CPEB3 Maintains Developmental Competence of the Oocyte
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA999673 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25452140_1.fastq.gz | Fastqsanger.gz | |||
| SRR25452140_2.fastq.gz | Fastqsanger.gz | |||
| SRR25452141_1.fastq.gz | Fastqsanger.gz | |||
| SRR25452141_2.fastq.gz | Fastqsanger.gz | |||
| SRR25452142_1.fastq.gz | Fastqsanger.gz |
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Project description:Mammalian oocyte development depends on the temporally controlled translation of maternal transcripts, particularly in the coordination of meiotic and early embryonic development when transcription has ceased. The translation of mRNA is regulated by various RNA-binding proteins. We show that the absence of cytoplasmic polyadenylation element-binding protein 3 (CPEB3) neg-atively affects female reproductive fitness. CPEB3-depleted oocytes undergo meiosis normally but experience early embryonic arrest due to a disrupted transcriptome, leading to aberrant protein expression and the subsequent failure of embryonic transcription initiation. We found that CPEB3 stabilizes a subset of mRNAs with a significantly longer 3’UTR that is enriched in its distal region with cytoplasmic polyadenylation elements. Overall, our results suggest that CPEB3 is an im-portant maternal factor that regulates the stability and translation of a subclass of mRNAs that are essential for the initiation of embryonic transcription and thus for embryonic development.
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Project description:Ovarian aging has reproductive and overall health implications with increased infertility, miscarriage rates, and adverse outcomes associated with menopause. Mitochondrial dysfunction is one of the main mechanisms of female reproductive aging. Mitochondrial protein homeostasis maintains mitochondrial function and globally dysregulated unfolded mitochondrial protein response accelerates reproductive aging. However, the role of oocyte mitochondrial proteostasis in determining oocyte quality is unknown. ClpX (Caseinolytic Protease X) is a mitochondrial protein unfoldase that maintains mitochondrial protein homeostasis. In this study, we uncovered that Clpx deficiency, either through genetic ablation or natural decline with aging in mice, leads to the disrupted mitochondrial proteostasis in oocytes. Oocyte-specific knockout of Clpx impaired oocyte quality and developmental competence, thereby leading to female subfertility. Transcriptomic and micro-proteomic analyses of Clpx null oocytes revealed dysregulated mitochondrial function, protein processing and meiosis. Notably, Clpx deficiency promoted PGD2 synthesis and DP1/PKA/cAMP and DP2/AKT/mTOR signaling pathways by upregulating Ptgds. The PGD2 synthesis inhibitor AT-56 restored the developmental competence of Clpx knockout and aged oocytes. Our findings indicate the pivotal role of oocyte mitochondrial proteostasis in the regulation of oocyte quality with aging and pave the way for future investigations assessing the potential therapeutic value of these pathways to improve infertility treatment outcomes.
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Project description:This SuperSeries is composed of the following subset Series: GSE36602: Transcriptional profiling of somatic cells differentiation throughout oocyte competence acquisition in rainbow trout ovarian follicles. GSE36603: Transcriptional profiling of somatic cells differentiation throughout oocyte competence acquisition in the xenopus ovarian follicles. GSE36604: Transcriptional profiling of cumulus cells differentiation throughout oocyte competence acquisition in the murine ovarian follicles. GSE36605: Transcriptional profiling of cumulus cells differentiation throughout oocyte competence acquisition in the bovine ovarian follicles. Refer to individual Series
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Project description:Ovarian aging has reproductive and overall health implications with increased infertility, miscarriage rates, and adverse outcomes associated with menopause. Mitochondrial dysfunction is one of the main mechanisms of female reproductive aging. Mitochondrial protein homeostasis maintains mitochondrial function and globally dysregulated unfolded mitochondrial protein response accelerates reproductive aging. However, the role of oocyte mitochondrial proteostasis in determining oocyte quality is unknown. ClpX (Caseinolytic Protease X) is a mitochondrial protein unfoldase that maintains mitochondrial protein homeostasis. In this study, we uncovered that Clpx deficiency, either through genetic ablation or natural decline with aging in mice, leads to the disrupted mitochondrial proteostasis in oocytes. Oocyte-specific knockout of Clpx impaired oocyte quality and developmental competence, thereby leading to female subfertility. Transcriptomic and micro-proteomic analyses of Clpx null oocytes revealed dysregulated mitochondrial function, protein processing and meiosis. Notably, Clpx deficiency promoted PGD2 synthesis and DP1/PKA/cAMP and DP2/AKT/mTOR signaling pathways by upregulating Ptgds. The PGD2 synthesis inhibitor AT-56 restored the developmental competence of Clpx knockout and aged oocytes. Our findings indicate the pivotal role of oocyte mitochondrial proteostasis in the regulation of oocyte quality with aging and pave the way for future investigations assessing the potential therapeutic value of these pathways to improve infertility treatment outcomes.
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Project description:Oocyte developmental competence is instructed by H3.3 chaperone Hira complex
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Project description:Gene expression profiles of granulosa cells from rat ovarian follicles by Affymetrix rat whole genome array showed that twelve genes were up-regulated, while one gene down-regulated more than 1.5 folds in the normal developmental competence group compared with those in the poor developmental competence group. Gene ontology classification showed that the up-regulated genes included lysyl oxidase and nerve growth factor receptor associated protein 1, which are important in the regulation of protein-lysine 6-oxidase activity, and in apoptosis induction, respectively. The down-regulated genes included glycoprotein-4-beta galactosyltransferase 2, which is involved in the regulation of extracellular matrix organization and biogenesis. Experiment Overall Design: Immature rats were injected with eCG and 24h thereafter with anti-eCG antibody to induce follicular atresia or with pre-immune serum to stimulate follicle development. A high percentage (30-50%, normal developmental competence, NDC) of oocytes from eCG/pre-immune serum group developed to term after embryo transfer compared to those from eCG/anti-eCG (0%, poor developmental competence, PDC). Gene expression profiles of granulosa cells from the above oocyte-collected follicles were assessed by Affymetrix rat whole genome array.
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