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Genome wide mapping of histone 3 lysine 79 mono, di and trimethylation and histone 3 lysine 27 trimethylation in LSKs, GMPs and retroviral MLL-AF9 driven murine leukemias

ABSTRACT: We report the genome wide distribution of the three states of H3K79 methylation (H3K79me1/me2/me3) and H3K27me3 in mouse lineage negative Sca-1 positive Kit positive cells (LSKs), granulocyte macrophage progenitors (GMPs) and LSK derived MLL-AF9 leukemias in the presence or absence of the Af10 OM-LZ domain. Legend- MIT:MSCV-IRES-tdTomato (Empty vector control) and CRE (MIT vector with the Cre recombinase).

ORGANISM(S): Mus musculus

PROVIDER: GSE55038 | GEO | 2014/09/08

SECONDARY ACCESSION(S): PRJNA238311

REPOSITORIES: GEO

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Genome wide mapping of histone 3 lysine 79 mono, di and trimethylation and histone 3 lysine 27 trimethylation in LSKs, GMPs and retroviral MLL-AF9 driven murine leukemias

Project description:We report the genome wide distribution of the three states of H3K79 methylation (H3K79me1/me2/me3) and H3K27me3 in mouse lineage negative Sca-1 positive Kit positive cells (LSKs), granulocyte macrophage progenitors (GMPs) and LSK derived MLL-AF9 leukemias in the presence or absence of the Af10 OM-LZ domain. Legend- MIT:MSCV-IRES-tdTomato (Empty vector control) and CRE (MIT vector with the Cre recombinase). We examined the H3K79 me1,me2,me3 and H3K27me3 profiles by ChIP-seq in lineage negative Sca-1 positive, Kit positive (LSK) cells, granulocyte macrophage progenitors (GMPs) and bone marrow cells from sacrificed terminally ill secondary MLL-AF9 positive leukemic mice. In case of the MLL-AF9 leukemias, the ChIP-seq experiments were performed in 2 conditions in the presence or absence of the Dot1l interacing octapeptide-motif leucine zipper (OM-LZ) domain of Af10. For the leukemia experiments, leukemias derived from the Af10 OM-LZ homozygous floxed background were transduced with MSCV-IRES-tdTomato control vector (MIT) or its Cre-recombinase expressing counterparts (CRE). Subsequently, we sorted tdTomato positive cells and injected them into sub-lethally irradiated syngenic secondary recipient mice. Seconday leukemias obtained from these MIT or CRE expressing cells were used for ChIP -seq studies.

2014-09-08 | E-GEOD-55038 | biostudies-arrayexpress

Assesment of gene expression upon AF10 deletion in MLL-AF9 secondary leukemia

Project description:Aberrant Hox gene activation is a recurrent feature in several different types of human leukemia, including leukemias with rearrangements of the mixed lineage leukemia (MLL) gene. In this study, we demonstrate that Hox gene expression is controlled by higher degree H3K79 methylation in acute myeloid leukemia (AML). We show that the deposition of progressive H3K79 methylation states at the genomic loci of critical Hox genes is dependent on the interaction of the H3K79 methyltransferase Dot1l with Af10, a protein that is found in the Dot1l complex isolated from diverse cell types. Furthermore, abrogation of the Dot1l-Af10 interaction reverses aberrant epigenetic profiles found in the leukemia epigenome and impairs the transforming ability of mechanistically distinct AML oncogenes. Primary MLL-AF9 leukemias in the AF10 floxed background (homozygous) were transduced with MSCV-IRES-tdTomato (MIT) or the Cre recombinase expressing MIT vector, cells were sorted and injected into secondary recipient mice to generate Af10 floxed (MIT) or deleted (CRE) leukemias. BM cells fresly harvested from these leukemias were sorted for tdTomato expression and used for microarrays. BM cells from Hoxa9-Meis1 transduced primary leukemias were used for comparison.

