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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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			Action	DRS
	SRR11624317.fastq.gz	Fastqsanger.gz
	SRR11624318.fastq.gz	Fastqsanger.gz
	SRR11624319.fastq.gz	Fastqsanger.gz
	SRR11624320.fastq.gz	Fastqsanger.gz
	SRR11624321.fastq.gz	Fastqsanger.gz

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

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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.

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Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte 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. Wilms tumor-1 (WT1) is a master regulator of gene expression in podocytes, binding nearly all genes known to be crucial for maintenance of the glomerular filtration barrier. Using murine models and human kidney organoids, we investigated WT1-mediated transcriptional reprogramming during the course of podocyte injury. Reprogramming the transcriptome involved highly dynamic changes in the binding of WT1 to target genes during a reparative injury response, affecting chromatin state and expression levels of target genes.

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

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