3K4 KMT（MLL1、MLL3、MLL4、SMYD2 和 SET7/9）和 H3K27 KMT（EZH2）都在脂肪生成过程中发挥积极作用，而 PRMT6/7 和 H3K9 KMT（G9a、SUV39H1、 SUV39H2 和 SETDB1) 在脂肪生成过程中发挥负面作用。