Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA99461 | ENA |
REPOSITORIES: ENA
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Project description:The objective of this study was to gain better understanding of the follicular conditions associated with low oocyte developmental competence. In summary, we demonstrated that differences in follicle maturity at collection could explain differences in oocyte competence associated with individual animals. We also revealed deficiencies in lipid metabolism and retinol signalling in granulosa cells from donors of mostly incompetent oocytes.
2016-10-19 | GSE88893 | GEO
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.
2008-06-15 | E-GEOD-7697 | biostudies-arrayexpress
Project description:Oocyte competence is a complex process that is directly associated with the ability of oocyte to develop a newborn. The generation of a viable gamete has a multifactorial origin directly related to follicle and oocyte growth. Several dynamic changes in the follicle have driven the oocyte to success or failure, such as storage of metabolites, epigenetic modifications, and maternal RNAs, among others. However, little is known about the precise factors of maternal RNAs associated with oocyte competence, once these RNAs are consumed during maternal embryonic transition. To investigate the oocyte transcriptome landscape, we used a biopsy method to remove ~1.5% of ooplasm followed by a Single-ooplasm-biopsy RNA-Seq approach after retrospectively tracking the oocyte fate. We identified factors driving competence and the feasibility of the technique in obtaining enough amount of sample and high-quality sequencing results, enabling the model establishment. Furthermore, we integrated data from granulosa and cumulus cell transcriptome. Besides that, the first polar body methylation showed high similarities with pathways enriched in the ooplasm-biopsy transcriptome. In granulosa and ooplasm-biopsy with high-competence, we found MAPK and Oxytocin signaling enriched, while the process of necroptosis and ferroptosis were associated with low-competence oocytes. Deep analysis in the ooplasm-biopsy transcriptome, shows MYC as the highest up-regulated gene, and GNAS as a central hub gene in the network analysis. In addition, TIMP1, APOA1, EZR1, and STAT1 were key genes in the low-competence group of oocytes. Importantly, we found that metabolic alteration in the low-low-competence group was constantly found in all transcriptomes data, suggesting a metabolic disturbance inherited since the follicle environment which is amplified in cumulus cells after oocyte maturation.
2025-09-30 | GSE242970 | GEO
Project description:During mammalian follicular development, the correct establishment of the epitranscriptome in oocytes is essential for precise gene repression and the acquisition of developmental competence. N4-acetylcytidine (ac4C) is a conserved posttranscriptional RNA modification catalyzed by the only known “writer”, N-acetyltransferase 10 (NAT10). NAT10-targeted transcripts in oocytes and their functions in supporting folliculogenesis are poorly understood. In this study, we showed that oocyte-specific knockout of Nat10 resulted in retardation of oocyte growth with defective follicular development, premature ovarian failure, and female sterility. We profiled the ac4C landscape in the ovarian transcriptome and identified many folliculogenesis-related oocyte genes with ac4C modifications. Loss of Nat10 in oocytes eliminated ac4C signals, resulting in the downregulation of numerous oocyte-derived transcripts with reduced stability. Moreover, Nat10-deletion in oocytes or mutations in these ac4C sites led to decreased levels of protein translation, whereas the introduction of ac4C into these mRNAs increased their translational efficiencies. In addition, our data showed that the distinct gene expression patterns in granulosa cells within arrested secondary follicles were disrupted, and the identity of granulosa cells was altered by Nat10 deletion in oocytes. Taken together, these findings provide evidence that NAT10-mediated ac4C modification is a crucial regulatory factor in the maintenance of oocyte competence and that it constitutes a checkpoint for ovarian folliculogenesis beyond the secondary follicle stage.
2026-05-04 | GSE266987 | GEO
Project description:During mammalian follicular development, the correct establishment of the epitranscriptome in oocytes is essential for precise gene repression and the acquisition of developmental competence. N4-acetylcytidine (ac4C) is a conserved posttranscriptional RNA modification catalyzed by the only known “writer”, N-acetyltransferase 10 (NAT10). NAT10-targeted transcripts in oocytes and their functions in supporting folliculogenesis are poorly understood. In this study, we showed that oocyte-specific knockout of Nat10 resulted in retardation of oocyte growth with defective follicular development, premature ovarian failure, and female sterility. We profiled the ac4C landscape in the ovarian transcriptome and identified many folliculogenesis-related oocyte genes with ac4C modifications. Loss of Nat10 in oocytes eliminated ac4C signals, resulting in the downregulation of numerous oocyte-derived transcripts with reduced stability. Moreover, Nat10-deletion in oocytes or mutations in these ac4C sites led to decreased levels of protein translation, whereas the introduction of ac4C into these mRNAs increased their translational efficiencies. In addition, our data showed that the distinct gene expression patterns in granulosa cells within arrested secondary follicles were disrupted, and the identity of granulosa cells was altered by Nat10 deletion in oocytes. Taken together, these findings provide evidence that NAT10-mediated ac4C modification is a crucial regulatory factor in the maintenance of oocyte competence and that it constitutes a checkpoint for ovarian folliculogenesis beyond the secondary follicle stage.
