Fosl2 orchestrates chromatin accessibility to determine granulosa cells developmental trajectories
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ABSTRACT:
PROVIDER: PRJNA1113965 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Fosl2 orchestrates chromatin accessibility to determine granulosa cells developmental trajectories [ATAC-seq]
| PRJNA1113521 | ENA
Project description:Fosl2 orchestrates chromatin accessibility to determine granulosa cells developmental trajectories [RNA-seq]
| PRJNA1113522 | ENA
Project description:Fosl2 orchestrates chromatin accessibility to determine granulosa cells developmental trajectories [CUT&Tag]
| PRJNA1113520 | ENA
Project description:Fosl2 orchestrates chromatin accessibility to determine granulosa cells developmental trajectories [scRNA-Seq]
| PRJNA1182281 | ENA
Project description:Granulosa cells (GCs) behave as the most dynamically responsive cell lineage to encourage continuous ovarian folliculogenesis; however, the determinants of their developmental trajectories and interplay with downstream transcription circuitry remain poorly understood. In this research, we delineate the genome-wide redistribution of accessible chromatin regions that drive broad developmental-related transcriptomic changes aacross porcine and murine follicular stages. We report the distinct GCs-activated accessibility regions (GAAs), are responsible for augmenting of flanking GCs-involved developmental genes (GDGs) expression, serving as a key requirement for transcription in response to developmental cues. Mechanistically, the transcription factor Fosl2 is robustly recruited to GAAs, facilitating chromatin accessibility state transition. The enlarged GAAs signal driven by Fosl2 loading subsequently induces a significant upregulation of adjacent GDG expression. Additionally, the germ cell-specific deletion of Fols2 induces perturbations in GCs cellularity, which consequently precipitate endocrine dysfunction and a progressive deterioration in reproductive competence in murine models. Together, our research provides a detailed depiction of the dynamic chromatin accessibility landscape throughout the developmental continuum of GCs, revealing the indispensable function of Fosl2 in controlling the transcriptional activation via the reconfiguration of the widespread chromatin state.
2024-11-10 | GSE281100 | GEO
Project description:Granulosa cells (GCs) behave as the most dynamically responsive cell lineage to encourage continuous ovarian folliculogenesis; however, the determinants of their developmental trajectories and interplay with downstream transcription circuitry remain poorly understood. In this research, we delineate the genome-wide redistribution of accessible chromatin regions that drive broad developmental-related transcriptomic changes aacross porcine and murine follicular stages. We report the distinct GCs-activated accessibility regions (GAAs), are responsible for augmenting of flanking GCs-involved developmental genes (GDGs) expression, serving as a key requirement for transcription in response to developmental cues. Mechanistically, the transcription factor Fosl2 is robustly recruited to GAAs, facilitating chromatin accessibility state transition. The enlarged GAAs signal driven by Fosl2 loading subsequently induces a significant upregulation of adjacent GDG expression. Additionally, the germ cell-specific deletion of Fols2 induces perturbations in GCs cellularity, which consequently precipitate endocrine dysfunction and a progressive deterioration in reproductive competence in murine models. Together, our research provides a detailed depiction of the dynamic chromatin accessibility landscape throughout the developmental continuum of GCs, revealing the indispensable function of Fosl2 in controlling the transcriptional activation via the reconfiguration of the widespread chromatin state.
2024-06-01 | GSE267851 | GEO
Project description:Granulosa cells (GCs) behave as the most dynamically responsive cell lineage to encourage continuous ovarian folliculogenesis; however, the determinants of their developmental trajectories and interplay with downstream transcription circuitry remain poorly understood. In this research, we delineate the genome-wide redistribution of accessible chromatin regions that drive broad developmental-related transcriptomic changes aacross porcine and murine follicular stages. We report the distinct GCs-activated accessibility regions (GAAs), are responsible for augmenting of flanking GCs-involved developmental genes (GDGs) expression, serving as a key requirement for transcription in response to developmental cues. Mechanistically, the transcription factor Fosl2 is robustly recruited to GAAs, facilitating chromatin accessibility state transition. The enlarged GAAs signal driven by Fosl2 loading subsequently induces a significant upregulation of adjacent GDG expression. Additionally, the germ cell-specific deletion of Fols2 induces perturbations in GCs cellularity, which consequently precipitate endocrine dysfunction and a progressive deterioration in reproductive competence in murine models. Together, our research provides a detailed depiction of the dynamic chromatin accessibility landscape throughout the developmental continuum of GCs, revealing the indispensable function of Fosl2 in controlling the transcriptional activation via the reconfiguration of the widespread chromatin state.
2024-06-01 | GSE267850 | GEO
Project description:Granulosa cells (GCs) behave as the most dynamically responsive cell lineage to encourage continuous ovarian folliculogenesis; however, the determinants of their developmental trajectories and interplay with downstream transcription circuitry remain poorly understood. In this research, we delineate the genome-wide redistribution of accessible chromatin regions that drive broad developmental-related transcriptomic changes aacross porcine and murine follicular stages. We report the distinct GCs-activated accessibility regions (GAAs), are responsible for augmenting of flanking GCs-involved developmental genes (GDGs) expression, serving as a key requirement for transcription in response to developmental cues. Mechanistically, the transcription factor Fosl2 is robustly recruited to GAAs, facilitating chromatin accessibility state transition. The enlarged GAAs signal driven by Fosl2 loading subsequently induces a significant upregulation of adjacent GDG expression. Additionally, the germ cell-specific deletion of Fols2 induces perturbations in GCs cellularity, which consequently precipitate endocrine dysfunction and a progressive deterioration in reproductive competence in murine models. Together, our research provides a detailed depiction of the dynamic chromatin accessibility landscape throughout the developmental continuum of GCs, revealing the indispensable function of Fosl2 in controlling the transcriptional activation via the reconfiguration of the widespread chromatin state.
2024-06-01 | GSE267849 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-06-01 | GSE267974 | GEO
Project description:The differentiation of Th17 cells is controlled by a complex network of transcription factors (TFs), including FOS and JUN proteins of the AP-1 family. The FOS-like proteins, FOSL1 and FOSL2 have recently been reported to control Th17 responses. The molecular mechanisms dictating their roles, however, are unclear. Moreover, although the functions of AP-1 TFs are largely governed by their protein-protein interactions, these are also poorly characterized in this milieu. Using affinity purification in combination with mass-spectrometry we established the first interactomes of FOSL1 and FOSL2 in human Th17 cells. In addition to their known interactions with JUN proteins, our analysis identified several novel binding partners of FOSL factors. Gene ontology analysis revealed RNA binding was enriched as the major functionality for FOSL1 and FOSL2 associated proteins, thereby suggesting possible mechanistic links that have not been studied before. Intriguingly, 29 interactors were found to be shared between FOSL1 and FOSL2, which included crucial regulators of Th17-fate. These findings, including unique and shared interactions, were validated using parallel reaction monitoring targeted mass-spectrometry (PRM-MS), with additional measurements with other laboratory methods. Overall, this study provides key insights into interaction-based signalling mechanisms of FOSL1 and FOSL2, which potentially control Th17 cell-development and associated pathologies.
2021-11-02 | PXD025729 | Pride