N6-methyladenosine (m6A) represents one of the most common RNA modifications in eukaryotes. Specific m6A writer, eraser, and reader proteins have been identified. As an m6A eraser, ALKBH5 specifically removes m6A from target mRNAs and inactivation of Alkbh5 leads to male infertility in mice. However, the underlying molecular mechanism remains unknown. Here, we report that ALKBH5-mediated m6A erasure in the nuclei of spermatocytes and round spermatids is essential for correct splicing and the production of longer 3′-UTR mRNAs, and failure to do so leads to aberrant splicing and production of shorter transcripts with elevated levels of m6A that are rapidly degraded. Our study identified reversible m6A modification as a critical mechanism of posttranscriptional control of mRNA fate in late meiotic and haploid spermatogenic cells.

中文翻译：

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依赖ALKBH5的m6A去甲基化控制雄性生殖细胞中长3'-UTR mRNA的剪接和稳定性

N6-甲基腺苷（m6A）代表真核生物中最常见的RNA修饰之一。已经确定了特定的m6A书写，擦除和阅读蛋白。作为一个M6A橡皮擦，ALKBH5专门从靶mRNA和失活除去M6A Alkbh5导致小鼠雄性不育。然而，潜在的分子机制仍然未知。在这里，我们报告说，ALKBH5介导的精子细胞和圆形精子细胞核中的m6A消除对于正确剪接和更长的3'-UTR mRNA的产生是必不可少的，否则，将导致异常的剪接和较短的转录物的产生，升高水平迅速下降的m6A。我们的研究确定可逆的m6A修饰是后期减数分裂和单倍体生精细胞中mRNA命运转录后控制的关键机制。