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G9a regulated chromatin accessibility programs during B cell differentiation [ATAC-seq]

ABSTRACT: G9a regulated chromatin accessibility programs during B cell differentiation [ATAC-seq]

PROVIDER: PRJNA1147200 | ENA |

REPOSITORIES: ENA

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G9a regulated chromatin accessibility programs during B cell differentiation [ATAC-seq]

Project description:B cell differentiation is tightly regulated through coordinated changes in metabolism, division, expression of transcription factors, and epigenetic programming mediated by histone modifying enzymes. In this study, we examined the role of an epigenetic writer, the histone H3K9 mono and dimethyltransferse G9a, in regulating the chromatin accessibility programs during B-cell development and plasma cell (PC) formation. Utilizing a B-cell specific G9afl/flCd19Cre/+ conditional mouse model we performed ATAC-seq on naive and activated B cells and plasma cells that formed in response to LPS.

2025-07-10 | GSE274552 | GEO

G9a regulated transcriptional programs during B cell differentiation [RNA-seq]

Project description:G9a regulated transcriptional programs during B cell differentiation [RNA-seq]

| PRJNA1147201 | ENA

G9a regulated transcriptional programs during B cell differentiation [RNA-seq]

Project description:B cell differentiation is tightly regulated through coordinated changes in metabolism, division, expression of transcription factors, and epigenetic programming mediated by histone modifying enzymes. In this study, we examined the role of an epigenetic writer, the histone H3K9 mono and dimethyltransferse G9a, in regulating the transcriptional programs during B-cell development and plasma cell (PC) formation. Utilizing a B-cell specific G9afl/flCd19Cre/+ conditional mouse model we performed RNA-seq on naive and activated B cells and plasma cells that formed in response to LPS.

2025-07-10 | GSE274553 | GEO

Chromatin accessibility underlies cell-type specific programs of amphetamine-regulated gene expression in Nucleus Accumbens interneurons [ATAC-Seq]

Project description:Chromatin accessibility underlies cell-type specific programs of amphetamine-regulated gene expression in Nucleus Accumbens interneurons [ATAC-Seq]

| PRJNA751926 | ENA

Chromatin accessibility underlies cell-type specific programs of amphetamine-regulated gene expression in Nucleus Accumbens interneurons [ATAC-Seq]

Project description:Parvalbumin-expressing (PV+) interneurons of the nucleus accumbens (NAc) play an essential role in the addictive-like behaviors induced by psychostimulant exposure. To identify molecular mechanisms of PV+ neuron plasticity, we isolated interneuron nuclei from the NAc of male and female mice following acute or repeated exposure to amphetamine (AMPH) and sequenced for cell type-specific RNA expression and chromatin accessibility. AMPH regulated the transcription of hundreds of genes in PV+ interneurons, and this program was largely distinct from that regulated in other NAc GABAergic neurons. Chromatin accessibility at enhancers predicted cell-type specific gene regulation, identifying transcriptional mechanisms of differential AMPH responses. Finally, we observed dysregulation of multiple PV-specific, AMPH-regulated genes in an Mecp2 mutant mouse strain that shows heightened behavioral sensitivity to psychostimulants, suggesting the functional importance of this transcriptional program. Together these data provide novel insight into the cell-type specific programs of transcriptional plasticity in NAc neurons that underlie addictive-like behaviors.

2021-08-06 | GSE181420 | GEO

Chromatin accessibility analysis of primary GCTB samples

Project description:Analysis of chromatin accessibility in primary GCTB samples with ATAC-seq

2020-08-31 | E-MTAB-9512 | biostudies-arrayexpress

Chromatin accessibility underlies cell-type specific programs of amphetamine-regulated gene expression in Nucleus Accumbens interneurons

Project description:Chromatin accessibility underlies cell-type specific programs of amphetamine-regulated gene expression in Nucleus Accumbens interneurons

| PRJNA751927 | ENA

G9a/GLP-dependent H3K9me2 patterning alters chromatin structure at CpG islands in hematopoietic progenitors.

Project description:We profiled chromatin accessibility across the genome of HSPCs treated with either a small molecule inhibitor of G9a/GLP or DMSO. We observed that chromatin accessibility is dramatically altered at the regions of H3K9me2 nucleation. We have characterized the regions of H3K9me2 nucleation, revealing that H3K9me2 is nucleated in HSPCs at CpG islands (CGIs) and CGI-like sequences across the genome. Our analysis furthermore revealed a bias of H3K9me2 nucleation towards regions with low rates of C->T deamination, which typically lack DNA methylation. Lastly we examined the interaction of H3K9me2 and DNA methylation and determined that chromatin accessibility changes upon loss of H3K9me2 are dependent on the presence of DNA methylation. Examination of chromatin remodeling with FAIRE-seq in HSPCs treated with either a small molecule inhibitor of G9a/GLP or DMSO

2014-09-25 | E-GEOD-59749 | biostudies-arrayexpress

Expression data from G9a knockdown ovarian cancer cell

Project description:G9a depleted SKCO3 cells were used to identify genes regulated by G9a-dependent epigenetic regulations We used microarrays to detail the global programme of gene expression underlying paritoneal dissemination and identified distinct classes of G9a-regulated genes during this process. SKOV3 cells receiving G9a-specific shRNAs were analyzed compare to cells receiving control shRNA

2013-07-18 | E-GEOD-41226 | biostudies-arrayexpress

Targeting G9a Regulated m6A Modification Pathway to Hinder SARS-CoV-2 Replication

Project description:N6-methyladenosine (m6A) modification pathway is hijacked by several RNA viruses, including SARS-CoV-2, making it an attractive host-directed target for development of broad-spectrum antivirals. Here, we show that histone methyltransferase G9a, through its interaction with METTL3, regulates SARS-CoV-2 mediated rewiring of host m6A methylome to ultimately promote turnover, abundance, secretion and/or phosphorylation of various viral receptors and proteases, transcription factors, cytokines/chemokines, coagulation & angiogenesis associated proteins, and fibrosis markers. More importantly, drugs targeting G9a and its associated protein EZH2 are potent inhibitors of SARS-CoV-2 replication and reverse multi-omic effects of coronavirus infection in human alveolar epithelial cells (A549-hACE2) and COVID-19 patient PBMCs - with similar changes seen in multiorgan autopsy samples from COVID-19 patients. Altogether, we extend G9a function(s) beyond transcription to translational regulation during COVID-19 pathogenesis and show that targeting this master regulatory complex represents a new strategy (drug-class) that can be leveraged to combat emerging anti-viral resistance and infections.

2025-04-14 | PXD058743 | Pride

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