Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA193681 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:During female reproductive life, the reserve of ovarian follicles is reduced by maturation and atresia until menopause ensues. Foxo3 is required to maintain the ovarian reserve in mice. We asked if overexpression of a constitutively active FOXO3 protein can increase long-lasting ovarian reproductive capacity in mice. Trangenic vs non-transgenic mice onto Foxo3+/- vs Foxo3-/- genotype
2013-06-08 | E-GEOD-45389 | biostudies-arrayexpress
Project description:During female reproductive life, the reserve of ovarian follicles is reduced by maturation and atresia until menopause ensues. Foxo3 is required to maintain the ovarian reserve in mice. We asked if overexpression of a constitutively active FOXO3 protein can increase long-lasting ovarian reproductive capacity in mice.
2013-06-08 | GSE45389 | GEO
Project description:Expression data from the mouse liver with constitutively active FoxO3
| PRJNA192681 | ENA
Project description:Ovarian reserve defines the female reproductive lifespan, which in humans spans decades due to the robust maintenance of meiotic arrest in non-growing oocytes residing in primordial follicles. Dynamic epigenomic reprogramming and programming occur during mammalian germline and early embryonic development. However, the chromatin-based mechanisms that underlie the establishment and maintenance of ovarian reserves are poorly defined. Here, we report a comprehensive epigenomic landscape of mouse perinatal oocytes and unravel Polycomb-based mechanisms underlying ovarian reserve development. By quantitatively profiling key histone modifications, including the Polycomb-mediated repressive marks H2AK119ub and H3K27me3, we identified two major epigenomic transitions: one for ovarian reserve formation from meiotic prophase I to dictyate-arrested non-growing oocytes, and another for ovarian reserve activation from non-growing to growing oocytes. Combining conditional loss-of-function mouse models for Polycomb Repressive Complex 1 or 2 (PRC1/2), we show that PRC1-H2AK119ub and PRC2-H3K27me3 undergo differential dynamics during perinatal oogenesis and have distinct biological functions in ovarian reserve formation and maintenance. Notably, PRC1-H2AK119ub presets the epigenetic states in non-growing oocytes and provides a blueprint for the PRC2-H3K27me3 profile, which is globally reprogrammed as oocytes exit the ovarian reserve and grow. Our study determines a comprehensive epigenomic roadmap of perinatal oogenesis, shedding light on how the ovarian reserve is formed, maintained, and activated, emphasizing a critical window of epigenetic programming during female germline development.
2026-02-23 | GSE311349 | GEO
Project description:Ovarian reserve defines the female reproductive lifespan, which in humans spans decades due to the robust maintenance of meiotic arrest in non-growing oocytes residing in primordial follicles. Dynamic epigenomic reprogramming and programming occur during mammalian germline and early embryonic development. However, the chromatin-based mechanisms that underlie the establishment and maintenance of ovarian reserves are poorly defined. Here, we report a comprehensive epigenomic landscape of mouse perinatal oocytes and unravel Polycomb-based mechanisms underlying ovarian reserve development. By quantitatively profiling key histone modifications, including the Polycomb-mediated repressive marks H2AK119ub and H3K27me3, we identified two major epigenomic transitions: one for ovarian reserve formation from meiotic prophase I to dictyate-arrested non-growing oocytes, and another for ovarian reserve activation from non-growing to growing oocytes. Combining conditional loss-of-function mouse models for Polycomb Repressive Complex 1 or 2 (PRC1/2), we show that PRC1-H2AK119ub and PRC2-H3K27me3 undergo differential dynamics during perinatal oogenesis and have distinct biological functions in ovarian reserve formation and maintenance. Notably, PRC1-H2AK119ub presets the epigenetic states in non-growing oocytes and provides a blueprint for the PRC2-H3K27me3 profile, which is globally reprogrammed as oocytes exit the ovarian reserve and grow. Our study determines a comprehensive epigenomic roadmap of perinatal oogenesis, shedding light on how the ovarian reserve is formed, maintained, and activated, emphasizing a critical window of epigenetic programming during female germline development.
