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Genome-wide analysis of gene expression in wild-type and KMT2D-deficient HT22 cells

ABSTRACT: Genome-wide analysis of gene expression in wild-type and KMT2D-deficient HT22 cells

PROVIDER: PRJNA521224 | ENA |

REPOSITORIES: ENA

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Genome-wide analysis of gene expression in wild-type and KMT2D-deficient HT22 cells

Project description:We conducted genome wide transcription profiling by RNA-seq in a mouse hippocampal cell line (HT22), comparing cells with CRISPR-Cas9 mediated deletion of the KMT2D enzymatic SET methyltransferase domain to the parental cell line

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Genome-wide analysis of gene expression in proliferative dentate gyrus (DG) nuclei of adult wild-type and KMT2D-deficient mice

Project description:We conducted genome wide transcription profiling by RNA-seq in proliferating neuronal progenitors after purifying EdU+ nuclei from micro-dissected DG of adult wild-type and KMT2D-deficient mice (Kmt2d +/Bgeo)

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Genome-wide transcriptome profiling of wild-type and Kmt2d-deficient ATDC5 differentiated chondrocytes and undifferentiated mesenchymal cells

Project description:We performed genome-wide transcriptome profiling in stable Kmt2d-/- (bi-allelic deletion of the catalytic SET domain) and Kmt2d+/+ ATDC5 chondrocyte cell lines 7 days after induction of differentiation and in stable Kmt2d-/- and Kmt2d+/+ undifferentiated ATDC5 cells.

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Expression data from J147-treated HT22 cells compared to untreated HT22 cells

Project description:The Neurotrophic Compound J147 Reverses Cognitive Impairment In Aged Alzheimer's Disease We used GeneChipM-BM-. Mouse Genome 430 2.0 Arrays to probe global gene expression changes when adding J147 compound to HT22 cells and compared to untreated cells. The hippocampal cell line HT22 were treated with the J147 compound for 1 hour and compared to HT22 treated only with vehicle (DMSO) for 1 hour. The gene expression profile from the J147-treated HT22 cells (1 hour exposure) was compared to HT22 cells treated with vehicle only (DMSO) for 1 hour. The DMSO/vehicle treated cells serve as the control and are referred to as untreated with drug.

2013-03-28 | E-GEOD-45534 | biostudies-arrayexpress

Genome-wide transcriptome profiling of wild-type and Kmt2d-deficient ATDC5 differentiated chondrocytes and undifferentiated mesenchymal cells

Project description:Genome-wide transcriptome profiling of wild-type and Kmt2d-deficient ATDC5 differentiated chondrocytes and undifferentiated mesenchymal cells

| PRJNA531019 | ENA

Expression data from J147-treated HT22 cells compared to untreated HT22 cells

Project description:The Neurotrophic Compound J147 Reverses Cognitive Impairment In Aged Alzheimer's Disease We used GeneChip® Mouse Genome 430 2.0 Arrays to probe global gene expression changes when adding J147 compound to HT22 cells and compared to untreated cells. The hippocampal cell line HT22 were treated with the J147 compound for 1 hour and compared to HT22 treated only with vehicle (DMSO) for 1 hour.

2013-03-28 | GSE45534 | GEO

Genome-wide analysis of gene expression in proliferative dentate gyrus (DG) nuclei of adult wild-type and KMT2D-deficient mice

Project description:Genome-wide analysis of gene expression in proliferative dentate gyrus (DG) nuclei of adult wild-type and KMT2D-deficient mice

| PRJNA521223 | ENA

Kmt2d deficiency promotes acute myeloid leukemia development and maintenance

Project description:The histone-3 lysine-4 methyltransferase KMT2D is frequently mutated in human cancers. However, knowledge of its role in the initiation and maintenance of acute myeloid leukemia (AML) is incomplete. Here, we show that KMT2D is generally downregulated in human AML. Using shRNA and CRISPR/Cas9 technologies, we show that Kmt2d loss, by cooperating with Trp53 and Nf1 loss, promoted mouse acute myeloid leukemogenesis through a differentiation block of hematopoietic stem and progenitor cells. Furthermore, using a doxycycline-induced shRNA system, we show that restoring Kmt2d impairs AML maintenance. Multi-omics analyses of Kmt2d-deficient and -restored AML cells showed that Kmt2d, via histone methyltransferase activity and chromatin remodeling, epigenetically regulates the expression of genes controlling hematopoietic stem cell differentiation. Lastly, we showed that 3-Deazaneplanocin A, a histone methyltransferase EZH2 inhibitor, could specifically repress Kmt2d-deficient AML cell growth and reverse pro-leukemia programs. Thus, our study indicate Kmt2d is a tumor suppressor, whose downregulation promotes AML development through differentiation blockage.

2022-09-18 | GSE147210 | GEO

Genome-wide maps of chromatin state in KMT2D Knockout and KMT2D WT melanoma in mice

Project description:Somatic mutations in various epigenetic regulators, including histone methyltransferases KMT2C and KMT2D, have emerged as important cancer-driving events. However, the mechanism of action and therapeutic vulnerability imparted by these mutations remain poorly understood. We identified KMT2D and 8 other epigenetic regulators as potential suppressors to melanoma initiation through an in vivo pooled epigenome-focused RNAi screen. Loss of KMT2D, which exhibits somatic mutations in human melanoma and other cancers, drastically enhanced melanoma progression in xenograft models and a BRAFV600E-driven genetically engineered mouse model of melanoma. Epigenome profiling of 6 histone marks and chromatin state alterations showed substantial reprogramming of H3K4me1- and H3K27ac-marked active enhancer states in KMT2D mutant tumors. Energy metabolic pathways such as glycolysis, OxPhos and TCA/electron transport showed high degree of deregulation which was confirmed with metabolic profiling. Pharmacological abrogation of glycolysis led to reduced proliferation and tumorigenesis preferentially in KMT2D mutant cells. Mechanistically, we find that enhancer loss at IGFBPs increases IGF signaling and downstream AKT phosphorylation that leads to upregulation of metabolic pathways rendering KMT2D mutant cells dependent on these energy metabolism pathways for their higher growth potential. Overall, we present evidence that KMT2D mutations promote tumorigenesis by reprogramming energy metabolism pathways through enhancer reprogramming.

2020-11-16 | GSE116851 | GEO

Identification of KMT2D regulated genes in germinal center B cells

Project description:Somatic mutations of the KMT2D methyltransferase gene represent a common genetic lesion in multiple cancer types. In diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL), these mutations are highly recurrent and occur early during tumorigenesis, suggesting a central role in transformation. Here we show that FL/DLBCL-associated KMT2D mutations impair its enzymatic activity and lead to diminished global H3K4 methylation in germinal center (GC) B cells and DLBCL, consistent with the enrichment of KMT2D binding at enhancer and promoter regions marked by mono- and tri-methylation. Conditional deletion of Kmt2d early during B cell development, but not after initiation of the GC reaction, leads to an increase in GC B cells, whose transcriptional profile is enriched in cell-cycle regulatory and B-cell receptor signaling genes. Consistently, Kmt2d-deficient B cells exhibit proliferative advantage ex vivo. Loss of Kmt2d combined with BCL2 deregulation, mimicking FL/DLBCL pathogenesis, leads to an increased incidence of clonal lymphoproliferations resembling the features of the human tumors. These findings suggest that early KMT2D loss facilitates lymphomagenesis by remodeling the epigenetic landscape of the cancer precursor cells. Eradication of KMT2D-deficient cells may represent a rational therapeutic approach targeting early tumorigenic events.

2015-09-10 | GSE67494 | GEO

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