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H3K79me2/3 controls enhancer promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells

ABSTRACT: H3K79me2/3 controls enhancer promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells

PROVIDER: PRJNA557180 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9853930_1.fastq.gz	Fastqsanger.gz
	SRR9853930_2.fastq.gz	Fastqsanger.gz
	SRR9853940_1.fastq.gz	Fastqsanger.gz
	SRR9853940_2.fastq.gz	Fastqsanger.gz
	SRR9853950_1.fastq.gz	Fastqsanger.gz

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H3K79me2/3 controls enhancer promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells (ATAC-seq)

Project description:MLL gene rearrangements (MLLr) are a common cause of aggressive, incurable acute lymphoblastic leukemias (ALL) in infants and children, most of which originate in utero. The most common MLLr produces an MLL-AF4 fusion protein. MLL-AF4 promotes leukemogenesis by activating key target genes, mainly through recruitment of DOT1L and increased histone H3 lysine 79 methylation (H3K79me2/3). One key MLL-AF4 target gene is PROM1 which encodes CD133 (Prominin-1). CD133 is a pentaspan transmembrane glycoprotein that represents a potential pan-cancer target as it is found on multiple cancer stem cells. Here we demonstrate that aberrant PROM1/CD133 expression is essential for leukemic cell growth, mediated by direct binding of MLL-AF4. Activation is controlled by an intragenic H3K79me2/3 enhancer element (KEE) leading to increased enhancer-promoter interactions between PROM1 and the nearby gene TAPT1. This dual locus regulation is reflected in a strong correlation of expression in leukemia. We find that in PROM1/CD133 non-expressing cells, the PROM1 locus is repressed by polycomb repressive complex 2 (PRC2) binding, associated with reduced expression of TAPT1, partially due to loss of interactions with the PROM1 locus. Together, these results provide the first detailed analysis of PROM1/CD133 regulation that explains CD133 expression in MLLr ALL.

2020-03-25 | GSE135025 | GEO

H3K79me2/3 controls enhancer promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells (ChIP-seq)

2020-03-25 | GSE135024 | GEO

H3K79me2/3 controls enhancer promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells (RNA-seq)

2020-03-25 | GSE135023 | GEO

H3K79me2/3 controls enhancer promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells (RNA-seq)

Project description:H3K79me2/3 controls enhancer promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells (RNA-seq)

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H3K79me2/3 controls enhancer promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells (ChIP-seq)

Project description:H3K79me2/3 controls enhancer promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells (ChIP-seq)

| PRJNA557189 | ENA

H3K79me2/3 controls enhancer promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells (ATAC-seq)

Project description:H3K79me2/3 controls enhancer promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells (ATAC-seq)

| PRJNA557190 | ENA

H3K79me2/3 controls enhancer-promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells.

Project description:MLL gene rearrangements (MLLr) are a common cause of aggressive, incurable acute lymphoblastic leukemias (ALL) in infants and children, most of which originate in utero. The most common MLLr produces an MLL-AF4 fusion protein. MLL-AF4 promotes leukemogenesis by activating key target genes, mainly through recruitment of DOT1L and increased histone H3 lysine-79 methylation (H3K79me2/3). One key MLL-AF4 target gene is PROM1, which encodes CD133 (Prominin-1). CD133 is a pentaspan transmembrane glycoprotein that represents a potential pan-cancer target as it is found on multiple cancer stem cells. Here we demonstrate that aberrant PROM1/CD133 expression is essential for leukemic cell growth, mediated by direct binding of MLL-AF4. Activation is controlled by an intragenic H3K79me2/3 enhancer element (KEE) leading to increased enhancer-promoter interactions between PROM1 and the nearby gene TAPT1. This dual locus regulation is reflected in a strong correlation of expression in leukemia. We find that in PROM1/CD133 non-expressing cells, the PROM1 locus is repressed by polycomb repressive complex 2 (PRC2) binding, associated with reduced expression of TAPT1, partially due to loss of interactions with the PROM1 locus. Together, these results provide the first detailed analysis of PROM1/CD133 regulation that explains CD133 expression in MLLr ALL.

| S-EPMC7116565 | biostudies-literature

H3K79me2/3 controls enhancer-promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells.

Project description:MLL gene rearrangements (MLLr) are a common cause of aggressive, incurable acute lymphoblastic leukemias (ALL) in infants and children, most of which originate in utero. The most common MLLr produces an MLL-AF4 fusion protein. MLL-AF4 promotes leukemogenesis by activating key target genes, mainly through recruitment of DOT1L and increased histone H3 lysine-79 methylation (H3K79me2/3). One key MLL-AF4 target gene is PROM1, which encodes CD133 (Prominin-1). CD133 is a pentaspan transmembrane glycoprotein that represents a potential pan-cancer target as it is found on multiple cancer stem cells. Here we demonstrate that aberrant PROM1/CD133 expression is essential for leukemic cell growth, mediated by direct binding of MLL-AF4. Activation is controlled by an intragenic H3K79me2/3 enhancer element (KEE) leading to increased enhancer-promoter interactions between PROM1 and the nearby gene TAPT1. This dual locus regulation is reflected in a strong correlation of expression in leukemia. We find that in PROM1/CD133 non-expressing cells, the PROM1 locus is repressed by polycomb repressive complex 2 (PRC2) binding, associated with reduced expression of TAPT1, partially due to loss of interactions with the PROM1 locus. Together, these results provide the first detailed analysis of PROM1/CD133 regulation that explains CD133 expression in MLLr ALL.

| S-EPMC7787973 | biostudies-literature

PROM1(CD133)-dependent expressed genes from mouse embryonic DRG neurons

Project description:Prom1, also knwon as CD133 is a stem cell marker that are down-regulated during developmental process. Here we first reports that PROM1 is a regulator of expression of specific sets of genes from DRG neurons.

2020-04-02 | GSE147936 | GEO

A novel human fetal model of infant ALL reveals a link between MLL-AF4, PAF1 and increased H3K79me2/3 [RNA-seq]

Project description:Acute Lymphoblastic Leukemia (ALL) caused by chromosomal translocation involving the Mixed Lineage Leukemia (MLL) gene remains a poor prognosis disease, especially in infants. The most common MLL-rearrangement in infant ALL (iALL), MLL-AF4, originates in utero where the properties of fetal target cells likely provide a permissive landscape for transformation. We describe the first faithful MLL-AF4 iALL model derived by CRISPR-Cas9 genome editing of primary human fetal liver (FL) cells. Using this model, we demonstrate that H3K79me2/3 is increased during transformation as a direct consequence of MLL-AF4 binding, but correlates weakly with changes in gene expression. DOT1L, the only known H3K79 methyltransferase, does not form part of the MLL-AF4 complex. Instead, we identify PAF1 as a key protein recruited by the MLL-AF4 complex, which in turn can recruit DOT1L. These results explain the previously unclear link between MLL-AF4 binding and increased H3K79me2/3, and introduce an iALL-specific model for future drug studies.

2021-10-25 | GSE162032 | GEO

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