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Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (ChIP-seq_2)

ABSTRACT: These data include the genome wide occupancy of H2AUbq and H3K27me3 by ChIP sequencing in Ring1a-/-;Ring1bf/f Cdkn2a-/- MLL-AF9 leukemic cells treated with OHT or EtOH

ORGANISM(S): Mus musculus

PROVIDER: GSE85327 | GEO | 2016/10/21

SECONDARY ACCESSION(S): PRJNA338175

REPOSITORIES: GEO

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Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (RNA-seq_2)

Project description:These data include RNA Seq data generated from wild type and Ring1a Ring1b dKO Cdkn2a-/- MLL-AF9 Leukemic cells

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Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (RNA-seq)

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Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (ChIP-seq)

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Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (ChIP-seq)

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MLL-AF9 lates transcriptional initiation in mixed lineage leukemic cells

Project description:MLL-fusion proteins (MLL-FPs) are believed to maintain gene activation and induce mixed lineage leukemia (MLL) through aberrantly stimulating transcriptional elongation, but the underlying mechanisms are incompletely understood. Here we show that both MLL1 and AF9, one of the major fusion partners of MLL1, mainly occupy promoters and distal intergenic regions, exhibiting chromatin occupancy patterns resembling that of RNA polymerase II (Pol II) in HEL, a human cell line without MLL1 arrangement (MLLr). MLL1 and AF9 only co-regulate over a dozen genes despite of their co-occupancy on thousands of genes. They do not interact with each other, and their chromatin occupancy is also independent of each other. Moreover, AF9 deficiency in HEL cells decreases global TBP occupancy while decreases CDK9 occupancy on a small number of genes, suggesting an accessory role of AF9 in CDK9 recruitment and a possible major role in transcriptional initiation via initiation factor recruitment. Importantly, MLL1 and MLL-AF9 occupy promoters and distal intergenic regions, exhibiting identical chromatin occupancy patterns in MLL cells, and MLL-AF9 deficiency decreased occupancy of TBP and TFIIE on major target genes of MLL-AF9 in iMA9, a murine acute myeloid leukemia (AML) cell line inducibly expressing MLL-AF9, suggesting that it can also regulate initiation. These results suggest that there is no difference between MLL1 and MLL-AF9 with respect to location and size of occupancy sites, contrary to what people have believed, and that MLL-AF9 may also regulate transcriptional initiation in addition to widely-believed elongation.

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