2026-02-23 | GSE280638 | GEO
Project description:Expression of constitutively active FOXO3 in murine forebrain leads to a loss of neural progenitors
| PRJNA126707 | ENA
Project description:The ovarian reserve, a finite pool of long-lived non-growing oocytes established at birth, determines female reproductive lifespan, yet how these oocytes establish long-term quiescence while retaining the capacity for future growth and embryogenesis remains poorly understood. Here, we define a regulatory logic by which Polycomb repressive complexes shape stage-specific active chromatin remodeling during ovarian reserve formation and early oocyte growth. During ovarian reserve formation, H3K27ac, an active promoter- and enhancer-associated mark, undergoes extensive genome-wide redistribution. A key feature of this transition is CpG island promoter remodeling, in which many loci lose H3K27ac while gaining PRC1-dependent H2AK119ub, a repressive mark. This early reprogramming is followed during oocyte growth by acquisition of PRC2-dependent H3K27me3, de novo establishment of bivalent promoters, and protection of promoter regions from de novo DNA methylation. Oocyte growth is also accompanied by broad gains in both H3K27ac and H3K4me3, an active promoter-associated mark. Analyses of PRC1- and PRC2-deficient oocytes reveal unequal Polycomb contributions: PRC2 broadly constrains H3K27ac, whereas PRC1 more selectively shapes genome-wide H3K27ac redistribution and restricts H3K4me3 accumulation at bivalent promoters. Together, these findings identify staged active chromatin remodeling as an integral feature of perinatal oocyte development and reveal that Polycomb shapes chromatin state transitions as oocytes enter quiescence and become poised for future growth.
2026-02-12 | GSE280637 | GEO
Project description:Although it is well established that the ovarian reserve diminishes with increasing age, and that a woman’s age is correlated to lower oocyte quality, the interplay of a diminished reserve and age on oocyte developmental competence is not clear. After maturation, oocytes are mostly transcriptionally quiescent, and developmental competence prior to embryonic genome activation (EGA) relies on maternal RNA and proteins. Age and ovarian reserve both affects oocyte developmental competence, however, their relative importance in this process are difficult to tease out, as ageing is accompanied by a decrease in ovarian reserve. Oocytes store large quantities of RNA, including several noncoding transcripts (ncRNAs) involved in early development transcription and translation modulation. Despite the central role of ncRNAs in maternal to zygote transition, no characterization of the ncRNA transcriptome in human oocytes has been reported. This study aims at identifying how the human oocyte transcriptome changes across reproductive ages and ovarian reserve levels, with the goal of identifying candidate markers of developmental competence, and to assess the independent relevance of age and ovarian reserve in the changes of the transcriptome
2017-08-29 | GSE87201 | GEO
Project description:Primary ovarian insufficiency (POI) and related infertility, early menopause, and endocrine disorders are major side effects in young female cancer patients undergoing cancer treatment. Current strategies preserving ovarian functions and fertility can be suboptimal due to concerns of feasibility, efficacy, or safety. Herein, we identify c-Jun N-terminal kinase (JNK) as a pivotal factor regulating the DNA damage response (DDR) signaling in oocytes of primordial follicles in response to DNA-damaging chemotherapy. Using pharmacological inhibition of JNK and a mouse model with oocyte-specific deletion of JNK, together with bioinformatic, molecular, and computational approaches, we show that inhibition of oogenic JNK prevents chemotherapy-induced oocyte apoptosis and POI as well as preserve long-term reproductive cycles and fertility. Mechanistically, JNK is activated upon chemotherapy-induced DNA damage in oocytes of primordial follicles, which further activates the transcription factor TAp63α and triggers oocyte apoptosis. we further used a breast cancer mouse model to demonstrate that JNK inhibition preserves the ovarian reserve without interfering with the anti-cancer efficacy of chemotherapy. Together, our research establishes JNK as a crucial determinant of oocyte apoptosis and POI following DNA-damaging cancer therapy, highlighting JNK as a promising target for developing ovarian protectant and preserving the ovarian reserve, fertility, and ovarian endocrine functions in young female cancer patients.
2026-04-28 | GSE314244 | GEO
Project description:The ovarian reserve defines the female reproductive lifespan, which in humans spans decades due to robust maintenance of meiotic arrest in oocytes residing in primordial follicles. Epigenetic reprogramming, including DNA demethylation, accompanies meiotic entry, but the chromatin changes that underpin the generation and preservation of ovarian reserves are poorly defined. We report that the Polycomb Repressive Complex 1 (PRC1) establishes repressive chromatin states in perinatal mouse oocytes that directly suppress the gene expression program of meiotic prophase-I and thereby enable the transition to dictyate arrest. PRC1 dysfuction causes depletion of the ovarian reserve and leads to premature ovarian failure. Our study demonstrates a fundamental role for PRC1-mediated gene silencing in female reproductive lifespan, and reveals a critical window of epigenetic programming required to establish ovarian reserve.
2022-06-26 | GSE184208 | GEO