ChIP-seq of histone marks H3K36, H3K27, and H3K9 in JMJD1C knockout or mutated MLL-AF9 leukemia cells
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PROVIDER: PRJNA532408 | ENA |
REPOSITORIES: ENA
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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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Project description:It has been recently reported that the pluripotency factor OCT4, the early neural inducing factor NR2F2, and the pluripotency-associated miRNA miR-302 are linked in a regulatory circuitry that critically regulate both pluripotency and neural differentiation of human embryonic stem cells (hESCs). We show here that JMJD1C, a H3K9 demethylase expressed in undifferentiated hESCs, plays a key role in the regulatory circuitry. hESCs with JMJD1C knockdown (KD) retain the state of self-renewal and pluripotency, but express lower miR-302c than control hESCs. JMJD1C directly binds to the miR-302 promoter in hESCs and reduces H3K9 methylation on the promoter. Upon withdrawal of bFGF (an inhibitor of neural initiation) from a defined culture medium, the KD, but not control, hESCs differentiate into neural progenitors within three days – the fastest ever reported, accompanied by rapid increase of NR2F2 expression. A miR-302c analogue or an inhibitor of H3K9 methylation reduces neural induction from the KD hESCs, whereas a miR-302c inhibitor promotes hESC differentiation. Together, our findings suggest that JMJD1C plays a central role in control of neural differentiation from hESCs, which involves sustained miR-302c expression, and that inhibition of JMJD1C is sufficient to rapidly induce neural progenitors from hESCs in the defined medium depleted of bFGF. This is also the first evidence, to our knowledge, for epigenetic modification of miR-302 in hESCs. 6 human ES cell lines were used in this microarray assay. Each line has two replicates.
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Project description:We used a mouse model of human AML induced by the MLL-AF9 fusion oncogene, and an epigenetic shRNA library to screen for novel potential drug targets. One of the best candidate drug targets identified in these screens was Jmjd1c. Depletion of Jmjd1c impairs growth and colony formation of mouse MLL-AF9 cells in vitro, as well as establishment of leukemia after transplantation. Depletion of JMJD1C impairs expansion and colony formation of human leukemic cell lines, with the strongest effect observed in the MLL-rearranged ALL cell line, SEM. In both mouse and human leukemic cells, the growth defect upon JMJD1C depletion appears to be primarily due to increased apoptosis, which implicates JMJD1C as a potential therapeutic target in leukemia.
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Project description:We used a mouse model of human AML induced by the MLL-AF9 fusion oncogene, and an epigenetic shRNA library to screen for novel potential drug targets. One of the best candidate drug targets identified in these screens was Jmjd1c. Depletion of Jmjd1c impairs growth and colony formation of mouse MLL-AF9 cells in vitro, as well as establishment of leukemia after transplantation. Depletion of JMJD1C impairs expansion and colony formation of human leukemic cell lines, with the strongest effect observed in the MLL-rearranged ALL cell line, SEM. In both mouse and human leukemic cells, the growth defect upon JMJD1C depletion appears to be primarily due to increased apoptosis, which implicates JMJD1C as a potential therapeutic target in leukemia.
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