ArticleCell death & disease2018
Loss of oocyte Rps26 in mice arrests oocyte growth and causes premature ovarian failure.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 61 citations in OpenAlex.
- Regulatory risk loci link disrupted androgen response to the pathophysiology of polycystic ovary syndrome.Journal of the Endocrine Society · 2026Article
- Epigenetic regulation by DNA methylation in PCOS and POI: mechanisms of ovarian dysfunction and implications for clinical research.Journal of ovarian research · 2026Review
- Natural degradation of RNA polymerase II is essential for oocyte chromatin reorganization and maternal-to-zygotic transition.Nature communications · 2025Article
- Article
- Absence of CDK12 in oocyte leads to female infertility.Cell death & disease · 2025Article
- Premeiotic deletion of Eif2s2 causes oocyte arrest at the early diplotene stage and apoptosis in mice.Cell proliferation · 2024Article
- DENND1A desensitizes granulosa cells to FSH by arresting intracellular FSHR transportation.Science China. Life sciences · 2024Article
- Oocyte-specific deletion of eukaryotic translation initiation factor 5 causes apoptosis of mouse oocytes within the early-growing follicles by mitochondrial fission defect-reactive oxygen species-DNA damage.Clinical and translational medicine · 2024Article
- Deletion of Fbxw7 in oocytes causes follicle loss and premature ovarian insufficiency in mice.Journal of cellular and molecular medicine · 2024Article
- Association of RPS26 gene polymorphism with different types of diabetes in Chinese individuals.Journal of diabetes investigation · 2024Article
- Understanding crosstalk of organ tropism, tumor microenvironment and noncoding RNAs in breast cancer metastasis.Molecular biology reports · 2023Review
- Article
- Maternal NAT10 orchestrates oocyte meiotic cell-cycle progression and maturation in mice.Nature communications · 2023Article
- Upregulated Ribosomal Pathway Impairs Follicle Development in a Polycystic Ovary Syndrome Mouse Model: Differential Gene Expression Analysis of Oocytes.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- Multidrug resistance transporter-1 dysfunction perturbs meiosis and Ca2+ homeostasis in oocytes.Reproduction (Cambridge, England) · 2023Article
- BNC1 deficiency-triggered ferroptosis through the NF2-YAP pathway induces primary ovarian insufficiency.Nature communications · 2022Article
- Mendelian Randomization Analysis Identified Potential Genes Pleiotropically Associated with Polycystic Ovary Syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- Genome-Wide Identification and Stage-Specific Expression Profile Analysis Reveal the Function of Ribosomal Proteins for Oogenesis ofFrontiers in physiology · 2022Article
- Umbilical Cord Mesenchymal Stem Cells Ameliorate Premature Ovarian Insufficiency in Rats.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Global transcriptional activity increases as oocytes grow and is silenced in fully grown oocytes. Thus, the chromatin configuration varies during oocyte growth, but the molecular mechanisms regulating these changes remain to be clarified. Here, we studied a susceptibility gene of polycystic ovary syndrome (PCOS), RPS26, which is a ribosomal protein-encoding gene that is highly expressed in the ovary, but the functions of which remain unknown. Specific knockout of Rps26 in mouse oocytes resulted in retarded follicle development from pre-antral follicles to antral follicles, while the chromatin configurations of the oocytes were arrested at the transition from the non-surrounded nucleolus (NSN) to surrounded nucleolus (SN)-type. As a consequence, all oocytes died by postnatal day 84 resulting in premature ovarian failure (POF). Loss of Rps26 in oocytes led to decreased mRNA transcription and low levels of histone trimethylation on H3K4/H3K9 and DNA methylation at 5-cytosine, high levels of which are required for oocytes to transform from NSN to SN-type. Low protein levels of oocyte-derived growth differentiation factor 9, bone morphogenetic protein 15, and the oocyte-granulosa cell gap junction protein connexin 37 inhibited oocyte growth and retarded follicle development. The disruption of the phosphoinositide 3-kinase/protein kinase B/Forkhead box O-3a pathway contributed to oocyte death and follicle atresia. These results provide genetic clues for the clinical diagnosis of POF, especially in PCOS patients without treatment.
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