Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance [P53-WT-cKO_BulkRNA]

ABSTRACT: Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance [P53-WT-cKO_BulkRNA]

PROVIDER: PRJNA1287484 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance

Project description:Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance

| PRJNA1145966 | ENA

Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance [RNA-seq]

Project description:Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance [RNA-seq]

| PRJNA1145955 | ENA

Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance [CUT&Run]

Project description:Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance [CUT&Run]

| PRJNA1229619 | ENA

Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance

Project description:Phenotypic plasticity of somatic cells is a principal feature of vertebrate adaptation as well as a hallmark of tumorigenesis. However, the determinants and mechanisms that regulate the stability of somatic cell identities remain unclear. Here, using the somatic plasticity of thymic epithelial cells – which facilitates the selection of a self-discriminating T cell repertoire – as a physiological model system, we show that stochastic fluctuations in background chromatin accessibility at nucleosome-dense regions are amplified by thymic epithelial cells to ectopically express thousands of genes highly restricted to other specialized cell types. We found broad regions of inaccessible chromatin flanking tissue-specific genes become ‘destabilized’ during thymic epithelial maturation independently of AIRE-induced transcription of these genes, but concurrently with the repression of the tumor suppressor p53. Augmenting p53 activity in thymic epithelial cells reduced noise in chromatin accessibility at nucleosome-dense regions, inhibited ectopic expression of tissue-specific genes and caused multi-organ autoimmunity. Furthermore, we found p53-regulated fluctuations in background chromatin accessibility in lung adenocarcinoma to be associated with high plasticity states that promote tumor progression. Taken together, our findings establish p53-dependent stabilization of nucleosomal barriers to cellular reprogramming as a fulcrum of cell fate integrity that underlies critical components of immune tolerance induction and oncogenic potential.

2025-06-30 | GSE274324 | GEO

Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance [P53-WT-cKO_BulkRNA]

2025-07-08 | GSE301724 | GEO

Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance [CUT&Run]

2025-06-30 | GSE290716 | GEO

Thymic epithelia amplify noise in chromatin accessibility via p53 repression to impose immune tolerance [RNA-seq]

2025-06-30 | GSE274320 | GEO

Expression data from mammary epithelia and mammary fibroblasts from mice with and without epithelial KrasG12D and with and without stromal p53 deletion

Project description:p53 is a known tumor suppressor. We have found that stromal p53 regulates breast cancer development, the immune landscape, and survival in an oncogene specific manner when comparing the epithelial oncogenes ErbB2 and KrasG12D In this dataset, we have evaluated mammary epithelia from mice with and without epithelial KrasG12D and with and without stromal p53 deletion. We have also evaluated mammary fibroblasts from mice with and without epithelial KrasG12D and with and without stromal p53 deletion.

2022-05-01 | GSE201935 | GEO

Comparative analysis between single-cell RNA-seq and single-molecule RNA FISH indicates that the pyrimidine nucleobase idoxuridine (IdU) globally amplifies transcriptional noise

Project description:Stochastic fluctuations (noise) in transcription generate substantial cell-to-cell variability, but the physiological roles of noise have remained difficult to determine in the absence of generalized noise-modulation approaches. Previous single-cell RNA-sequencing (scRNA-seq) suggested that the pyrimidine-base analog (5′-iodo-2′-deoxyuridine, IdU) could generally amplify noise without substantially altering mean-expression levels but scRNA-seq technical drawbacks potentially obscured the penetrance of IdU-induced transcriptional noise amplification. Here we quantify global-vs.-partial penetrance of IdU-induced noise amplification by assessing scRNA-seq data using numerous normalization algorithms and complement our previous results with data from Human Jurkat T Lymphocytes, including two biological replicates to allow rigorous statistical analysis. Collectively, this analysis indicates which scRNA-seq algorithms are appropriate for quantifying noise and argues that IdU is a globally penetrant noise-enhancer molecule that could enable investigations of the physiological impacts of transcriptional noise in various cell types and organisms.

2024-08-28 | GSE263194 | GEO

Nucleosome noise

Project description:Fuzziness and noise in nucleosomal architecture

| PRJEB4709 | ENA