2026-05-04 | GSE266989 | GEO
Project description:The objective of this study was to gain better understanding of the follicular conditions associated with low oocyte developmental competence in younger donors. In summary, we demonstrated that differences in follicle maturity at collection could explain differences in oocyte competence associated with individual animals.
2018-02-14 | GSE110578 | GEO
Project description:The oocyteâs capacity to complete maturation, to succeed fertilization and to reach the blastocyst stage is what defines the oocyteâs competence. The oocyte acquires this competence working closely with somatic cells of the follicle. Cumulus and granulosa cells provided support for the oocyteâs development and conversely the oocyte influence follicular cell growth and differentiation. Existing studies support the idea that follicular-stimulated hormone and luteinizing hormone play an essential role in oocyte competence acquisition through protein kinase A (PKA) and protein kinase C (PKC) signalling in granulosa cells. Therefore, human-like granulosa cells (KGN) were treated with forskolin 10 μM and phorbol 12-myristate 13-acetate 0.1 μM for 24 hours in order to process a transcriptomic analysis of differentially express genes between treatment. Over 2000 genes were founded to be differentially express at cut-off fold change of 1.5 and a p-value of 0.05. Five major upstreams, EGF, TGFB1, VEGF, FGF2 and HGF were founded to play an important role in competence acquisition thought PKA and PKC signalling. Differentially expressed targeted genes of both signalling pathways were classified in seven major ovarian functions such as PTGS2, IL8 and IL6 in inflammation, STAR, CYP11A1, CYP19A1 in steroidogenesis, VEGFC, VEGFA, CXCR4 in angiogenesis, AREG, EGFR, SPRY2 in differentiation, BAX, BCL2L12, CASP1 in apoptosis, CCND1, CCNB1, CCNB2 in division and MMP1, MMP9, TIMP1 in ovulation. Taken together, the results of this study suggest that PKA and PKC signalling potentiate their effects in some functions such as inflammation and apoptosis while some others are more specific to one or the other protein kinase like differentiation, ovulation and angiogenesis that are thought to be more PKC-dependent in human granulosa cells. 8 samples were analysed, 4 controls compared to 4 Forskolin treatments (total of 4 replicates).
2016-07-20 | E-GEOD-84541 | biostudies-arrayexpress
Project description:The oocyteâs capacity to complete maturation, to succeed fertilization and to reach the blastocyst stage is what defines the oocyteâs competence. The oocyte acquires this competence working closely with somatic cells of the follicle. Cumulus and granulosa cells provided support for the oocyteâs development and conversely the oocyte influence follicular cell growth and differentiation. Existing studies support the idea that follicular-stimulated hormone and luteinizing hormone play an essential role in oocyte competence acquisition through protein kinase A (PKA) and protein kinase C (PKC) signalling in granulosa cells. Therefore, human-like granulosa cells (KGN) were treated with forskolin 10 μM and phorbol 12-myristate 13-acetate 0.1 μM for 24 hours in order to process a transcriptomic analysis of differentially express genes between treatment. Over 2000 genes were founded to be differentially express at cut-off fold change of 1.5 and a p-value of 0.05. Five major upstreams, EGF, TGFB1, VEGF, FGF2 and HGF were founded to play an important role in competence acquisition thought PKA and PKC signalling. Differentially expressed targeted genes of both signalling pathways were classified in seven major ovarian functions such as PTGS2, IL8 and IL6 in inflammation, STAR, CYP11A1, CYP19A1 in steroidogenesis, VEGFC, VEGFA, CXCR4 in angiogenesis, AREG, EGFR, SPRY2 in differentiation, BAX, BCL2L12, CASP1 in apoptosis, CCND1, CCNB1, CCNB2 in division and MMP1, MMP9, TIMP1 in ovulation. Taken together, the results of this study suggest that PKA and PKC signalling potentiate their effects in some functions such as inflammation and apoptosis while some others are more specific to one or the other protein kinase like differentiation, ovulation and angiogenesis that are thought to be more PKC-dependent in human granulosa cells. 8 samples were analysed, 4 controls compared to 4 Phorbol 12-myristate 13-acetate treatments (total of 4 replicates).
2016-07-20 | E-GEOD-84542 | biostudies-arrayexpress
Project description:Inflammation is a key component of pathological angiogenesis. Here we induce cornea neovascularisation using sutures placed into the cornea, and sutures are removed to induce a regression phase. We used whole transcriptome microarray to monitor gene expression profies of several genes
2016-08-18 | GSE81418 | GEO
Project description:TGF-β/Smad3 Stimulates Stem Cell/Developmental Gene Expression and Vascular Smooth Muscle Cell De-Differentiation
| PRJNA237211 | ENA