Mettl3-mediated m ^6A regulates spermatogonial differentia- tion and meiosis initiation

METTL3 catalyzes the formation of N%methyl-adenosine （m6A） which has important roles in regulating various biological processes. However, the in vivo function of Mettl3 remains largely unknown in mammals. Here we gener- ated germ cell-specific Mettl3 knockout mice and demonstrated that Mettl3 was es...

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Published in细胞研究：英文版 Vol. 27; no. 9; pp. 1100 - 1114
Main Author Kai Xu Ying- Yang Gui-Hai Feng Bao-Fa Sun Jun-Qing Chen Yu-Fei Li Yu-Sheng Chen Xin-Xin Zhang Chen-Xin Wang Li-Yuan Jiang Chao Liu Ze-Yu Zhang Xiu-Jie Wang Qi Zhou Yun-Gui Yang Wei Li
Format Journal Article
LanguageEnglish
Published 2017
Subjects
减数分裂
哺乳动物
基因敲除
差异化
生殖细胞
精原细胞
精子介导
精子发生过程
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Summary:METTL3 catalyzes the formation of N%methyl-adenosine （m6A） which has important roles in regulating various biological processes. However, the in vivo function of Mettl3 remains largely unknown in mammals. Here we gener- ated germ cell-specific Mettl3 knockout mice and demonstrated that Mettl3 was essential for male fertility and sper- matogenesis. The ablation of Mettl3 in germ cells severely inhibited spermatogonial differentiation and blocked the initiation of meiosis. Transcriptome and m6A profiling analysis revealed that genes functioning in spermatogenesis had altered profiles of expression and alternative splicing. Our findings provide novel insights into the function and regulatory mechanisms of MettD-mediated m6A modification in spermatogenesis and reproduction in mammals.
Bibliography:Mettt3; m6A; spermatogenesis; spermatogonial differentiation; meiosis; alternative splicing
31-1568
METTL3 catalyzes the formation of N%methyl-adenosine （m6A） which has important roles in regulating various biological processes. However, the in vivo function of Mettl3 remains largely unknown in mammals. Here we gener- ated germ cell-specific Mettl3 knockout mice and demonstrated that Mettl3 was essential for male fertility and sper- matogenesis. The ablation of Mettl3 in germ cells severely inhibited spermatogonial differentiation and blocked the initiation of meiosis. Transcriptome and m6A profiling analysis revealed that genes functioning in spermatogenesis had altered profiles of expression and alternative splicing. Our findings provide novel insights into the function and regulatory mechanisms of MettD-mediated m6A modification in spermatogenesis and reproduction in mammals.
ISSN:1001-0602
1748-7838