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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE126165 | GEO | 2019/02/07

REPOSITORIES: GEO

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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

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.

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Chromatin profiling in HT22 hippocampal cells

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

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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.

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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

Effects of NMDAR on mouse hippocampal neuron (HT22) mRNA and lncRNA expression during hypoxia/reoxygenation injury

Project description:To investigate the changes of the transcriptome in neuronal cells under the condition of NMDAR hypofunction and H/R injury, we compared the changes of mRNA and lncRNA expression levels in mouse hippocampal neuron HT22 cell with or without NMDAR knockdown and H/R stimulation by RNA sequencing.

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Identification of Klf9-regulated genes in HT22 tissue culture cells [RNA-Seq]

Project description:Krueppel-like factor 9 (Klf9) is a DNA-binding transcription factor that has been implicated in neuronal development and regeneration. We used mouse hippocampus-derived HT22 cell line to identify genes differentially regulated by forced Klf9 expression. We stably transfected HT22 cells with pCDNA6:TR (encoding the Tet repressor) and pCDNA6:TO-Klf9 (encoding Klf9 downstream of the Tet operator), allowing doxycycline(dox)-inducible expression of Klf9. We chose a stably transfected clone with baseline Klf9 mRNA level similar to that of untransfected HT22 cells (parent line) and approximately 10-fold induction after dox treatment. We conducted RNA-seq on stably transfected HT22 cells treated with or without dox for 8 hours; we also conducted RNA-seq on parent cells subjected to the same dox treatment to separate nonspecific effects of dox from the effects of forced Klf9 expression. Analysis of RNA-seq data found 217 gene repressed and 21 upregulated by forced Klf9 expression (FDR-adjusted p<.005; because fold changes were small we used a stringent p value cutoff to ensure that we were studying genes likely to be bona fide targets), showing that Klf9 functions primarily as a transcriptional repressor. Gene ontology analysis showed that Klf9-repressed genes were enriched in cytoskeletal and Wnt signaling-related genes.

2019-09-19 | GSE87093 | GEO

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