Ontology highlight
ABSTRACT:
PROVIDER: PRJNA504853 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8179971_1.fastq.gz | Fastqsanger.gz | |||
| SRR8179971_2.fastq.gz | Fastqsanger.gz | |||
| SRR8179972_1.fastq.gz | Fastqsanger.gz | |||
| SRR8179972_2.fastq.gz | Fastqsanger.gz | |||
| SRR8179973_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:Coupling the release of pituitary hormones to the developmental stage of the oocyte is essential for female fertility. It requires estrogen to restrain kisspeptin (Kiss1) neuron pulsatility in the arcuate hypothalamic nucleus, while also exerting a surge-like effect on Kiss1 neuron activity in the AVPV hypothalamic nucleus. However, a mechanistic basis for this region-specific effect has remained elusive. Here, we provide functional insight into hypothalamic estrogen sensing by analyzing estrogen receptor alpha (ERα/ESR1) DNA binding events in the arcuate and AVPV nuclei of the hypothalamus in female mice.
2023-04-25 | GSE227540 | GEO
Project description:Posttranslational modification of proteins by N-linked glycosylation is crucial for many life processes. However, the exact contribution of N-glycosylation to mammalian female reproduction remains largely undefined. Here, DPAGT1, the enzyme that catalyzes the first step of protein N-glycosyation, is identified to be indispensable for oocyte development in mice. A recessive missense mutation (c. 497A>G; p. Asp166Gly) of Dpagt1 causes female subfertility without grossly affecting other functions. Mutant females ovulate fewer eggs owing to defects of follicular development beyond the late secondary stage. Oocytes ovulated by mutants carry a thin and fragile zona pellucida, and display poor developmental competence after fertilization in vitro. Moreover, completion of the first meiosis is accelerated in mutant oocytes, which is coincident with the elevation of aneuploidy. Mechanistically, transcriptomic analysis reveals the downregulation of a number of transcripts essential for oocyte meiotic progression and preimplantation development (e.g., Pttgt1, Esco2, Orc6, and Npm2) in mutant oocytes, which could account for the defects observed. Furthermore, conditional knockout (CKO) of Dpagt1 in oocytes recapitulates the phenotypes observed in Dpagt1 mutant females, and causes complete infertility. Taken together, these data indicate that protein N-glycosylation in oocytes is essential for female fertility in mammals by specific control of oocyte development.
2021-09-09 | PXD018531 | Pride
Project description:Basonuclin, which is a zinc-finger protein found in abundance only in the keratinocytes of the stratified epithelium, male germ cells and oocytes, qualifies as a maternal-effect gene because the source of pre-implantation embryonic basonuclin is maternal. Using a transgenic-RNAi approach, we knocked-down basonuclin specifically in mouse oocytes, which led to female sub-fertility. Basonuclin deficiency in oocytes perturbed both RNA polymerase I- and II-mediated transcription and oocyte morphology was affected as evidenced by cytoplasmic and cell surface abnormalities. The affected oocytes, however, could still mature to and arrest at metaphase II and be ovulated, suggesting the impaired pathways were not essential for oocyte development and maturation. Nevertheless, an early embryonic failure in pre-implantation development was identified and likely accounted for the sub-fertility phenotype. These results suggest that basonuclin is a new member of the mammalian maternal-effect genes and interestingly, differs from the previously reported mammalian maternal-effect genes in that it also apparently perturbs oogenesis.
2007-07-06 | E-GEOD-4029 | biostudies-arrayexpress
Project description:To investigate the effect of mitochondrial fission factor (MFF) on oocyte competence and female fertility using an oocyte-specific Mff knockout mouse model. Oocyte-specific Mff deficiency hindered oocyte maturation and early embryonic development via regulation of mitochondrial dynamics, resulting in female subfertility. What is known already: Emerging studies have demonstrated that mitochondrial dynamics play a vital role in oocyte maturation and early embryo development. MFF is one of the crucial proteins regulating mitochondrial dynamics. Our previous studies have indicated that Mff is necessary for oocyte competence and fertility using a global Mff knockout mouse model. However, further investigation is needed to determine whether the deletion of Mff in oocytes could affect oocyte competence and early embryonic development by regulating mitochondrial dynamics.The Mfffl/fl; Gdf9-Cre mice consistently exhibited reduced fertility with a significant decrease in litter size, number of litters per female, and number of pups per female compared to the Mfffl/fl mice. The numbers of GV oocytes, ovulated oocytes and 2-cell embryos were significantly lower in the Mfffl/fl; Gdf9-Cre mice. The blastocyst (32.32% vs. 68.44%, p<0.05) embryo development rate per 2-cell embryos was also significantly lower. In vitro maturation revealed that of Mfffl/fl; Gdf9-Cre GV oocytes had significantly lower rates of GV break-down and polar body extrusion . The ratios of aberrant spindle and misaligned chromosomesin ovulated oocytes from Mfffl/fl; Gdf9-Cre mice were significantly increased. In terms of mitochondrial dynamics, the mitochondrial size and the ratio of abnormal mitochondrial distribution (unevenly aggregated) in Mfffl/fl; Gdf9-Cre oocytes significantly elevated. This study found that the Mff played a crucial role in oocyte maturation and early embryonic development. These results shed light on the important role played by MFF in ensuring proper mitochondrial dynamics in oocytes and underscore the significance of this protein in female fertility. This study provides insights into potential therapeutic targets for infertility and related diseases in humans.
