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多组学研究表明,DCP1A和SPDL1决定了排卵后老化卵母细胞中的胚胎发生缺陷。

Multi-omics revealed that DCP1A and SPDL1 determine embryogenesis defects in postovulatory ageing oocytes.

作者信息

Kong Li, Gong Yutian, Wang Yongyong, Yuan Mengjiao, Liu Wenxiang, Zhou Heyang, Meng Xiangyue, Guo Xinru, Liu Yongbin, Zhou Yang, Zhang Teng

机构信息

State Key Laboratory of Reproductive Regulation & Breeding of Grassland Livestock, College of Life Sciences, Inner Mongolia University, Hohhot, China.

Department of Reproductive Medicine, Qingdao Municipal Hospital, University of Health and Rehabilitation Sciences, Qingdao, China.

出版信息

Cell Prolif. 2025 Mar;58(3):e13766. doi: 10.1111/cpr.13766. Epub 2024 Dec 4.

Abstract

Growing evidence indicates that the deterioration of egg quality caused by postovulatory ageing significantly hampers embryonic development. However, the molecular mechanisms by which postovulatory ageing leads to a decline in oocyte quality have not been fully characterized. In this study, we observed an accelerated decay of maternal mRNAs through RNA-seq analyses in postovulatory-aged (PostOA) oocytes. We noted that these downregulated mRNAs should be degraded during the 2-cell stage. Proteomic analyses revealed that the degradation of maternal mRNAs is associated with the accumulation of DCP1A. The injection of exogenous Dcp1a mRNA or siRNA into MII stage oocytes proved that DCP1A could accelerate the degradation of maternal mRNAs. Additionally, we also found that SPDL1 is crucial for maintaining spindle/chromosome structure and chromosome euploidy in PostOA oocytes. Spdl1-mRNA injection remarkably recovered the meiotic defects in PostOA oocytes. Collectively, our findings provide valuable insights into the molecular mechanisms underlying postovulatory ageing.

摘要

越来越多的证据表明,排卵后老化导致的卵子质量下降显著阻碍胚胎发育。然而,排卵后老化导致卵母细胞质量下降的分子机制尚未完全阐明。在本研究中,我们通过RNA测序分析观察到排卵后老化(PostOA)卵母细胞中母体mRNA的加速降解。我们注意到这些下调的mRNA应该在二细胞阶段被降解。蛋白质组学分析表明,母体mRNA的降解与DCP1A的积累有关。将外源Dcp1a mRNA或siRNA注入MII期卵母细胞证明,DCP1A可以加速母体mRNA的降解。此外,我们还发现SPDL1对于维持PostOA卵母细胞中的纺锤体/染色体结构和染色体整倍性至关重要。Spdl1-mRNA注射显著恢复了PostOA卵母细胞中的减数分裂缺陷。总的来说,我们的发现为排卵后老化的分子机制提供了有价值的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/11882766/18fad1da20e0/CPR-58-e13766-g004.jpg

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