Bcl11b and Atoh8 binding on chromatin in MEFs
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA751042 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15305462.fastq.gz | Fastqsanger.gz | |||
| SRR15305463.fastq.gz | Fastqsanger.gz | |||
| SRR15305464.fastq.gz | Fastqsanger.gz | |||
| SRR18246867.fastq.gz | Fastqsanger.gz | |||
| SRR18246868.fastq.gz | Fastqsanger.gz |
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Project description:Coordinated changes of cellular plasticity and cellular identity are critical for pluripotent reprogramming and oncogenic transformation. However, the sequences of cellular/molecular events that orchestrate these intermingled modifications have never been comparatively dissected. Here, we deconvoluted the cellular trajectories of reprogramming (via Oct4/Sox2/Klf4/c-Myc) and transformation (via Ras/c-Myc) at the single-cell resolution and revealed how the two processes intersect prior to bifurcate. This approach also led to identify the transcription factor (TF) Bcl11b as a broad-range regulator of cell fate changes, as well as a pertinent marker to capture early cellular intermediates that emerge simultaneously during reprogramming and transformation. Multi-omics characterization of these intermediates led to unveil a c-Myc/Atoh8/Sfrp1 regulatory axis that constrains rodent and human reprogramming but also cancer cell plasticity and neuron transdifferentiation. Mechanistically, we found that the TF Atoh8 restrains cellular plasticity, independently of cellular identity, by binding a specific enhancer network. This study provides insights into the partitioned control of cellular plasticity and identity for both regenerative and cancer biology.
2022-05-06 | GSE181196 | GEO
Project description:The differentiation of preadipocytes into adipocytes is controlled by several transcription factors, including peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), which are known as master regulators of adipogenesis. BCL11B is a zinc finger-type transcription factor that regulates the development of the skin and central nervous and immune systems. Here, we found that BCL11B was expressed in the white adipose tissue (WAT), particularly the subcutaneous WAT and that BCL11Bâ/â mice had a reduced amount of subcutaneous WAT. During adipogenesis, BCL11B expression transiently increased in 3T3-L1 preadipocytes and mouse embryonic fibroblasts (MEFs). The ability for adipogenesis was reduced in BCL11B knockdown 3T3-L1 cells and BCL11Bâ/â MEFs, whereas the ability for osteoblastogenesis was unaffected in BCL11Bâ/â MEFs. Luciferase reporter gene assays revealed that BCL11B stimulated C/EBPβ activity. Furthermore, the expression of downstream genes of the Wnt/β-catenin signaling pathway was not suppressed in BCL11Bâ/â MEFs during adipogenesis. Thus, this study identifies BCL11B as a novel regulator of adipogenesis, which works, at least in part, by stimulating C/EBPβ activity and suppressing the Wnt/β-catenin signaling pathway. MEFs were derived from embryonic day 12.5 BCL11B+/+ and BCL11Bâ/â C57BL6 mice embryos. After 2 times passage, MEFs were differentiated using the adipocyte differentiation medium and 10 μM pioglitazone. After 12 h of adipocyte differentiation, gene expression profiles were analyzed by DNA microarray.
2016-09-05 | E-GEOD-83980 | biostudies-arrayexpress
Project description:The differentiation of preadipocytes into adipocytes is controlled by several transcription factors, including peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), which are known as master regulators of adipogenesis. BCL11B is a zinc finger-type transcription factor that regulates the development of the skin and central nervous and immune systems. Here, we found that BCL11B was expressed in the white adipose tissue (WAT), particularly the subcutaneous WAT and that BCL11B−/− mice had a reduced amount of subcutaneous WAT. During adipogenesis, BCL11B expression transiently increased in 3T3-L1 preadipocytes and mouse embryonic fibroblasts (MEFs). The ability for adipogenesis was reduced in BCL11B knockdown 3T3-L1 cells and BCL11B−/− MEFs, whereas the ability for osteoblastogenesis was unaffected in BCL11B−/− MEFs. Luciferase reporter gene assays revealed that BCL11B stimulated C/EBPβ activity. Furthermore, the expression of downstream genes of the Wnt/β-catenin signaling pathway was not suppressed in BCL11B−/− MEFs during adipogenesis. Thus, this study identifies BCL11B as a novel regulator of adipogenesis, which works, at least in part, by stimulating C/EBPβ activity and suppressing the Wnt/β-catenin signaling pathway.
