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RNA-seq and ChIP-seq in mouse MLL-AF9 leukmemia cells with CRISPR knockout of Sgf29

ABSTRACT: RNA-seq and ChIP-seq in mouse MLL-AF9 leukmemia cells with CRISPR knockout of Sgf29

PROVIDER: PRJNA927233 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23215956_1.fastq.gz	Fastqsanger.gz
	SRR23215956_2.fastq.gz	Fastqsanger.gz
	SRR23215957_1.fastq.gz	Fastqsanger.gz
	SRR23215957_2.fastq.gz	Fastqsanger.gz
	SRR23215958_1.fastq.gz	Fastqsanger.gz

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LC-MS3 analysis of Herc1-knockout mouse MLL/AF9 acute myeloid leukemia cells

Project description:Our CRISPR-based pharmacogenomic screening identified the E3 ubiquitin ligase Herc1 as a key modulator of sensitivity to cytarabine (Ara-C) chemotherapy in the MLL/AF9 (MA) mouse AML model both in vitro and in vivo. To identify the intracellular proteins whose abundance is modulated by Herc1, we performed comparative LC-MS3 analysis of in vitro-cultured MA mouse AML cells that were transduced with either a small-guide RNA targeting Herc1 (i.e., CRISPR-mediated Herc1-knockout) or a control non-targeting small-guide RNA, at steady state or after brief exposure to Ara-C (200 nMol for 6 hours).

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RNA-seq and ChIP-seq in mouse MLL-AF9 leukmemia cells with CRISPR knockout of Sgf29

Project description:This dataset examined the effect of Sgf29 knockout in mouse MLL-AF9 cells. The gene expression profiling (RNA-seq) and the chromatin targeting of SGF29 (TST-ChIP-seq) are reported.

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ChIP-seq of histone marks H3K36, H3K27, and H3K9 in JMJD1C knockout or mutated MLL-AF9 leukemia cells

Project description:We performed genome-wide profiling of H3K9me3, H3K9me1, H3K27me3, and H3K36me3 by ChIP-seq in JMJD1C knockout or mutated MLL-AF9 leukemia cells. For ChIP-seq in JMJD1C mutated cells, we transduced sgRNA targeting the zinc finger, jumonji domain of JMJD1C or Renilla control and sorted on day 6 for GFP (MLL-AF9) Tdtomato (sgRNA) double positive cells. For ChIP-seq in JMJD1C knockout cells, we transduced Jmjd1c flox/flox MLL-AF9 leukemia cells with CRE TdTomato and sorted on day 6 for GFP (MLL-AF9) Tdtomato (CRE) double positive cells. These cells were subjected to ChIP-seq analysis with either H3K27me3, H3K9me3, H3K9me1 (JMJD1C knockout cells) or H3K36me3 (both knockout and mutated cells) antibody. We found increased H3K36me3 level at promoters of differentially expressed genes between control and JMJD1C loss or mutated leukemia cells.

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POLR2M-mediated paused transcription silences tumor suppressor MIR139 in MLL-AF9 AML

Project description:MIR139 is a critical tumor suppressor and commonly silenced in human cancer, including acute myeloid leukemia (AML). Here, we found that depletion of identified MIR139 targets affects AML outgrowth. We unraveled the mechanism of MIR139 gene inactivation in AML expressing the Mixed-Lineage Leukemia (MLL)-AF9 oncogene. Epigenetic analyses revealed two well-conserved putative enhancer regions in close proximity of transcriptional start sites (TSS) of MIR139. These regions were silenced by the Polycomb-Repressive Complex-2 (PRC2) downstream of MLL-AF9. Genomic deletion of these regions abolished MIR139 transcriptional regulation in normal and oncogenic conditions. Genome-wide knockout screens revealed the transcriptional pausing factor of RNA Polymerase-II, POLR2M, as a critical MIR139-silencing factor. Furthermore, direct POLR2M binding to the MIR139 TSS induced paused transcription, which was abrogated upon PRC2 inhibition. We present evidence for an oncogenic POLR2M-mediated MIR139 silencing mechanism, downstream of MLL-AF9 and PRC2. Together, our findings highlight the importance of POLR2M-mediated paused transcription in AML.

