YTHDF2 promotes spermagonial adhesion through modulating MMPs decay via m6A/mRNA pathway.,Cell Death & Disease

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YTHDF2 promotes spermagonial adhesion through modulating MMPs decay via m6A/mRNA pathway.
Cell Death & Disease ( IF 8.1 ) Pub Date : 2020-01-20 , DOI: 10.1038/s41419-020-2235-4
Tao Huang ₁ , Zidong Liu ₁ , Yi Zheng ₁ , Tongying Feng ₁ , Qiang Gao ₁ , Wenxian Zeng ₁

Affiliation

As the foundation of male fertility, spermatogenesis is a complicated and highly controlled process. YTHDF2 plays regulatory roles in biological processes through accelerating the degradation of target mRNAs. However, the function of YTHDF2 in spermatogenesis remains elusive. Here, we knocked out Ythdf2 in mouse spermatogonia via CRISPR/Cas9, and found that depletion of Ythdf2 mainly downregulated the expression of matrix metallopeptidase (MMPs), thus affecting cell adhesion and proliferation. m6A-IP-PCR and RIP-PCR analysis showed that Mmp3, Mmp13, Adamts1 and Adamts9 were modified with m6A and simultaneously interacted with YTHDF2. Moreover, inhibition of Mmp13 partially rescued the phenotypes in Ythdf2-KO cells. Taken together, YTHDF2 regulates cell-matrix adhesion and proliferation through modulating the expression of Mmps by the m6A/mRNA degradation pathway.

中文翻译：

YTHDF2 通过 m6A/mRNA 途径调节 MMPs 衰变来促进精原细胞粘附。

作为男性生育能力的基础，精子发生是一个复杂且高度受控的过程。YTHDF2 通过加速目标 mRNA 的降解在生物过程中发挥调节作用。然而，YTHDF2 在精子发生中的功能仍然难以捉摸。在这里，我们通过 CRISPR/Cas9 敲除小鼠精原细胞中的 Ythdf2，发现 Ythdf2 的缺失主要下调基质金属肽酶 (MMPs) 的表达，从而影响细胞粘附和增殖。m6A-IP-PCR 和 RIP-PCR 分析表明 Mmp3、Mmp13、Adamts1 和 Adamts9 被 m6A 修饰并同时与 YTHDF2 相互作用。此外，Mmp13 的抑制部分挽救了 Ythdf2-KO 细胞中的表型。综合起来，

更新日期：2020-01-21

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