The comparative roadmaps of reprogramming and transformation unveiled that cellular plasticity is broadly controlled by Bcl11b and Atoh8
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA564325 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10882106_1.fastq.gz | Fastqsanger.gz | |||
| SRR10882106_2.fastq.gz | Fastqsanger.gz | |||
| SRR10882107_1.fastq.gz | Fastqsanger.gz | |||
| SRR10882107_2.fastq.gz | Fastqsanger.gz | |||
| SRR10882108_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 109 |
Similar Datasets
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.
2022-05-06 | GSE137050 | 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 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:Bcl11b and Atoh8 binding on chromatin in MEFs
| PRJNA751042 | ENA
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 | GSE181451 | 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 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 | GSE181800 | 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 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 | GSE181799 | GEO
Project description:Atoh8 is a transcription factor of the basic-helix-loop-helix (bHLH) family that is expressed in multiple tissues during embryonic development but whose specific functions remain unknown. The gene encoding Atoh8 is induced by various lineage- determining bHLH transcription factors in cell culture, suggesting a possible common role of this gene in multiple bHLH-driven differentiation programs. In the pancreas, the pro-endocrine bHLH factors Neurogenin3 (Neurog3) and NeuroD1 activate Atoh8 expression. Moreover, Atoh8 is expressed in the embryonic pancreas confirming its participation in the pancreatic transcriptional cascade. This work aims at gaining insight into the molecular function of Atoh8 during the endocrine differentiation program initiated by Neurog3 in the pancreas. To this aim, we have generated a recombinant adenovirus encoding an Atoh8-specific shRNA (Ad-shAtoh8) and used it to down-regulate expression of the Atoh8 gene in Neurog3-expressing pancreatic ductal cells (mPAC), a cellular model of endocrine cell differentiation. Thus, we have compared global changes in gene expression profiles between cells treated with Ad-Neurog3+shControl and cells treated with Ad-Neurog3+shAtoh8 using Affymetrix microarrays. Our results show that Atoh8 silencing significantly affects the expression of 293 genes in Neurog3-expressing mPAC cells. Gene Ontology analysis has revealed cell cycle as the biological function most significantly represented among the modified genes. These results uncover a potential function of Math6 as a regulator of cell cycle progression and provide novel insights into the link between Neurog3 and the regulation of the cell cycle. mPAC cells (mouse pancreatic duct cells) overexpressing Neurogenin3 were divided in 2 groups according to the shRNA encoded by the recombinant adenoviruses used: 1) Scramble shRNA (control for the infection effect), 2) Atonal Homolog 8-specific shRNA. Experiment was performed three independent times (3 independent biological replicates).
2014-10-10 | E-GEOD-43536 | biostudies-arrayexpress
Project description:B-cell leukemia/lymphoma 11B (Bcl11b) is a transcription factor showing predominant expression in the striatum. To date, there are no known gene targets of Bcl11b in the nervous system. Here, we define targets for Bcl11b in striatal cells by performing genome-wide expression profiling. Transcriptome-wide analysis revealed that 694 genes were significantly altered in striatal cells over-expressing Bcl11b, including genes showing striatal-enriched expression similar to Bcl11b. Functional analysis on the gene target list identified significant association of Bcl11b to brain-derived neurotrophic factor/neurotrophin signaling. These data implicate Bcl11b as a novel regulator of the BDNF signaling pathway, which is disrupted in many neurological disorders. n=4 wt STHdh striatal cells and n=4 Bcl11b-transfected STHdh striatal cells
2011-08-01 | E-GEOD-31096 | biostudies-arrayexpress
Project description:Transcriptional profiling of mouse iNKT cells comparing wild type and Bcl11b deficient cell. The mice were treated with 4 μg of α-galactosylceramide. Goal was to determine the effects of transcription factor Bcl11b removal in iNKT cells. Intraperitoneal treatment with 4 μg of α-Galactosylceramide. Two pair of wild type (BCL11b F/F Vα14 transgenic) and Knock out (BCL11b F/F PLZF-Cre Vα14 transgenic)) mice were treated. Lymphocytes from spleen and liver were enriched and stain with PBS-57 Loaded CD1d tetramer. Pure iNKT cells were collected through cell sorter.
2016-08-10 | E-GEOD-73679 | biostudies-arrayexpress