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Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury

ABSTRACT: Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury

PROVIDER: PRJNA648052 | ENA |

REPOSITORIES: ENA

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Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [ChIP-seq]

Project description:We profiled Wt1, a key transcription factor, in purified murine podocytes based on ChIP-seq during the time course of podocyte injury by ADR.

2020-08-04 | GSE149486 | GEO

Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [RNA-seq]

Project description:Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [RNA-seq]

| PRJNA648054 | ENA

Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [ChIP-seq]

Project description:Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [ChIP-seq]

| PRJNA628872 | ENA

FOXC2 and WT1 regulate transcriptional reprogramming during the podocyte response to injury

Project description:In the context of human disease, the mechanisms whereby transcription factors reprogram gene expression in reparative responses to injury are not well understood. We have studied the mechanisms of transcriptional reprogramming in disease using murine kidney podocytes as a model for tissue injury. Podocytes are a crucial component of glomeruli, the filtration units of each nephron. Podocyte injury is the initial event in many processes that lead to End Stage Kidney Disease. FOXC2 is a transcription factor known to regulate gene expression in podocytes. FOXC2 and WT1 are both required for podocyte differentiation. Using murine models and human kidney organoids, we investigated FOXC2-mediated transcriptional reprogramming during the course of podocyte injury. Correlating FOXC2 and WT1 ChIP-seq analyses demonstrated that they co-bind many genes expressed in podocytes. Reprogramming the transcriptome involved highly dynamic changes in the binding of FOXC2 and WT1 to target genes during a reparative injury response.

2023-11-01 | GSE213174 | GEO

Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [RNA-seq]

Project description:We profiled total-RNA data in isolated murine podocytes during the time course of podocyte injury by ADR.

2020-08-04 | GSE154955 | GEO

Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury

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

2020-08-04 | GSE154956 | GEO

Genome-wide analysis of WT1-controlled gene expression in podocytes

Project description:We identified binding sites of the Wilms' tumor suppressor protein WT1 in the mouse podocyte genome in vivo by ChIP-seq. Furthermore, we provide a podocyte transcriptome derived from primary podocytes that were isolated by FACS on mouse glomeruli. In short, we show that WT1 activates a highly specific podocyte transcriptome by binding to putative podocyte-specific enhancers and TSS of target genes. Genes bound by WT1 in podocytes include the majority of genes mutated in hereditary podocytopathies as well as components of the slit diaphragm, actin cytoskeleton, extracellular matrix, and within endocytosis pathways. Furthermore, we infer a podocyte TF network from DNA-binding motifs enriched at WT1-bound loci that includes Tead, Lmx1b, Mafb, Tcf21, and Fox-class transcription factors. Examination of transcription factor binding sites for WT1 by ChIP-seq. Transcriptome analysis of podocytes by RNA-seq.

2014-12-11 | E-GEOD-64063 | biostudies-arrayexpress

Genome-wide analysis of WT1-controlled gene expression in podocytes

2014-12-11 | GSE64063 | GEO

EWS-WT1 Oncogene Activates a Neuronal Reprogramming Factor ASCL1 and Mediates Partial Neural Differentiation

Project description:A chromosomal translocation fusion gene product EWS-WT1 is the defining genetic event in Desmoplastic Small Round Cell Tumor (DSRCT), a rare but aggressive tumor with a high rate of mortality. EWS-WT1 oncogene acts as an aberrant transcription factor that drives tumorigenesis, but the mechanism by which EWS-WT1 causes tumorigenesis is not well understood. To delineate the oncogenic mechanisms, we generated the EWS-WT1 fusion in the mouse using a gene targeting (knock-in) approach, enabling physiologic expression of EWS-WT1 under the native Ews promoter. We derived mouse embryonic fibroblasts (MEFs) and performed genome-wide expression profiling to identify transcripts directly regulated by EWS-WT1. Remarkably, expression of EWS-WT1 led to a dramatic induction of many neuronal genes. Notably, a neural reprogramming factor, ASCL1 (achaete-scute complex-like 1), was highly induced by EWS-WT1 in MEFs and in primary DSRCT. Further analysis demonstrated that EWS-WT1 directly binds to the proximal promoter region of ASCL1 and activates its transcription through multiple WT1-responsive elements. Depletion of EWS-WT1 in a DSRCT cell line resulted in severe reduction in ASCL1 expression and cell viability. Remarkably, when stimulated with neuronal induction media, cells expressing EWS-WT1 expressed neural markers and generated neurite-like projections. These results demonstrate for the first time that EWS-WT1 activates neural gene expression and is capable of directing partial neuronal differentiation, likely via ASCL1. These findings suggest that stimulating DSRCT tumor cells with biological or chemical agents that promote neural differentiation might be a useful approach to develop novel therapeutics against this incurable disease. mouse embryonic fibroblasts (MEFs) and performed genome-wide expression profiling to identify transcripts directly regulated by EWS-WT1 in 0 vs. 24 Hours in three replications (WT+KTS, or WT-KTS in 0, 24 H; CRE in 0 and 24H)

2014-09-11 | E-GEOD-53301 | biostudies-arrayexpress

EWS-WT1 Oncogene Activates a Neuronal Reprogramming Factor ASCL1 and Mediates Partial Neural Differentiation

2014-09-11 | GSE53301 | GEO

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