2014-09-08 | E-GEOD-54499 | biostudies-arrayexpress

Effect of Dot1l deletion on LSKs and GMPs

Project description:We wanted to investigate the effects of Dot1l deletion on gene expression in LSKs and GMPs of C57/BL6 mice Aberrant Hox gene activation is a recurrent feature in several different types of human leukemia, including leukemias with rearrangements of the mixed lineage leukemia (MLL) gene. In this study, we demonstrate that Hox gene expression is controlled by higher degree H3K79 methylation in acute myeloid leukemia (AML). We show that the deposition of progressive H3K79 methylation states at the genomic loci of critical Hox genes is dependent on the interaction of the H3K79 methyltransferase Dot1l with Af10, a protein that is found in the Dot1l complex isolated from diverse cell types. Furthermore, abrogation of the Dot1l-Af10 interaction reverses aberrant epigenetic profiles found in the leukemia epigenome and impairs the transforming ability of mechanistically distinct AML oncogenes. Lineage negative Sca-1 positive Kit positive (LSK) cells and granulocyte macrophage progenitors (GMPs) were sorted from Dot1 wt/wt x Mx-Cre mice or Dot1l fl/fl x Mx-Cre mice were injected with PIPC. PIPC injection induced biallelic deletion of the Dot1l allele in the Dot1l fl/fl mice but not the Dot1l wt/wt mice. The Dot1l wt/wt LSKs and GMPs were compared to the Dot1l -/- counterparts by RNA extraction and Microarrays.

2014-09-08 | E-GEOD-54498 | biostudies-arrayexpress

Genome wide mapping of histone 3 lysine 79 dimethylation in MLL-AF6 murine leukemias

Project description:We report the genome wide distribution of H3K79 dimethylation in mouse MLL-AF6 positive leukemias to assess whether this epigenetic mark drives MLL-target gene expression. Examination of H3K79 dimethylation in bone marrow cells from sacrificed terminally ill MLL-AF6 positive leukemic mice. The retroviral MSCV-IRES-neo-MLL-AF6 construct was transduced into mouse bone marrow lineage negative Kit +, Sca + (LSK) cells and these cells were injected after G418 selection into irradiated syngenic mice to establish MLL-AF6 positive leukemias.

2013-04-03 | E-GEOD-43062 | biostudies-arrayexpress

Effect of Dot1l deletion on LSKs and GMPs

2014-09-08 | GSE54498 | GEO

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.

2023-04-01 | GSE214139 | GEO

Expression data of cultured MCF10A cells transduced with MYB or MYB-NFIB expression vectors

Project description:This experiment investigates differences between control cells (empty vector) and cells with MYB or MYB-NFIB (M14N9) overexpression using MSCV vectors

2020-01-31 | GSE136095 | GEO

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse Dot1l ko RNA-seq]

Project description:Purpose: To characterize transcriptional changes associated with homozygous inactivation of Dot1l or Mll1 in MN1 driven AML Methods: We sequenced mRNA from murine LSK-cells transformed using forced expression of MN1 (MSCV-MN1-IRES-GFP), and transduced with Cre-vector to inactivate either Dot1l or Mll1. Cells were sorted for Cre-expression (pTomato fluorescent marker) or expression of an inert control vector. Results: Inactivation of either Dot1l or Mll1 in this model leads to a substantial delay or complete abrogation of leukemia development. Loss of Dot1l or Mll1 are associated with gene expression changes that have substantial overlap. In addition, genes that are downregulated follwing inactivation of Dot1l or Mll1 have substantial overlap with the gene set upregulated in MN1 transduced CMPs. Conclusions: MN1 mediated leukemogenesis is associated with a gene expression program that dependes on Mll1 and Dot1l

2016-01-12 | GSE76748 | GEO

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse Mll1 ko RNA-seq]

Project description:Purpose: To characterize transcriptional changes associated with homozygous inactivation of Dot1l or Mll1 in MN1 driven AML Methods: We sequenced mRNA from murine LSK-cells transformed using forced expression of MN1 (MSCV-MN1-IRES-GFP), and transduced with Cre-vector to inactivate either Dot1l or Mll1. Cells were sorted for Cre-expression (pTomato fluorescent marker) or expression of an inert control vector. Results: Inactivation of either Dot1l or Mll1 in this model leads to a substantial delay or complete abrogation of leukemia development.Loss of Dot1l or Mll1 are associated with gene expression changes that have substantial overlap. In addition, genes that are downregulated follwing inactivation of Dot1l or Mll1 have substantial overlap with the gene set upregulated in MN1 transduced CMPs. Conclusions: MN1 mediated leukemogenesis is associated with a gene expression program that dependes on Mll1 and Dot1l

2016-01-12 | GSE76749 | GEO

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.

2023-04-01 | GSE214141 | GEO

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