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ATAC-seq, H3K9ac ChIP-seq and 4sU-seq in WT, SAGA and ATAC mutant mouse embryonic stem cells

ABSTRACT: ATAC-seq, H3K9ac ChIP-seq and 4sU-seq in WT, SAGA and ATAC mutant mouse embryonic stem cells

PROVIDER: PRJNA734278 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14701300_1.fastq.gz	Fastqsanger.gz
	SRR14701300_2.fastq.gz	Fastqsanger.gz
	SRR14701301_1.fastq.gz	Fastqsanger.gz
	SRR14701301_2.fastq.gz	Fastqsanger.gz
	SRR14701302_1.fastq.gz	Fastqsanger.gz

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ATAC-seq, H3K9ac ChIP-seq and 4sU-seq in WT, SAGA and ATAC mutant mouse embryonic stem cells

Project description:This SuperSeries is composed of the ATAC-seq, H3K9ac ChIP-seq and 4sU-seq SubSeries.

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H3K9ac ChIP-seq in WT, SAGA and ATAC mutant mouse embryonic stem cells

Project description:Assess H3K9ac levels in WT and mutant ES E14 strains using ChIP-seq. Mutant strains are depleted for subunits of the coactivator complexes SAGA (Supt7l KO) or ATAC (AID-Yeats2) or of HAT subunits (AID-Tada3, Tada2a+Tada2b KO) using constitutive knock-out (KO) or the auxin-inducible degron (AID) system.

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Project description:H3K9ac ChIP-seq in WT, SAGA and ATAC mutant mouse embryonic stem cells

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Project description:SAGA and ATAC are two related transcriptional coactivator complexes, sharing the same histone acetyltransferase (HAT) subunit. The HAT activities of SAGA and ATAC are required for metazoan development but the precise role of the two complexes in RNA polymerase II transcription in mammals is less understood. To determine whether SAGA and ATAC have redundant or specific functions dependent on their HAT activities, we compared the effects of HAT inactivation in each complex with that of inactivation of either SAGA or ATAC core subunits in mouse embryonic stem cells (ESCs). We show that core subunits of SAGA or ATAC subunits are required for complex assembly, mouse ESC growth and self-renewal. Additionally, ATAC, but not SAGA subunits are required for ESC viability by regulating the transcription of translation-related genes. Surprisingly, depletion of specific or shared HAT module subunits caused a global decrease in histone H3K9 acetylation, but did not result in significant phenotypic or transcriptional defects. Thus, our results indicate that SAGA and ATAC are differentially required for viability and self-renewal of mouse ESCs by regulating transcription through different pathways, in a HAT-independent manner.

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