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Single-cell sequencing of JMJD1C Jumonji domain mutated MLL-AF9 Leukemia cells

ABSTRACT: We performed single-cell sequencing on mouse MLL-AF9-cas9 leukemia cells 7 days after transduction with sgRNA against Renilla or JMJD1C JmjC domain. We revealed heterogeneity within each population.

ORGANISM(S): Mus musculus

PROVIDER: GSE129662 | GEO | 2019/04/12

REPOSITORIES: GEO

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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.

2019-04-12 | GSE129661 | GEO

RNA-seq study on MLL-AF9 leukemia cells harboring JMJD1C sgRNAs targeting jumonji and zinc finger domains.

Project description:We transduced clonally MLL-AF9 leukemia cells expressing cas9 with sgRNA targeting the jumonji and zinc finger domains of JMJD1C. GFP (MLL-AF9) and TdTomato (sgRNA) double positive cells were sorted on Day 6 after transduction. Total RNA was isolated followed by mRNA selection. cDNA libraries were generated and NextGen Sequencing was performed.

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Effect of loss of Jmjd1c on MLL-AF9 leukemia

Project description:Analysis of gene expression profile of MLL-AF9 leukemia cells 6 days after loss of Jmjd1c. Loss of Jmjd1c induces differentiation and apoptosis in MLL-AF9 leukemia cells. These results provide insight into the role of Jmjd1c in MLL leukemia.

2016-06-09 | GSE75576 | GEO

Single-cell sequencing of JMJD1C Jumonji domain mutated MLL-AF9 Leukemia cells

Project description:Single-cell sequencing of JMJD1C Jumonji domain mutated MLL-AF9 Leukemia cells

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Gene expression profiling of Hox-driven AML overexpressing JMJD1C

Project description:JMJD1C, a Jumonji C (JmjC) domain-containing histone demethylase, has been reported as a direct cofactor of oncogenic transcription factor HOXA9. To identify JMJD1C downstream effectors, we performed a genome-wide gene expression profiling experiment. Our microarray analysis identified a new role for JMJD1C in regulating a cancer metabolic program in HOX-driven AML. GFP+ HOXA9/MEIS1-mediated pre-leukemic stem cells were transduced with retroviruses carrying JMJD1C or empty vector for the microarray experiment. Each group has 4 samples.

2018-12-30 | E-MTAB-5760 | biostudies-arrayexpress

Effect of loss of Jmjd1c on H3K9me2 level across the genome

Project description:Analysis of H3K9me2 level in MLL-AF9 leukemia cells upon deletion of Jmjd1c. Jmjd1c has been shown to be a H3K9me1/2 demethylase and these results provide insight into its role in MLL-Af9 leukemia

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shRNA Screening Identifies JMJD1C as being required for Leukemia Maintenance (Agilent)

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. To assess the effect of JMJD1C depletion on transcription, we compared the transcriptome of shJMJD1C- and shScr-transduced mouse MLL-AF9 transformed cells 48h after infection. A total of 451 transcripts were detected as changing between the two conditions (FDR<0.25)

2014-01-23 | E-GEOD-54311 | biostudies-arrayexpress

RNA-seq study on MLL-AF9 leukemia cells harboring JMJD1C sgRNAs targeting jumonji and zinc finger domains.

Project description:RNA-seq study on MLL-AF9 leukemia cells harboring JMJD1C sgRNAs targeting jumonji and zinc finger domains.

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shRNA Screening Identifies JMJD1C as being required for Leukemia Maintenance

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Critical role of Jumonji domain of JMJD1C in MLL-rearranged leukemia.

Project description:JMJD1C, a member of the lysine demethylase 3 family, is aberrantly expressed in mixed lineage leukemia (MLL) gene-rearranged (MLLr) leukemias. We have shown previously that JMJD1C is required for self-renewal of acute myeloid leukemia (AML) leukemia stem cells (LSCs) but not normal hematopoietic stem cells. However, the domains within JMJD1C that promote LSC self-renewal are unknown. Here, we used clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein-9 nuclease (Cas9) negative-selection screening and identified a requirement for the catalytic Jumonji (JmjC) domain and zinc finger domain for leukemia cell survival in vitro and in vivo. In addition, we found that histone H3 lysine 36 methylation (H3K36me) is a marker for JMJD1C activity at gene loci. Moreover, we performed single cell transcriptome analysis of mouse leukemia cells harboring a single guide RNA (sgRNA) against the JmjC domain and identified increased activation of RAS/MAPK and the JAK-STAT pathway in cells harboring the JmjC sgRNA. We discovered that upregulation of interleukin 3 (IL-3) receptor genes mediates increased activation of IL-3 signaling upon JMJD1C loss or mutation. Along these lines, we observed resistance to JMJD1C loss in MLLr AML bearing activating RAS mutations, suggesting that RAS pathway activation confers resistance to JMJD1C loss. Overall, we discovered the functional importance of the JMJD1C JmjC domain in AML leukemogenesis and a novel interplay between JMJD1C and the IL-3 signaling pathway as a potential resistance mechanism to targeting JMJD1C catalytic activity.

| S-EPMC6517669 | biostudies-literature

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