N6-methyladenosine (m6 A) is the most abundant mRNA chemical modification, and is modulated by m6 A‘writers’, ‘erasers’ and ‘readers’ proteins [1-3]. In vitro experiments suggest that m6 A regulates several aspects of RNA metabolism, including RNA decay, splicing and translation [1]. Recent genetic analyses in vivo showed that m6 A functions in sex determination in Drosophila [4,5], in maternal-to-zygotic transition and haematopoietic stem cell specification during zebrafish embryogenesis [6, 7], in mouse spermatogenesis [8-10], and in mouse brain development [11]. We recently discovered that lineage-specific deletion of the m6 A ‘writer’ enzyme METTL3 in CD4+ T cells (Mettl3f/f; CD4-Cre) led to disruption of naïve T cell homeostasis [12]. CD4+ regulatory T cells (Tregs) comprise a critical subset of effector T cells, which are involved in resolution of inflammation and immunosuppression in tumor microenvironments [13]. However, the potential roles of m6 A mRNA modification in Treg functions in vivo are unknown.

中文翻译：

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m6 A mRNA 甲基化维持 Treg 抑制功能

N6-甲基腺苷 (m6 A) 是最丰富的 mRNA 化学修饰，由 m6 A'writers'、'erasers' 和 'readers' 蛋白调节 [1-3]。体外实验表明，m6 A 调节 RNA 代谢的多个方面，包括 RNA 衰变、剪接和翻译 [1]。最近的体内遗传分析表明，m6 A 在果蝇性别决定中发挥作用 [4,5]、斑马鱼胚胎发生过程中的母体到合子转变和造血干细胞特化 [6, 7]、小鼠精子发生 [8-10] ，以及小鼠大脑发育 [11]。我们最近发现 CD4+ T 细胞 (Mettl3f/f; CD4-Cre) 中 m6 A 'writer' 酶 METTL3 的谱系特异性缺失导致幼稚 T 细胞稳态的破坏 [12]。CD4+ 调节性 T 细胞 (Tregs) 包括效应 T 细胞的关键子集，参与解决肿瘤微环境中的炎症和免疫抑制 [13]。然而，m6 A mRNA 修饰在体内 Treg 功能中的潜在作用尚不清楚。