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Role of the histone demethylase KDM2B in hematopoietic homeostasis and malignancies [ChIP-seq]

ABSTRACT: Development of the hematopoietic system is dynamically controlled by the interplay of transcriptional and epigenetic networks to determine cellular identity. Those networks are critical for homeostasis and frequently dysregulated in leukemias. We identified histone demethylase Kdm2b as a critical regulator of definitive hematopoiesis and lineage specification of hematopoietic stem and progenitor cells (HSPCs). RNA sequencing in murine HSPCs and genome-wide chromatin immunoprecipitation studies in human leukemias revealed that Kdm2b regulates differentiation, lineage choice, cytokine signaling, and quiescence. Identify the binding of KDM2B in seven human leukemia cell lines

ORGANISM(S): Homo sapiens

SUBMITTER: Alexandros Tzatsos

PROVIDER: E-GEOD-70624 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Histone demethylase KDM2B regulates lineage commitment in normal and malignant hematopoiesis.

Andricovich Jaclyn J Kai Yan Y Peng Weiqun W Foudi Adlen A Tzatsos Alexandros A

The Journal of clinical investigation 20160125 3

The development of the hematopoietic system is a dynamic process that is controlled by the interplay between transcriptional and epigenetic networks to determine cellular identity. These networks are critical for lineage specification and are frequently dysregulated in leukemias. Here, we identified histone demethylase KDM2B as a critical regulator of definitive hematopoiesis and lineage commitment of murine hematopoietic stem and progenitor cells (HSPCs). RNA sequencing of Kdm2b-null HSPCs and ...[more]

PMID: 26808549

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Role of the histone demethylase KDM2B in hematopoietic homeostasis and malignancies [RNA-seq]

Project description:Development of the hematopoietic system is dynamically controlled by the interplay of transcriptional and epigenetic networks to determine cellular identity. Those networks are critical for homeostasis and frequently dysregulated in leukemias. We identified histone demethylase Kdm2b as a critical regulator of definitive hematopoiesis and lineage specification of hematopoietic stem and progenitor cells (HSPCs). RNA sequencing in murine HSPCs and genome-wide chromatin immunoprecipitation studies in human leukemias revealed that Kdm2b regulates differentiation, lineage choice, cytokine signaling, and quiescence. Comparison of gene expression in wild-type and knockout HSPCs

2016-02-22 | E-GEOD-70728 | biostudies-arrayexpress

Role of the histone demethylase KDM2B in hematopoietic homeostasis and malignancies [human cell line gene expression]

Project description:Development of the hematopoietic system is dynamically controlled by the interplay of transcriptional and epigenetic networks to determine cellular identity. Those networks are critical for homeostasis and frequently dysregulated in leukemias. We identified histone demethylase Kdm2b as a critical regulator of definitive hematopoiesis and lineage specification of hematopoietic stem and progenitor cells (HSPCs). RNA sequencing in murine HSPCs and genome-wide chromatin immunoprecipitation studies in human leukemias revealed that Kdm2b regulates differentiation, lineage choice, cytokine signaling, and quiescence. Identify the KDM2B dependent transcriptome in human leukemia cell lines by using the GeneChipÂ® PrimeViewâ¢ Human Gene Expression Array

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Role of the histone demethylase KDM2B in hematopoietic homeostasis and malignancies [ChIP-seq]

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ZNF384 fusion oncoproteins drive lineage aberrancy in acute leukemia

Project description:ZNF384-rearranged fusion oncoproteins (FO) define a subset of lineage ambiguous leukemias, but the mechanistic role of ZNF384 FO in leukemogenesis and lineage ambiguity is poorly understood. Here, using viral expression in mouse and human hematopoietic stem and progenitor cells (HSPCs) and a Ep300-Zfp384 mouse model we show that ZNF384 FO promote hematopoietic expansion, myeloid lineage skewing, and self-renewal. In mouse HSPCs, concomitant lesions such as NRASG12D, were required for fully penetrant leukemia, whereas expression of ZNF384 FO drove development of B/myeloid leukemia in human HSPCs, with sensitivity of human ZNF384r leukemia to FLT3 inhibition in vivo. Mechanistically, ZNF384 FO occupy a subset of predominantly intragenic/enhancer regions with increased histone 3 lysine acetylation suggesting enhancer function. These data define a paradigm for FO-driven lineage ambiguous leukemia, in which expression in HSPCs results in deregulation of lineage-specific genes and hematopoietic skewing, progressing to full leukemic transformation in the presence of proliferative stress.

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Kdm2b maintains murine embryonic stem cell status by recruiting PRC1 complex to CpG islands of lineage genes [ChIP-Seq]

Project description:Polycomb group (PcG) proteins play important roles in repressing lineage-specific genes and maintaining the undifferentiated state of mouse embryonic stem cells (mESCs). However, the mechanisms by which PcG proteins are recruited to their targets are largely unknown. Here, we show that the histone demethylase Kdm2b is highly expressed in mESCs and regulated by the pluripotent factors Oct4/Sox2 directly. Depletion of Kdm2b in mESCs causes de-repression of lineage-specific genes and induces early differentiation. The function of Kdm2b depends on its CXXC-ZF domain, which mediates Kdm2b’s genome-wide binding to CpG islands (CGIs). Kdm2b interacts with the core components of the Polycomb repressive complex 1 (PRC1) and recruits the complex to the CGIs of early lineage-specific genes. Thus, our study not only reveals a novel Oct4/Sox2-Kdm2b-PRC1-CGI regulatory axis and its function in maintaining undifferentiated state of mESCs, but also demonstrates a critical function of Kdm2b in recruiting PRC1 to the CGIs of lineage-specific genes to repress their expression. In this dataset, we include the ChIP-seq data of Kdm2b, Ezh2 and Ring1b in both control and Kdm2b knock down mouse embryonbic stem cells.

2013-02-20 | E-GEOD-41314 | biostudies-arrayexpress

Deletion of KDM2B DNA-binding domain affects RING1B and SUZ12 occupancy

Project description:The histone lysine demethylase protein, KDM2B, associates with the PCGF1/PRC1 complex and binds to non-methylated DNA through its ZF-CxxC domain, providing a possible molecular link between CpG island elements and polycomb nucleation (Farcas et al., 2012, Wu et al., 2013). Here, a novel genetic system was designed in which PCGF1/PRC1 targeting could be disrupted in vivo through the ablation of KDM2B-mediated DNA binding. To ablate PCGF1/PRC1 targeting, an exon that encodes most of the KDM2B ZF-CxxC domain and is shared by both the long and short form of the protein was flanked by loxP sites (Kdm2bfl/fl). Homozygous mouse ES cell lines were derived that also stably express a tamoxifen inducible form of CRE-recombinase. CRE induced deletion of the ZF-CxxC domain by the addition of tamoxifen yields KDM2B long and short form proteins that are incapable of binding to CpG island DNA but still remain associated with the PCGF1/PRC1 variant complex. We then assessed genome-wide occupancy of the PRC1 component RING1B and the PRC2 component SUZ12 to examine the impact of losing KDM2B-dependent targeting of polycomb. KDM2Bfl/fl ES cells were treated with 800M-BM-5M tamoxifen for 72hours and compared to untreated control cells by ChIP-seq for KDM2B, RING1B and SUZ12, and RNA-seq.

2014-05-27 | E-GEOD-52619 | biostudies-arrayexpress

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