2016-09-05 | GSE83980 | GEO
Project description:Coordinated changes of cellular plasticity and cellular identity are critical for pluripotent reprogramming and oncogenic transformation. However, the sequences of cellular/molecular events that orchestrate these intermingled modifications have never been comparatively dissected. Here, we deconvoluted the cellular trajectories of reprogramming (via Oct4/Sox2/Klf4/c-Myc) and transformation (via Ras/c-Myc) at the single-cell resolution and revealed how the two processes intersect prior to bifurcate. This approach also led to identify the transcription factor (TF) Bcl11b as a broad-range regulator of cell fate changes, as well as a pertinent marker to capture early cellular intermediates that emerge simultaneously during reprogramming & transformation. Multi-omics characterization of these intermediates led to unveil a c-Myc/Atoh8/Sfrp1 regulatory axis that constrains rodent and human reprogramming but also cancer cell plasticity and neuron transdifferentiation. Mechanistically, we found that the TF Atoh8 restrains cellular plasticity, independently of cellular identity, by binding a specific enhancer network. This study provides insights into the partitioned control of cellular plasticity and identity for both regenerative and cancer biology.
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Project description:Upon Atoh8 downregulation by shRNA in MEFs, KRas512D mutation c-Myc over-expression and depletion of p53 were induced in mouse embryonic fibroblasts. After 10 passages, cells were collected and RNA extracted.
2022-05-06 | GSE143593 | GEO
Project description:Upon Atoh8 downregulation by shRNA, cells were cultivated for 5 days and RNA extracted for sequencing.
2022-05-06 | GSE143592 | GEO
Project description:Mucosal associated invariant T (MAIT) cells, already differentiated and located at mucosal sites, are critical in the body’s first wave of defenses against invading pathogens. Bcl11b KO MAIT cells fail to be maintained both in the thymus and peripheral organs. Furthermore, MAIT cells fail to fully develop in the thymus without Bcl11b, failing to upregulate RORγt, and that phenotype remains in the lungs and livers of these mice. Bcl11b deletion in MAIT cells causes dramatic shifts in the activation and TH17 programs, due to the binding of Bcl11b in many of those genes, which we have seen in the human MAIT cells. MAIT cells rely on PLZF and RORγt for their development and function, while also heavily relying on Bcl11b. These data show the key interplay of Bcl11b with PLZF and RORγt in a T cell leading to its development and necessary function to protect the body against diseases.
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Project description:Mapping Bcl11b binding in regulatory T cells
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Project description:Mapping Bcl11b binding in human MAIT cells
| PRJNA608199 | ENA
Project description:T regulatory (Treg) cells have been studied in depth since their discovery for their potential use in therapies of autoimmune diseases. Treg cells have a suppression program that includes surface molecules CD25 (IL2R), cytotoxic T-lymphocyte associated protein 4 (CTLA4), and glucocorticoid-induced TNFR family (GITR) to limit aberrant and excessive inflammatory immune responses. We have shown that Bcl11b can bind to the CNS2 region in Foxp3 as well as the gene loci of those essential surface molecules for Treg suppression. Furthermore, we have identified a subset of Foxp3-independent genes in Treg cells directly regulated by Bcl11b binding. Bcl11b also directly represses expression of innate molecules such as transcription factors PU.1 and ID2 in Treg cells. Finally, we have also shown that removal of Bcl11b accelerates apoptosis in Treg cells as cleaved caspase 3 levels were significantly elevated in Bcl11b KO Treg cells when compared with WT Treg cells.
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