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Single-cell transcriptomics and translatomics dual-omics analysis reveals the potential mechanism of HFD-induced maternal RNA degradation abnormalities

ABSTRACT: This study explores the impact of high-fat diet (HFD)-induced obesity on maternal RNA degradation and its implications for oocyte quality and development in mice, using a novel transcriptome and translatome sequencing (T&T-seq) strategy. By combining RiboLace for translatome profiling and Smart-seq for transcriptome analysis, the research investigates how HFD disrupts RNA degradation pathways during oocyte maturation, particularly from the germinal vesicle (GV) to metaphase II (MII) stages. The findings reveal that HFD impairs the degradation of key transcripts such as BTG4 and CNOT7, and alters the translation efficiency of meiotic regulators, which are crucial for proper meiotic progression. This study provides new insights into how maternal dietary factors influence oocyte quality at the molecular level, with potential implications for fertility and embryonic development.

ORGANISM(S): Mus musculus

PROVIDER: GSE294093 | GEO | 2025/04/14

REPOSITORIES: GEO

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CNOT6L Couples the Selective Degradation of Maternal Transcriptsto Meiotic Cell Cycle Progression in Mouse Oocyte [polysome RNA-seq]

Project description:Purpose: The goals of this study are to study the function of Cnot6l during oocyte maturation . Methods: Comparing the polysome-bounded transcripts at GV, MI and MII stage in WT and Cnot6l-/- oocytes by RNA sequencing. Results: Using an optimized data analysis workflow, we mapped about 15 million sequence reads per sample to the mouse genome (build mm9) and identified 23236 transcripts with TopHat workflow. Conclusions: CNOT6L stimulated degradation of maternal transcriptsto oocyte meiotic maturation.

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LSM14B is essential for oocyte meiotic maturation by regulating maternal mRNA storage and clearance

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2023-10-17 | PXD042761 | Pride

CNOT6L Couples the Selective Degradation of Maternal Transcriptsto Meiotic Cell Cycle Progression in Mouse Oocyte [total RNA-seq]

Project description:Purpose: The goals of this study are to study the function of Cnot6l during oocyte maturation and the differences between loss of Cnot6l and Btg4 during oocyte maturation. Methods:Comparing the degration of transcripts at different stage in WT, Btg4-/- and Cnot6l-/- oocytes by RNA sequencing. Results: Using an optimized data analysis workflow, we mapped about 15 million sequence reads per sample to the mouse genome (build mm9) and identified 23236 transcripts with TopHat workflow. Conclusions: CNOT6L stimulated degradation of maternal transcriptsto oocyte meiotic maturation.

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The CCR4-NOT complex suppresses untimely translational activation of maternal mRNAs.

Project description:Control of mRNA poly(A) tail has central role to regulate mRNA metabolism: translation efficiency and mRNA stability. Gene expression in maturing oocytes largely relies on the regulation of mRNA metabolism as they are transcriptionally silent. The CCR4-NOT complex is a major deadenylase for mammals and regulates poly(A) tails of maternal mRNAs, however their function to translational regulation was not well understood. Here we show that CCR4-NOT suppresses translational activity of maternal mRNAs during oocyte maturation. Oocytes which lack entire deadenylase activity of CCR4-NOT by genetic deletion of its catalytic subunits: CNOT7 and CNOT8 showed increase of both expression of maternal mRNAs and translational activity of them during oocyte maturation.

2023-10-01 | GSE224308 | GEO

NLRP14 deficiency contributes to female infertility and early embryo arrest

Project description:Oocyte maturation is vital to attain full competence required fertilization and embryogenesis. As a maternal effect factor, NLRP14 is preferentially expressed in mammalian oocytes and early embryos. Yet the role and molecular mechanism of NLRP14 in oocyte maturation and early embryogenesis is largely unknown. Whether NLRP14 deficiency accounts for human infertility with oocyte and embryo defects remains to be elucidated. Here, NLRP14 is identified essential for establishment of competent oocytes that can sustain early embryo development. Maternal deficiency of Nlrp14 results in sterility characterized by oocyte maturation defects and early embryo arrest. Nlrp14 ablation leads to compromised oocyte quality and developmental competence due to impaired oocyte cytoplasmic and nuclear maturation. Mechanistically, NLRP14 interacts with UHRF1 in oocyte cytoplasm to protect it from proteasome-dependent degradation, and perturbs maternal mRNA zygotic-decay and zygotic genome activation during maternal-zygotic transition. Furthermore, compound heterozygous pathogenic variants in NLRP14 gene are identified in infertile women with early embryonic arrest, which interrupt the NLRP14-UHRF1 interaction or UHRF1 protein expression. Our data uncover a vital role of NLRP14 as a new cytoplasmic-specific modulator of UHRF1 in oocyte meiotic maturation and early embryogenesis, which should provide new insights into risk prediction and genetic diagnosis for female infertility.

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Transcriptome assay of materal mRNA degradation in Btg4-deleted oocytes

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Project description:In order to establish an obese mouse model, female mice were continuously fed with a high-fat diet (HFD) or a normal diet (control) for 16 weeks beginning at three weeks of age. In this paper, these mice are termed ‘HFD mice’ and ‘control mice’, respectively. Accordingly, we call their oocytes ‘HFD oocytes’ and ‘control oocytes’. Substantial evidence indicates that the effects of maternal obesity on embryo/offspring development can be attributed to factors within the oocyte (9). To identify such potential effectors, we performed a comparative proteomic analysis of ovulated MII oocytes from control and HFD mice.

2018-05-24 | PXD006641 | Pride

Dynamic mRNA Degradome Analyses Indicate a Role of Histone H3K4 Trimethylation in Association with Meiosis-coupled mRNA Decay in Oocyte Aging

Project description:A decrease in oocyte developmental potential is a major obstacle for successful pregnancy in women of advanced age. However, the age-related epigenetic modifications associated with dynamic transcriptome changes, particularly meiotic maturation-coupled mRNA clearance, have not been adequately characterized in human oocytes. This study demonstrate a decreased storage of transcripts encoding key factors regulating the maternal mRNA degradome in fully grown oocytes of women of advanced age. A similar defect in meiotic maturation-triggered mRNA clearance was also detected in aged mouse oocytes. Mechanistically, the epigenetic and cytoplasmic aspects of oocyte maturation are synchronized in both the normal development and aging processes. The level of histone H3K4 trimethylation (H3K4me3) was high in fully grown mouse and human oocytes derived from young females but decreased during aging due to the decreased expression of epigenetic factors responsible for H3K4me3 accumulation. Oocyte-specific knockout of the gene encoding CxxC-finger protein 1 (CXXC1), a DNA-binding subunit of SETD1 methyltransferase, caused ooplasm changes associated with accelerated aging and impaired maternal mRNA translation and degradation. These results suggest that a network of CXXC1-maintained H3K4me3, in association with mRNA decay competence, sets a timer for oocyte deterioration and plays a role in oocyte aging in both mouse and human oocytes.

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The role of ALKBH5 in maternal RNA decay during mammalian oocyte meiosis [RNA-seq]

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Transcription profiling of polysomal mRNA populations of mouse oocytes and zygotes

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