PGC7通过小鼠卵母细胞中AKT1-YBX1相互作用调节母体mRNA翻译。

IF 8.2 2区 生物学 Q1 CELL BIOLOGY Cell Communication and Signaling Pub Date : 2024-12-18 DOI:10.1186/s12964-024-01976-1
Yingxiang Liu, Peiwen Feng, Xing Wei, Hongyu Xu, Mengying Yu, Lei Zhang, Weijie Hao, Zekun Guo
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引用次数: 0

摘要

母体mRNA的及时准确翻译对于卵母细胞成熟和早期胚胎发育至关重要。先前的研究强调了原始生殖细胞7 (PGC7)作为维持受精卵中母体印迹位点DNA甲基化的母体因子的重要性。然而,PGC7是否参与调控母体mRNA翻译尚不清楚。在本研究中,我们发现PGC7-AKT1-YBX1轴参与促进母体mrna的翻译。PGC7不仅通过对抗PP2A去磷酸化和促进PDK1-AKT1结合来维持AKT1的活性,而且还帮助AKT1磷酸化翻译抑制剂YBX1。在缺乏PGC7的情况下,尽管PIK3CA表达和AKT1磷酸化增加,但AKT1无法磷酸化YBX1。PGC7促进AKT1与YBX1的相互作用,增强YBX1- serine 100磷酸化,导致YBX1与eIF4E分离,从而激活母体Cyclin B1和YAP1的翻译。这些发现证明了PGC7对哺乳动物卵母细胞翻译激活的不可或缺性,并提供了一个由PGC7调控的早期卵子发生的潜在网络。
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PGC7 regulates maternal mRNA translation via AKT1-YBX1 interactions in mouse oocytes.

Timely and accurate translation of maternal mRNA is essential for oocyte maturation and early embryonic development. Previous studies have highlighted the importance of Primordial Germ cell 7 (PGC7) as a maternal factor in maintaining DNA methylation of maternally imprinted loci in zygotes. However, it is still unknown whether PGC7 is involved in the regulation of Maternal mRNA Translation. In this study, we have identified that PGC7-AKT1-YBX1 axis is involved in promoting the translation of maternal mRNAs. PGC7 not only sustains AKT1 activity by counteracting PP2A dephosphorylation and facilitating PDK1-AKT1 binding but also assists AKT1 in phosphorylating the translation inhibitor YBX1. In the absence of PGC7, despite increased PIK3CA expression and AKT1 phosphorylation, AKT1 is unable to phosphorylate YBX1. PGC7 facilitates the interaction between AKT1 and YBX1, enhancing YBX1-Serine 100 phosphorylation, which leads to YBX1 dissociation from eIF4E, thereby activating the translation of maternal Cyclin B1 and YAP1. The findings demonstrate the indispensability of PGC7 for translation activation in mammalian oocytes and provide a potential network regulated by PGC7 in early oogenesis.

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来源期刊
CiteScore
11.00
自引率
0.00%
发文量
180
期刊介绍: Cell Communication and Signaling (CCS) is a peer-reviewed, open-access scientific journal that focuses on cellular signaling pathways in both normal and pathological conditions. It publishes original research, reviews, and commentaries, welcoming studies that utilize molecular, morphological, biochemical, structural, and cell biology approaches. CCS also encourages interdisciplinary work and innovative models, including in silico, in vitro, and in vivo approaches, to facilitate investigations of cell signaling pathways, networks, and behavior. Starting from January 2019, CCS is proud to announce its affiliation with the International Cell Death Society. The journal now encourages submissions covering all aspects of cell death, including apoptotic and non-apoptotic mechanisms, cell death in model systems, autophagy, clearance of dying cells, and the immunological and pathological consequences of dying cells in the tissue microenvironment.
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