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The genome-wide maps of H3K27me3 in MLL-AF10 (Tip60 flox/flox, Cre-ERT2) cells (MATIP cells) with or without the treatment of 4-OHT

ABSTRACT: The genome-wide maps of H3K27me3 in MLL-AF10 (Tip60 flox/flox, Cre-ERT2) cells (MATIP cells) with or without the treatment of 4-OHT

PROVIDER: PRJNA597558 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10761091_1.fastq.gz	Fastqsanger.gz
	SRR10761091_2.fastq.gz	Fastqsanger.gz
	SRR10761092_1.fastq.gz	Fastqsanger.gz
	SRR10761092_2.fastq.gz	Fastqsanger.gz
	SRR10761093_1.fastq.gz	Fastqsanger.gz

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The quantitative analysis of transcriptomes derived from MLL-AF10 flox cells and MLL-AF10 (Tip60 flox/flox, Cre-ERT2) cells with or without the treatment of 4-OHT

Project description:The quantitative analysis of transcriptomes derived from MLL-AF10 flox cells and MLL-AF10 (Tip60 flox/flox, Cre-ERT2) cells with or without the treatment of 4-OHT

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The quantitative analysis of transcriptomes derived from MLL-AF10 flox cells and MLL-AF10 (Tip60 flox/flox, Cre-ERT2) cells with or without the treatment of 4-OHT

Project description:Chromosome translocations involving the MLL gene are common rearrangements in leukemia. Such translocations fuse the MLL 5’-region in frame to partner genes , and the resultant fusion proteins can cause MLL-related leukemia. MLL-fusions activate transcription of target genes such as the HoxA cluster and Meis1, but the underlying mechanisms remain elusive. We found that the MLL-AF10 fusion recruits Tip60 to the Hoxa9 locus, where it acetylates H2A.Z, thereby promoting Hoxa9 expression. Following conditional deletion of Tip60, hypoacetylation of H2A.Z was accompanied by recruitment of Ezh2, the catalytic subunit of PRC2, suggesting that nucleosomes with hypoacetylated H2A.Z are the preferential targets of Ezh2. Our findings suggest that MLL-AF10 achieves active chromatin states by recruiting Tip60, which acetylates H2A.Z to prevent gene silencing by Ezh2.

2021-06-30 | GSE142558 | GEO

The genome-wide maps of H3K27me3 in MLL-AF10 (Tip60 flox/flox, Cre-ERT2) cells (MATIP cells) with or without the treatment of 4-OHT

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RNA-seq on Zfp961 GFP flox/flox mESCs to verify ERVKs repression by Zfp961.

Project description:To investigate the functional consequences in the absence of ZFP961 in mESCs, we treated the Zfp961-GFPflox/flox cells with 4-OHT to deplete the ZFP961 alleles, and then performed RNA-seq on three independent Zfp961-GFPflox/flox ESC lines before and after Cre mediated excision. Considerate that stable DNA methylation may remain upon Zfp961 absent, therefore ERVKs could still be repressed, we then treated Zfp961-GFPflox/flox cells with 5aza, which a inhibitor of DNA methylation, 24h before Zfp961 deletion with 4-OHT addition. After 4-OHT treatment，we performed RNAseq again, and this time we observed a ETnERV2-int, with belongs to ERVK elements, was upregulated after Zfp961 deletion.

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The role of AF10 (Mllt10) in maintaining cell identity (RNA-Seq)

Project description:AF10 is a cofactor of the H3K79 methyltransferase DOT1L. To uncover the role of H3K79me in reprogramming to induced pluripotent stem cells (iPSCs), we bred reprogrammable mice encoding doxycycline inducible Oct4-2A-Klf4-2A-IRES-Sox2-2A-c-Myc (OKSM) transgene with conditional flox (fl)-AF10 (Mllt10). We isolated mouse embryonic fibroblasts (MEFs), deleted AF10 with CRE-recombinase or treated cells with empty vector control, and initiated reprogramming in DOT1L chemical inhibitor SGC0946 or DMSO control. Gene expression was assessed using RNA-Seq and genome wide localization of H3K79me1 and H3K79me2 was determined by ChIP-Seq on day 4 of reprogramming.

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The role of AF10 (Mllt10) in maintaining cell identity (ChIP-Seq)

Project description:AF10 is a cofactor of the H3K79 methyltransferase DOT1L. To uncover the role of H3K79me in reprogramming to induced pluripotent stem cells (iPSCs), we bred reprogrammable mice encoding doxycycline inducible Oct4-2A-Klf4-2A-IRES-Sox2-2A-c-Myc (OKSM) transgene with conditional flox (fl)-AF10 (Mllt10). We isolated mouse embryonic fibroblasts (MEFs), deleted AF10 with CRE-recombinase or treated cells with empty vector control, and initiated reprogramming in DOT1L chemical inhibitor SGC0946 or DMSO control. Gene expression was assessed using RNA-Seq and genome wide localization of H3K79me1, H3K79me2, and RNA Polymerase II (RNAPII) was determined by ChIP-Seq on day 4 of reprogramming.

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Project description:Purpose: The goal of this study is to compare the gene expression profiles of H460, H460-ERT2-RUNX3-WT and H460-ERT2-RUNX3-MT(K94/171R) cells. Methods: H460, H460-ERT2-RUNX3 WT, and H460-ERT2-RUNX3-MT(K94/171R) cells were serum-starved for 24 hr, and then stimulated with 10% serum or 10% serum + 1 uM 4-OHT for 0, 8, or 16 hr. RNA was extracted from the cells. Isolated total RNA was processed for preparation of an RNA-seq library using the Illumina TruSeq Stranded mRNA Sample Preparation kit (Illumina, San Diego, CA, USA). Quality and size of libraries were assessed using the Agilent 2100 Bioanalyzer DNA kit (Agilent, Santa Clara, CA, USA). All libraries were quantified by qPCR using a CFX96 Real Time System (Bio-Rad, Hercules, CA, USA) and sequenced on NextSeq500 sequencers (Illumina). Sequencing adapters and low-quality bases in the raw reads were trimmed using the Cutadapt software. The cleaned high-quality reads were mapped to the human reference genome hg19 (https://genome.ucsc.edu) using STAR software. Genes differentially expressed between two selected biological conditions were identified by Cuffdiff in the Cufflinks package (http://cole-trapnell-lab.github.io/cufflinks/papers/). Results: RNA-Sequencing Data suggest that the R-point defends against oncogenic K-RAS–induced tumorigenesis not only by regulating intracellular programs (cell cycle, apoptosis, and metabolic pathways), but also by regulating extracellular programs (inflammatory response and immune response).

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