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HNF1A, H3K4me3 and H3K27ac ChIP-seq in control and Haster-deficient mouse livers

ABSTRACT: HNF1A, H3K4me3 and H3K27ac ChIP-seq in control and Haster-deficient mouse livers

PROVIDER: PRJEB51128 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR8772260.fastq.gz	Fastqsanger.gz
	ERR8772270.fastq.gz	Fastqsanger.gz
	ERR8772261.fastq.gz	Fastqsanger.gz
	ERR8772271.fastq.gz	Fastqsanger.gz
	ERR8772262.fastq.gz	Fastqsanger.gz

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HNF1A, H3K4me3 and H3K27ac ChIP-seq in control and Haster-deficient mouse livers

Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription of HNF1A, preventing silencing or overexpression. We have generated a mouse model where the promoter of Haster has been specifically deleted in liver (Haster loxP/loxP; AlbCre). In liver the prevailing consequence is upregulation of HNF1A. We performed HNF1A, H3K4me3 and H3K27ac ChIP-seq to assess the impact of HNF1A upregulation on the chromatin landscape of Haster KO liver.

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RNA-seq in control and Haster-deficient mouse livers

Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription of HNF1A, preventing silencing or overexpression. We have generated a mouse model where the promoter of Haster has been specifically deleted in liver (Haster loxP/loxP; AlbCre). In liver the prevailing consequence is upregulation of HNF1A. We performed RNA-seq from control and KO livers to assess the transcriptional impact of the HNF1A upregulation in the Haster KO liver.

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Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription HNF1A. If HASTER is deleted after beta cells have been formed and HNF1A is already stably expressed, HASTER is not required to maintain HNF1A activity, and is only required to provide negative feedback on HNF1A. HNF1A binding to the HASTER promoter mediates the repression of the HNF1A gene itself. To determine whether HNF1A binding to the HASTER promoter remodels 3D chromatin interactions of the HNF1A promoter, we performed UMI-4C experiments in wild type and HASTER-promoter KO EndoC-betaH3 cells with or without doxycycline-induced HNF1A overexpression using the HNF1A promoter as viewpoint.

2022-05-01 | E-MTAB-11473 | biostudies-arrayexpress

UMI-4C in control and Haster-deficient mouse livers

Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription of HNF1A, preventing silencing or overexpression. We have generated a mouse model where the promoter of Haster has been specifically deleted in liver (Haster loxP/loxP; AlbCre). In liver the prevailing consequence is upregulation of HNF1A. We performed UMI-4C experiments to assess how Haster inactivation remodel 3D chromatin interactions of the Hnf1a promoter using the Hnf1a promoter as viewpoint (V1, Hnf1a promoter upstream CTCF site viewpoint; V2, Hnf1a promoter VP).

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UMI-4C in control and HASTER-deficient EndoC-betaH3 cells overexpressing HNF1A

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UMI-4C in control and Haster-deficient mouse livers

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