2026-01-01 | GSE285731 | GEO
Project description:<p>Advanced maternal age is a key factor in female infertility, primarily due to declines in ovarian reserve and oocyte quality. However, the metabolic mechanisms underlying reproductive aging are still poorly understood. Here, we show that uridine levels in the plasma and ovaries of aged mice are significantly reduced compared with young controls. Building on this, we find that uridine supplementation significantly improves meiotic maturation, fertilization, and early embryonic development of aged oocytes, both in vivo and in vitro. Further microtranscriptomic analyses reveal that uridine enhances oocyte quality by inhibiting ferroptosis, enhancing mitochondrial function and removing excessive reactive oxygen species (ROS). Moreover, integrating Limited Proteolysis-Small Molecule Mapping (LiP-SMap), surface plasmon resonance (SPR) analyses and siRNA-based functional assays, we identify that uridine binds Poly(rC)-binding protein 1 (PCBP1), thereby suppressing ferroptosis and preserving mitochondrial function. In conclusion, this study demonstrates that uridine supplementation can effectively improve fertility of aged female mice. Our research also provides important insights into the role of ferroptosis in oocyte aging, thereby advancing our understanding of reproductive aging mechanisms.</p>
2026-03-03 | MTBLS13957 | MetaboLights
Project description:Alternative splicing(AS) contributes to gene diversification through RNA-binding proteins, but AS regulation during germline development remains largely undefined. Here, we report a comprehensive set of mRNA splicing events mediated by epithelial splicing regulatory proteins 1(Esrp1) to regulate mouse oocyte development. Collectively, our data highlights that ESRP1-mediated AS program are required for oocyte development and female fertility maintainance.
2020-12-20 | GSE149355 | GEO
Project description:In-vitro-grow (IVG) of preantral follicles is essential for female fertility preservation, while effective approach to improve it is far from being explored. Here, we report the dynamic location of TRKB in human and mouse ovaries, and a positive relation between human oocyte maturation and NT-4 level in follicular fluid. For the first time, we observe the improving effect of NT-4 on mice preantral follicle IVG, including follicle diameter, hormone production and oocyte maturation. Single-cell transcriptome analysis shows that the reparative effect of NT-4 on oocyte maturation in IVG may be mediated by regulation of PI3K-Akt signaling pathway and subsequent organization of F-actin. Suppression of advanced stimulated complement system in granulosa cells may also contribute to the improvement. Cell-specific network analysis reveals that NT-4 may recover the inflammation damage induced by abnormal lipid metabolism in IVG environment. Collectively, our data suggest that NT-4 is involved in the ovarian physiology and may serve to improve the efficiency of preantral follicle IVG for fertility preservation.
2021-09-08 | GSE176516 | GEO
Project description:In-vitro-grow (IVG) of preantral follicles is essential for female fertility preservation, while effective approach to improve it is far from being explored. Here, we report the dynamic location of TRKB in human and mouse ovaries, and a positive relation between human oocyte maturation and NT-4 level in follicular fluid. For the first time, we observe the improving effect of NT-4 on mice preantral follicle IVG, including follicle diameter, hormone production and oocyte maturation. Single-cell transcriptome analysis shows that the reparative effect of NT-4 on oocyte maturation in IVG may be mediated by regulation of PI3K-Akt signaling pathway and subsequent organization of F-actin. Suppression of advanced stimulated complement system in granulosa cells may also contribute to the improvement. Cell-specific network analysis reveals that NT-4 may recover the inflammation damage induced by abnormal lipid metabolism in IVG environment. Collectively, our data suggest that NT-4 is involved in the ovarian physiology and may serve to improve the efficiency of preantral follicle IVG for fertility preservation.
2021-09-08 | GSE177030 | GEO
Project description:Advanced maternal age is a key factor in female infertility, primarily due to declines in ovarian reserve and oocyte quality. However, the metabolic mechanisms underlying reproductive aging remain unclear. Here, we show that uridine levels in the plasma and ovaries of aged mice are significantly reduced compared with young controls. Building on this, we find that uridine supplementation significantly improves meiotic maturation, fertilization, and early embryonic development of aged oocytes, both in vivo and in vitro. Further microtranscriptomic analyses reveal that uridine enhances oocyte quality by inhibiting ferroptosis and enhancing mitochondrial function. Moreover, integrating Limited Proteolysis-Small Molecule Mapping, western blot and siRNA-based functional assays, we identify that uridine binds Poly(rC)-binding protein 1, thereby suppressing ferroptosis and preserving mitochondrial function. Collectively, these findings demonstrate that uridine supplementation improves fertility in aged female mice and provide mechanistic insight into ferroptosis in oocyte aging.
2026-03-05 | PXD075265 | Pride