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P53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [RNA-seq]

ABSTRACT: p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [RNA-seq]

PROVIDER: PRJNA988080 | ENA |

REPOSITORIES: ENA

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p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response

Project description:p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response

| PRJNA988078 | ENA

p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [HiC]

Project description:p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [HiC]

| PRJNA988081 | ENA

p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [PCHiC]

Project description:p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [PCHiC]

| PRJNA990725 | ENA

p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [ChIP-seq]

Project description:p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [ChIP-seq]

| PRJNA990719 | ENA

p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [HiC]

Project description:Activation of the p53 tumor suppressor triggers a transcriptional program to control cellular response to stress. However, the molecular mechanisms by which p53 controls gene transcription are not completely understood. Here, using a multi-omics integration framework, we uncover the critical role of spatio-temporal genome architecture in this process. We demonstrate that p53 drives direct and indirect changes in genome compartments, topologically associating domains and DNA loops within minutes of its activation, which escort the p53 transcriptional program along time. Focused on p53-bound enhancers, we report a core transcriptional program of 340 genes directly regulated by p53 over distance, most of these not previously identified. Finally, we showcase that p53 controls transcription of distal genes through newly formed and pre-existing enhancer-promoter loops in a cohesin dependent manner. Taken together, our findings demonstrate a previously unappreciated architectural role of p53 as regulator at distinct topological layers and provide a reliable set of new p53 direct target genes that may help future designs of p53-based cancer therapies.

2024-04-17 | GSE235944 | GEO

p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [PCHiC]

2024-04-17 | GSE236373 | GEO

p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [ChIP-seq]

2024-04-17 | GSE236372 | GEO

p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response [RNA-seq]

2024-04-17 | GSE235946 | GEO

p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-17 | GSE235947 | GEO

Lentiviral Vectors Escape Innate Sensing but Trigger p53 In Human Hematopoietic Stem Cells

Project description:In the context of lentiviral vector (LV)-mediated gene correction of hematopoietic stem and progenitor cells (HSPC), the viral origin of LV could trigger cellular responses with potential functional consequences that have not been investigated to date. Here, a time-course genome-wide transcriptional profiling of transduced human HSPC reveals a remarkably limited impact of LV on cellular gene expression, supporting some stealth features of the vector. In particular, LV efficiently escaped innate immune sensing that instead led to robust type I IFN signaling upon transduction with a gamma-retroviral vector. However, recognition of LV DNA prior to integration did trigger DNA damage responses that were activated also by non-integrating Adeno-associated vector DNA. As a consequence of this transient p53 activation, transduced HSPC showed increased apoptosis in vitro and reduced engraftment in vivo at limiting cell doses, but no long-term impact or competitive disadvantage were detected. Pharmacological inhibition of the LV signaling partially rescued both apoptosis and engraftment, potentially providing a novel strategy to further dampen the impact of ex vivo gene therapy on HSPC. Overall, our results shed light on the molecular mechanisms of viral vector sensing in HSPC and provide critical insight for the development of more stealth gene therapy strategies.

2017-06-28 | GSE92652 | GEO

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