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Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [RNA-Seq]

ABSTRACT: Identification of histone acetylation targets of Kat2a activity in murine models of acute myeloid leukaemia (AML) driven by the MLL-AF9 oncogenic fusion

ORGANISM(S): Mus musculus

PROVIDER: GSE118768 | GEO | 2020/02/03

REPOSITORIES: GEO

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Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [ChIP-Seq]

Project description:Identification of histone acetylation targets of Kat2a activity in murine models of acute myeloid leukemia (AML) driven by the MLL-AF9 oncogenic fusion

2020-02-03 | GSE118576 | GEO

Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells.

Project description:Acute Myeloid Leukemia (AML) is an aggressive hematological malignancy with abnormal progenitor self-renewal and defective white blood cell differentiation. Its pathogenesis comprises subversion of transcriptional regulation, through mutation and by hijacking normal chromatin regulation. Kat2a is a histone acetyltransferase central to promoter activity, that we recently associated with stability of pluripotency networks, and identified as a genetic vulnerability in AML. Through combined chromatin profiling and single-cell transcriptomics of a conditional knockout mouse, we demonstrate that Kat2a contributes to leukemia propagation through preservation of leukemia stem-like cells. Kat2a loss impacts transcription factor binding and reduces transcriptional burst frequency in a subset of gene promoters, generating enhanced variability of transcript levels. Destabilization of target programs shifts leukemia cell fate out of self-renewal into differentiation. We propose that control of transcriptional variability is central to leukemia stem-like cell propagation, and establish a paradigm exploitable in different tumors and distinct stages of cancer evolution.

| S-EPMC7039681 | biostudies-literature

Distinct contributions of KAT2A histone acetyl-transferase complexes to human erythropoiesis

Project description:KAT2A is a histone acetyl-transferase involved in stabilization of transcriptional activity through acetylation of lysine residue 9 of Histone 3. Mouse knockout models suggest that Kat2a is dispensable for haematopoietic stem and progenitor cell activity, despite a central role in survival and maintenance of Acute Myekoid Leukaemia cells through block of differentiation. Herein, we investigate KAT2A activity in human cord blood haematopoiesis and identify a specific requirement in the establishment of the erythroid lineage. KAT2A is required for specification and survival of Erythroid-Megakaryocytic progenitors, with regulation of expression of the erythropoietin receptor (EPOR) gene, which participates in lineage commitment, as well as of later effector genes in the platelet and erythroid lineages. Early and late lineage roles can be distinctly attributed to the ATAC and SAGA complexes in which context KAT2A exerts its activity. ATAC is active earlier in erythroid lineage development and mediates MEP specification from HSC, whilst SAGA activity is required post-commitment, including in expression of haemoglobin genes. We thus position KAT2A as a novel regulator of human erythropoiesis and separate early and later effects in lineage development with complex specificity. This has implications for putative therapeutic targeting of KAT2A complexes in leukaemia.

2021-09-28 | GSE128512 | GEO

Distinct contributions of KAT2A histone acetyl-transferase complexes to human erythropoiesis [RNA-seq]

2021-09-28 | GSE128902 | GEO

Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells

Project description:Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells

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Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-02-03 | GSE118769 | GEO

Genes differentially expressed in MLL-AF9-transduced versus HOXA9/MEIS1-transduced LSK cells

Project description:HOXA9 and MEIS1 are essential downstream effectors of the MLL-AF9 oncoprotein during leukaemia induction. Leukaemia derived from MLL-AF9-transduced LSK cells has a more aggressive phenotype than that derived from HOXA9/MEIS1-transduced LSK cells. To determine differential gene expression that contributes to increased aggressiveness in MLL-AF9-induced leukaemia, microarray was performed on LSK cells transduced with MLL-AF9 versus HOXA/MEIS1 oncogenes.

2019-07-03 | E-MTAB-7355 | biostudies-arrayexpress

Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [ChIP-Seq]

Project description:Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [ChIP-Seq]

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Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [RNA-Seq]

Project description:Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [RNA-Seq]

| PRJNA486775 | ENA

Glucose partitioning in the bone marrow micro-environment in acute myeloid leukaemia [single-cell RNA-seq]

Project description:To identify the metabolic transcriptome landscape within leukaemic cells we performed scRNA-Seq on the sorted leukaemia cells (GFP+) cells from MLL-AF9 mice.

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