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Single cell transcriptome of ESCs upon MLL1 inhibition/deletion

ABSTRACT: Single cell transcriptome of ESCs upon MLL1 inhibition/deletion

PROVIDER: PRJNA525848 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8690190_1.fastq.gz	Fastqsanger.gz
	SRR8690190_2.fastq.gz	Fastqsanger.gz
	SRR8690188_1.fastq.gz	Fastqsanger.gz
	SRR8690188_2.fastq.gz	Fastqsanger.gz
	SRR8690189_1.fastq.gz	Fastqsanger.gz

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Project description:This study describes the transcriptome profiling of: 1) Mll1fl/fl mESCs in LIF/Serum medium as control; 2) Mll1fl/fl mESCs with 4-OHT (Mll1-/-), MM-401 (Mll1i) in LIF/serum medium ; 2) Mll1fl/fl mESCs with 2i in LIF/serum-free (KSR) medium.

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Transcriptome and epigenome of ESCs upon MLL1 inhibition/deletion

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

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The histone methyltransferase activity of MLL1 is dispensable for hematopoiesis and leukemogenesis

Project description:Despite correlations between histone methyltransferase (HMT) activity and gene regulation, direct evidence that HMT activity is responsible for gene activation is sparse. We address the role of the HMT activity for MLL1, a histone H3 lysine 4 (H3K4) methyltransferase critical for maintaining hematopoietic stem cells (HSCs). Here we show that the SET domain and thus HMT activity of MLL1 is dispensable for maintaining HSCs and for supporting leukemogenesis driven by the MLL-AF9 fusion oncoprotein. Upon Mll1 deletion, histone H4 lysine 16 (H4K16) acetylation was selectively depleted at MLL1 target genes in conjunction with reduced transcription. Surprisingly, inhibition of SIRT1 was sufficient to prevent the loss of H4K16 acetylation and the reduction in MLL1 target gene expression. Thus, recruited MOF activity, and not the intrinsic HMT activity of MLL1, is central for the maintenance of HSC target genes. In addition, this work reveals a role for SIRT1 in opposing MLL1 function. 11 Samples, 5 controls and 5 KOs with antibodies H3K4me1, H3K4me3, and H3K27Ac. One input Sample.

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2019-12-02 | GSE107406 | GEO

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