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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE154956 | GEO | 2020/08/04

REPOSITORIES: GEO

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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 [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

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

| PRJNA648052 | ENA

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

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

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

| PRJNA879448 | ENA

Activation of podocyte Notch mediates early Wt1 glomerulopathy.

Project description:The Wilms' tumor suppressor gene, WT1, encodes a zinc finger protein that regulates podocyte development and is highly expressed in mature podocytes. Mutations in the WT1 gene are associated with the development of renal failure due to the formation of scar tissue within glomeruli, the mechanisms of which are poorly understood. Here, we used a tamoxifen-based CRE-LoxP system to induce deletion of Wt1 in adult mice to investigate the mechanisms underlying evolution of glomerulosclerosis. Podocyte apoptosis was evident as early as the fourth day post-induction and increased during disease progression, supporting a role for Wt1 in mature podocyte survival. Podocyte Notch activation was evident at disease onset with upregulation of Notch1 and its transcriptional targets, including Nrarp. There was repression of podocyte FoxC2 and upregulation of Hey2 supporting a role for a Wt1/FoxC2/Notch transcriptional network in mature podocyte injury. The expression of cleaved Notch1 and HES1 proteins in podocytes of mutant mice was confirmed in early disease. Furthermore, induction of podocyte HES1 expression was associated with upregulation of genes implicated in epithelial mesenchymal transition, thereby suggesting that HES1 mediates podocyte EMT. Lastly, early pharmacological inhibition of Notch signaling ameliorated glomerular scarring and albuminuria. Thus, loss of Wt1 in mature podocytes modulates podocyte Notch activation, which could mediate early events in WT1-related glomerulosclerosis.

| S-EPMC6169130 | biostudies-literature

Histone acetylation mediates epigenetic regulation of transcriptional reprogramming in insects during metamorphosis, wounding and infection.

Project description:UnlabelledBackgroundGene expression in eukaryotes is regulated by histone acetylation/deacetylation, an epigenetic process mediated by histone acetyltransferases (HATs) and histone deacetylases (HDACs) whose opposing activities are tightly regulated. The acetylation of histones by HATs increases DNA accessibility and promotes gene expression, whereas the removal of acetyl groups by HDACs has the opposite effect.ResultsWe explored the role of HDACs and HATs in epigenetic reprogramming during metamorphosis, wounding and infection in the lepidopteran model host Galleria mellonella. We measured the expression of genes encoding components of HATs and HDACs to monitor the transcriptional activity of each enzyme complex and found that both enzymes were upregulated during pupation. Specific HAT inhibitors were able to postpone pupation and to reduce insect survival following wounding, whereas HDAC inhibitors accelerated pupation and increased survival. The administration of HDAC inhibitors modulated the expression of effector genes with key roles in tissue remodeling (matrix metalloproteinase), the regulation of sepsis (inhibitor of metalloproteinases from insects) and host defense (antimicrobial peptides), and simultaneously induced HAT activity, suggesting that histone acetylation is regulated by a feedback mechanism. We also discovered that both the entomopathogenic fungus Metarhizium anisopliae and the human bacterial pathogen Listeria monocytogenes can delay metamorphosis in G. mellonella by skewing the HDAC/HAT balance.ConclusionsOur study provides for the first evidence that pathogenic bacteria can interfere with the regulation of HDACs and HATs in insects which appear to manipulate host immunity and development. We conclude that histone acetylation/deacetylation in insects mediates transcriptional reprogramming during metamorphosis and in response to wounding and infection.

| S-EPMC3538701 | biostudies-literature

Targeted removal of epigenetic barriers during transcriptional reprogramming.

Project description:Master transcription factors have the ability to direct and reverse cellular identities, and consequently their genes must be subject to particular transcriptional control. However, it is unclear which molecular processes are responsible for impeding their activation and safeguarding cellular identities. Here we show that the targeting of dCas9-VP64 to the promoter of the master transcription factor Sox1 results in strong transcript and protein up-regulation in neural progenitor cells (NPCs). This gene activation restores lost neuronal differentiation potential, which substantiates the role of Sox1 as a master transcription factor. However, despite efficient transactivator binding, major proportions of progenitor cells are unresponsive to the transactivating stimulus. By combining the transactivation domain with epigenome editing we find that among a series of euchromatic processes, the removal of DNA methylation (by dCas9-Tet1) has the highest potential to increase the proportion of cells activating foreign master transcription factors and thus breaking down cell identity barriers.

| S-EPMC6509258 | biostudies-literature

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