N6-methyladenosine (m6A) is the most prevalent, conserved, and abundant RNA modification of the mRNAs of most eukaryotes, including mammals. Similar to epigenetic DNA modifications, m6A has been proposed to function as a critical regulator for gene expression. This modification is installed by m6A methylation “writers” (Mettl3/Mettl14 methyltransferase complex), and it can be reversed by demethylase “erasers” (Fto and Alkbh5). Furthermore, m6A can be recognized by “readers” (Ythdf and Ythdc families), which may be interpreted to affect mRNA splicing, stability, translation or localization. Levels of m6A methylation appear to be highest in the brain, where it plays important functions during embryonic stem cell differentiation, brain development, and neurodevelopmental disorders. Depletion of the m6A methylation writer Mettl14 from mouse embryonic nervous systems prolongs cell cycle progression of radial glia and extends cortical neurogenesis into postnatal stages. Recent studies further imply that dysregulated m6A methylation may be significantly correlated with neurodegenerative diseases. In this review, we give an overview of m6A modifications during neural development and associated disorders, and provide perspectives for studying m6A methylation.

中文翻译：

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m6A 表观转录组对神经发育和退化的影响

N6-甲基腺苷 (m6A) 是大多数真核生物（包括哺乳动物）mRNA 中最普遍、最保守和最丰富的 RNA 修饰。与表观遗传 DNA 修饰类似，m6A 已被提议作为基因表达的关键调节因子。这种修饰是由 m6A 甲基化“写入器”（Mettl3/Mettl14 甲基转移酶复合物）安装的，它可以被去甲基化酶“擦除器”（Fto 和 Alkbh5）逆转。此外，m6A 可以被“阅读器”（Ythdf 和 Ythdc 家族）识别，这可能会被解释为影响 mRNA 的剪接、稳定性、翻译或定位。m6A 甲基化水平似乎在大脑中最高，它在胚胎干细胞分化、大脑发育和神经发育障碍过程中发挥重要作用。小鼠胚胎神经系统中 m6A 甲基化编写器 Mettl14 的消耗延长了放射状胶质细胞的细胞周期进程，并将皮层神经发生延伸到出生后阶段。最近的研究进一步暗示 m6A 甲基化失调可能与神经退行性疾病显着相关。在这篇综述中，我们概述了神经发育和相关疾病过程中的 m6A 修饰，并提供了研究 m6A 甲基化的观点。