IlFabAdip1
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB43990 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Fabriciana adippe (high brown fritillary) genome assembly, ilFabAdip1, alternate haplotype
| PRJEB43991 | ENA
Project description:Fabriciana adippe (high brown fritillary), genomic and transcriptomic data
| PRJEB43780 | ENA
Project description:β3-adrenergic receptor (β3-AR) hormonal signaling is imperative for adaptative thermogenesis, facilitating heat generation during cold exposure. This study explores how β3-AR signaling regulates thermogenic gene activation by altering the three-dimensional (3D) genome organization. Our findings reveal a rapid 3D genome reorganization in brown adipocytes following 4 hours of β3-AR stimulation, highlighted by high-resolution Micro-C analysis. This reorganization involves substantial dynamic changes in chromatin loops, coupled with activation of genes involved in thermogenesis. Mechanistically, β3-AR signaling promotes the p18Hamlet/SRCAP complex assembly, catalyzing the chromatin incorporation of the histone variant H2A.Z. H2A.Z incorporation enhances chromatin accessibility at loop anchors, facilitating loop formation. Disruption of H2A.Z impairs loop dynamics and thermogenic function of brown adipocytes, with implications for both mice and humans. Notably, human homologous loop anchors are associated with obesity-related genetic variants. This study underscores the critical role of 3D genome architecture in thermogenic regulation, offering new dimensions into obesity’s molecular underpinnings.
2026-02-17 | GSE261410 | GEO
Project description:β3-adrenergic receptor (β3-AR) hormonal signaling is imperative for adaptative thermogenesis, facilitating heat generation during cold exposure. This study explores how β3-AR signaling regulates thermogenic gene activation by altering the three-dimensional (3D) genome organization. Our findings reveal a rapid 3D genome reorganization in brown adipocytes following 4 hours of β3-AR stimulation, highlighted by high-resolution Micro-C analysis. This reorganization involves substantial dynamic changes in chromatin loops, coupled with activation of genes involved in thermogenesis. Mechanistically, β3-AR signaling promotes the p18Hamlet/SRCAP complex assembly, catalyzing the chromatin incorporation of the histone variant H2A.Z. H2A.Z incorporation enhances chromatin accessibility at loop anchors, facilitating loop formation. Disruption of H2A.Z impairs loop dynamics and thermogenic function of brown adipocytes, with implications for both mice and humans. Notably, human homologous loop anchors are associated with obesity-related genetic variants. This study underscores the critical role of 3D genome architecture in thermogenic regulation, offering new dimensions into obesity’s molecular underpinnings.
2026-02-17 | GSE261412 | GEO
Project description:Recent molecular advancements have revolutionized our understanding of the role of three-dimensional (3D) genome organization in gene regulation. Yet, the impact of acute hormonal signaling on reshaping genome structure and its consequences for metabolic processes remain largely unexplored. β3-adrenergic receptor (β3-AR) hormonal signaling is imperative for brown adipose tissue (BAT) thermogenesis. Here, we demonstrate that β3-AR signaling induces rapid reorganization of fine-scale genome architecture in murine and human brown adipocytes within four hours. High-resolution Micro-C profiling reveals dynamic chromatin loop formation associated with activation of thermogenic genes. Mechanistically, β3-AR signaling promotes p18Hamlet/SRCAP complex assembly, catalyzing incorporation of the histone variant H2A.Z into nucleosomes. ATAC-sequencing reveals that H2A.Z enhances chromatin accessibility at loop anchors, supporting loop formation by facilitating the recruitment of looping factors such as the Mediator complex. Disruption of H2A.Z compromises dynamic chromatin looping and transcriptional activation of thermogenic genes in both species. Mice with BAT-specific H2A.Z deficiency exhibit reduced thermogenic activity and impaired glucose tolerance. Revisiting genome-wide association study analysis reveals that H2A.Z-occupied loops are linked to genetic variants associated with obesity and its related metabolic disorders. Together, these findings highlight the rapid adaptability of 3D genome organization to acute β3-AR signaling and its critical role in brown adipocyte thermoregulation.
2026-02-17 | GSE301360 | GEO
Project description:Recent molecular advancements have revolutionized our understanding of the role of three-dimensional (3D) genome organization in gene regulation. Yet, the impact of acute hormonal signaling on reshaping genome structure and its consequences for metabolic processes remain largely unexplored. β3-adrenergic receptor (β3-AR) hormonal signaling is imperative for brown adipose tissue (BAT) thermogenesis. Here, we demonstrate that β3-AR signaling induces rapid reorganization of fine-scale genome architecture in murine and human brown adipocytes within four hours. High-resolution Micro-C profiling reveals dynamic chromatin loop formation associated with activation of thermogenic genes. Mechanistically, β3-AR signaling promotes p18Hamlet/SRCAP complex assembly, catalyzing incorporation of the histone variant H2A.Z into nucleosomes. ATAC-sequencing reveals that H2A.Z enhances chromatin accessibility at loop anchors, supporting loop formation by facilitating the recruitment of looping factors such as the Mediator complex. Disruption of H2A.Z compromises dynamic chromatin looping and transcriptional activation of thermogenic genes in both species. Mice with BAT-specific H2A.Z deficiency exhibit reduced thermogenic activity and impaired glucose tolerance. Revisiting genome-wide association study analysis reveals that H2A.Z-occupied loops are linked to genetic variants associated with obesity and its related metabolic disorders. Together, these findings highlight the rapid adaptability of 3D genome organization to acute β3-AR signaling and its critical role in brown adipocyte thermoregulation.
2026-02-17 | GSE301368 | GEO
Project description:Recent molecular advancements have revolutionized our understanding of the role of three-dimensional (3D) genome organization in gene regulation. Yet, the impact of acute hormonal signaling on reshaping genome structure and its consequences for metabolic processes remain largely unexplored. β3-adrenergic receptor (β3-AR) hormonal signaling is imperative for brown adipose tissue (BAT) thermogenesis. Here, we demonstrate that β3-AR signaling induces rapid reorganization of fine-scale genome architecture in murine and human brown adipocytes within four hours. High-resolution Micro-C profiling reveals dynamic chromatin loop formation associated with activation of thermogenic genes. Mechanistically, β3-AR signaling promotes p18Hamlet/SRCAP complex assembly, catalyzing incorporation of the histone variant H2A.Z into nucleosomes. ATAC-sequencing reveals that H2A.Z enhances chromatin accessibility at loop anchors, supporting loop formation by facilitating the recruitment of looping factors such as the Mediator complex. Disruption of H2A.Z compromises dynamic chromatin looping and transcriptional activation of thermogenic genes in both species. Mice with BAT-specific H2A.Z deficiency exhibit reduced thermogenic activity and impaired glucose tolerance. Revisiting genome-wide association study analysis reveals that H2A.Z-occupied loops are linked to genetic variants associated with obesity and its related metabolic disorders. Together, these findings highlight the rapid adaptability of 3D genome organization to acute β3-AR signaling and its critical role in brown adipocyte thermoregulation.
2026-02-17 | GSE301366 | GEO