Philaethria dido
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA686711 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The prevalence of overweight and obesity continues to rise in the population worldwide. Because it is an important predisposing factor for cancer, cardiovascular diseases, diabetes mellitus, and COVID-19, obesity reduces life expectancy. Adipose tissue (AT), the main fat storage organ with endocrine capacity, plays fundamental roles in systemic metabolism and obesity-related diseases. Dysfunctional AT can induce excess or reduced body fat (lipodystrophy). Dido1 is a marker gene for stemness; gene-targeting experiments compromised several functions ranging from cell division to embryonic stem cell differentiation, both in vivo and in vitro. We report that mutant mice lacking the DIDO N terminus show a lean phenotype. This consists of reduced AT and hypolipidemia, even when mice are fed a high-nutrient diet. DIDO mutation caused hypothermia due to lipoatrophy of white adipose tissue (WAT) and dermal fat thinning. Deep sequencing of the epididymal white fat (Epi WAT) transcriptome supported Dido1 control of the cellular lipid metabolic process. We found that, by controlling the expression of transcription factors such as C/EBPα or PPARγ, Dido1 is necessary for adipocyte differentiation, and that restoring their expression reestablished adipogenesis capacity in Dido1 mutants. Our model differs from other lipodystrophic mice and could constitute a new system for the development of therapeutic intervention in obesity.
2024-01-09 | GSE236036 | GEO
Project description:The analysis of interactome of different DIDO isoforms and mutants upon transient overexpression of FLAG-tagged constructs in HEK293T cells.
2023-10-25 | PXD039540 | Pride
Project description:The prevalence of overweight and obesity continues to rise in the population worldwide. Because it is an important predisposing factor for cancer, cardiovascular diseases, diabetes mellitus, and COVID-19, obesity reduces life expectancy. Adipose tissue (AT), the main fat storage organ with endocrine capacity, plays fundamental roles in systemic metabolism and obesity-related diseases. Dysfunctional AT can induce excess or reduced body fat (lipodystrophy). Dido1 is a marker gene for stemness; gene-targeting experiments compromised several functions ranging from cell division to embryonic stem cell differentiation, both in vivo and in vitro. We report that mutant mice lacking the DIDO N terminus show a lean phenotype. This consists of reduced AT and hypolipidemia, even when mice are fed a high nutrient diet. DIDO mutation caused hypothermia due to lipoatrophy of white adipose tissue (WAT) and dermal fat thinning. Deep sequencing of the epididymal white fat (Epi WAT) transcriptome supported Dido1 control of the lipid metabolic process. We found that, by controlling expression of transcription factors such as C/EBPα or PPARγ, Dido1 is necessary for adipocyte differentiation, and that restoring their expression reestablished adipogenesis capacity in Dido1 mutants. Our model differs from other lipodystrophic mice and could constitute a new system for the development of therapeutic intervention in obesity.
2024-01-09 | GSE236034 | GEO
Project description:The analysis of differential interactome of Pol II pS5 in DIDO WT, KO and ΔSPOC HEK293T cells using Pol II pS5 (3E8) antibody coupled to Protein G beads (no crosslinking).
2023-10-25 | PXD039567 | Pride
Project description:Transition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation.
2017-03-16 | GSE85028 | GEO
Project description:Data demonstrating utility of diDO-IPTL labeling method for quantitative proteomics
2017-01-08 | MSV000080457 | MassIVE
Project description:Rates of overweight and obesity continue to rise in the population worldwide. Obesity reduces life expectancy because it is an important predisposing factor for cancer, cardiovascular diseases and diabetes mellitus. Adipose tissue (AT), the main organ for fat storage with endocrine capacity, plays fundamental roles in systemic metabolism and in obesity-related diseases. Adiposity and lipodystrophy are associated with metabolic disorders, indicating that normal AT function is required for metabolic health. Dido1 is a marker gene for stemness and gene-targeting experiments compromised several functions from cell division to embryonic stem cell differentiation, in vivo and in vitro. Using animals carrying a DIDO mutant without the N-terminal, we report that these mice display a lean phenotype with reduced adipose tissue and hypolipidemia even when fed with an obesogenic diet. The phenotype related to impaired adipogenesis, partially corrected by transcription factors C/EBPα or PPARγ expression and to hypothermia subsequent to dermal fat thinning. Deep sequencing of the epididymal white fat (Epi WAT) transcriptome shows the role of Dido1 in the control of cellular lipases. The molecular analysis involves Dido1 in orchestrating adipogenesis and altogether offers a model different from described lipodystrophies in mice and pioneers a new path to understand obesity and identify mechanism for obesity intervention.
2024-01-09 | GSE195908 | GEO
Project description:DIDO is necessary for adipogenesis promoting diet-induced obesity [I]
| PRJNA802653 | ENA
Project description:Transition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation. We used microarrays to determine how the deletion of exon 16 (C-terminal truncation) of the Dido3 affects gene expression that results in the suppression of ESC differentiation.
2017-03-16 | GSE85026 | GEO
Project description:Transition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation. We used microarrays to determine how the deletion of exon 16 (C-terminal truncation) of the Dido3 affects gene expression that results in the suppression of ESC differentiation.
2017-03-16 | GSE85025 | GEO