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mRNA 3′ uridylation and poly(A) tail length sculpt the mammalian maternal transcriptome

机译:mRNA 3尿苷化和poly(A)尾巴长度雕刻了哺乳动物母本转录组

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摘要

A fundamental principle in biology is that the program for early development is established during oogenesis in the form of the maternal transcriptome,. How the maternal transcriptome acquires the appropriate content and dosage of transcripts is not fully understood. Here we show that TUT4/7-mediated mRNA 3′ terminal uridylation sculpts the mouse maternal transcriptome by eliminating transcripts during oocyte growth. TUT4/7-mediated uridylation is essential for both oocyte maturation and fertility. In comparison to somatic cells, the oocyte transcriptome displays shorter poly(A) tail length and a high relative proportion of terminal oligo-uridylation. TUT4/7 deletion leads to the accumulation of a cohort of transcripts with a high frequency of very short poly(A) tails and a loss of 3′ oligo-uridylation. In contrast, TUT4/7-deficiency does not alter gene expression in a variety of somatic cells. In summary, we show essential and specific functions for poly(A) tail length and 3′ terminal uridylation in sculpting a functional maternal transcriptome.
机译:生物学的基本原理是在卵子发生期间以母体转录组 的形式建立早期发育程序。母体转录组如何获得适当的转录物含量和剂量的方法尚未完全了解。在这里,我们显示TUT4 / 7介导的mRNA 3'末端尿苷化通过消除卵母细胞生长过程中的转录本来雕刻小鼠母本转录组。 TUT4 / 7介导的尿酸化对于卵母细胞的成熟和受精都至关重要。与体细胞相比,卵母细胞转录组显示较短的poly(A)尾巴长度和较高的末端寡尿苷化相对比例。 TUT4 / 7删除导致大量的非常短的poly(A)尾巴出现,并且丢失3'寡尿苷酸化,从而导致大量的转录物积累。相反,TUT4 / 7缺陷不会改变多种体细胞中的基因表达。总之,我们在雕刻功能性母体转录组时显示了poly(A)尾巴长度和3'末端尿苷化的基本功能和特定功能。

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