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2022-03-08 | GSE188291 | GEO

Aberrant chromatin acetylation in MLL-AF9 leukemia mediates the response to HDAC inhibition (ChIP-Seq)

Project description:We studied the chromatin modification patterns induced by the presence of the MLL-AF9 fusion protein in a model of human hematopoietic stem/progenitor cells (HSPC) transduced with retrovirus expressing MLL-AF9cDNA (HSPC-MA9). Comparative ChIP-seq analysis between HSPC-MA9 and control HSPC, revealed a massive hyperacetylation of histones that was consistent with the transcriptional profile in the presence of MLL-AF9 fusion protein. Furthermore, we identified 66 MLL-AF9 targets, and found that H4ac was present along with H3K4me3 and H3K79me2 chromatin marks in over 50% of the MLL-AF9 target genes. Examination of histone aceylation and methylation changes upon expression of MLL-AF9 fusion protein in human hematopoietic stem/progenitor cells.

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Gene expression changes upon Mof knockout in MLL-AF9 transformed murine LSKs

Project description:We report Illumina next generation RNA sequencing (RNAseq) of MLL-AF9 in vitro transformed murine LSKs upon genetic deletion of Mof. These gene expression data illustrate that Mof regulates the expression of genes involved in DNA damage response and chromatin stability in MLL-AF9 transformed cells.

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Controlled MLL-AF9 Expression in Human Induced Pluripotent Stem Cells Reveals MLL-AF9-specific Oncogene Program [hiMLLAF9_scRNAseq]

Project description:A t(9;11)(p22;q23) translocation produces the MLL-AF9 fusion protein, which is found in up to 25% of de novo AML cases in children. Despite major advances, obtaining a comprehensive under-standing of context-dependent MLL-AF9-mediated gene programs during early hematopoiesis is challenging. Here, we generated a human inducible pluripotent stem cell (hiPSC) model with a doxycycline dose-dependent MLL-AF9 expression. We exploited MLL-AF9 expression as an onco-genic hit to uncover epigenetic and transcriptomic effects on iPSC-derived hematopoietic develop-ment and the transformation into (pre-)leukemic states. In doing so, we observed a disruption in early myelomonocytic development. Accordingly, we identified gene profiles that were consistent with primary MLL-AF9 AML and uncovered high-confidence MLL-AF9-associated core genes that are faithfully represented in primary MLL-AF9 AML, including known and presently unknown factors. Using single-cell RNA-sequencing, we identified an increase of CD34 expressing early hematopoietic progenitor-like cell states as well as granulocyte-monocyte progenitor-like cells upon MLL-AF9 activation. Our system allows for careful chemically controlled and stepwise in vitro hiPSC-derived differentiation under serum-free and feeder-free conditions. For a disease that cur-rently lacks effective precision medicine, our system provides a novel entry-point into exploring po-tential novel targets for personalized therapeutic strategies.

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Project description:ASH1L and MLL1 are two histone methyltransferases that facilitate transcriptional activation during normal development. However, the roles of ASH1L and its enzymatic activity in the development of MLL-rearranged leukemias are not fully elucidated in Ash1L gene knockout animal models. In this study, we used an Ash1L conditional knockout mouse model to show that loss of ASH1L in hematopoietic progenitor cells impaired the initiation of MLL-AF9-induced leukemic transformation in vitro. Furthermore, genetic deletion of ASH1L in the MLL-AF9-transformed cells impaired the maintenance of leukemic cells in vitro and largely blocked the leukemia progression in vivo. Importantly, the loss of ASH1L function in the Ash1L-deleted cells could be rescued by wild-type but not the catalytic-dead mutant ASH1L, suggesting the enzymatic activity of ASH1L was required for its function in promoting MLL-AF9-induced leukemic transformation. At the molecular level, ASH1L enhanced the MLL-AF9 target gene expression by directly binding to the gene promoters and modifying the local histone H3K36me2 levels. Thus, our study revealed the critical functions of ASH1L in promoting the MLL-AF9-induced leukemogenesis, which provides a molecular basis for targeting ASH1L and its enzymatic activity to treat MLL-arranged leukemias.

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