PDF(Pubmed)
Abstract：
Oocyte in vitro maturation is a technique in assisted reproductive technology. Thousands of genes show abnormally high expression in in vitro maturated metaphase II (MII) oocytes compared to those matured in vivo in bovines, mice, and humans. The mechanisms underlying this phenomenon are poorly understood. Here, we use poly(A) inclusive RNA isoform sequencing (PAIso-seq) for profiling the transcriptome-wide poly(A) tails in both in vivo and in vitro matured mouse and human oocytes. Our results demonstrate that the observed increase in maternal mRNA abundance is caused by impaired deadenylation in in vitro MII oocytes. Moreover, the cytoplasmic polyadenylation of dormant Btg4 and Cnot7 mRNAs, which encode key components of deadenylation machinery, is impaired in in vitro MII oocytes, contributing to reduced translation of these deadenylase machinery components and subsequently impaired global maternal mRNA deadenylation. Our findings highlight impaired maternal mRNA deadenylation as a distinct molecular defect in in vitro MII oocytes.
摘要：
卵母细胞体外成熟是辅助生殖技术中的一项技术。与牛体内成熟的卵母细胞相比，数千个基因在体外成熟的中期II（MII）卵母细胞中显示出异常高的表达，老鼠,和人类。对这种现象的潜在机制知之甚少。这里,我们使用poly（A）包容性RNA同种型测序（PAIso-seq）在体内和体外成熟的小鼠和人卵母细胞中分析转录组范围的poly（A）尾巴。我们的结果表明，观察到的母体mRNA丰度的增加是由体外MII卵母细胞的死蛋白化受损引起的。此外，休眠Btg4和Cnot7mRNA的细胞质多腺苷酸化，对去端化机器的关键部件进行编码，在体外MII卵母细胞受损，导致这些死酶机制成分的翻译减少，并随后损害了全局母体mRNA的死酶化。我们的发现强调了受损的母体mRNA去端化是体外MII卵母细胞的明显分子缺陷。
