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

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

PROVIDER: PRJNA1147201 | ENA |

REPOSITORIES: ENA

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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

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

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

| PRJNA1147200 | ENA

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 and ZNF644 physically associate to suppress progenitor gene expression during neurogenesis

Project description:Proliferating progenitor cells undergo unidirectional changes in competence to give rise to post-mitotic progeny of specialized function. These transitions in cell fate typically involve the dynamic regulation of gene expression programs by histone methyltransferase (HMT) complexes. However, the composition, roles and regulation of these HMT complexes in regulating cell fate decisions in vivo are poorly understood. Using affinity purification and mass spectrometry (AP-MS), we identified the uncharacterized C2H2-like zinc finger (ZF) protein ZNF644, which is putatively causally linked to high-grade (degenerative) myopia, as a novel G9a/GLP-interacting protein and co-regulator of histone methylation. Using zebrafish embryos, we characterized the function of two ZNF644 orthologues, znf644a and znf644b, revealing critical neural- specific roles in regulating G9a/H3K9me2-mediated gene silencing in the retina. In addition, by virtue of additional non-overlapping requirements for znf644a and znf644b during retinal differentiation, we gained further insights regarding additional facets of retinal differentiation regulated by the G9a-ZNF644 physical association, such as maintaining retinal cell viability and in transitioning proliferating progenitor cells towards differentiation. Collectively, our data points to the G9a-ZNF644 physical interaction as a critical neural progenitor-specific co-factor of G9a/H3K9me2-mediated gene silencing during neuronal differentiation.

2015-11-13 | GSE63225 | GEO

Transcriptional programs regulated by MYCN in liver tumorigenesis

Project description:Transcriptional programs regulated by MYCN in liver tumorigenesis

| PRJNA1291076 | ENA

H3K9 methyltransferase G9a negatively regulates UHRF1 transdcription during leukemia cell differentiation.

Project description:Posttranslational modifications of histone N-terminal tails influence the status of chromatin and eventually control the transcriptional outcome of a particular gene. As a histone H3K9 methyltransferase (HMTase) in higher eukaryotes, G9a-mediated transcriptional repression is the major epigenetic silencing machinery. UHRF1 (ubiquitin-like with PHD and ring finger domains I) binds to hemi-methylated DNA and plays essential role in maintenance of DNA methylation by recruiting DNMT1. Here, we provide evidence that UHRF1 is transcriptionally downregulated by H3K9 HMTase G9a. We found that increased expression of G9a along with transcription factor YY1 specifically represses UHRF1 transcription. We uncovered showed that G9a regulates UHRF1-mediated H3K23 ubiquitylation and proper DNA replication maintenance by FACS analysis and propose that H3K9 HMTase G9a is a specific epigenetic regulator of UHRF1.

2018-12-31 | GSE63149 | GEO

The impact of G9a-inhibitors in T-cell and Treg differentiation [ATAC-seq]

Project description:As methyltransferase G9a has been implicated in immune cell differentiation we have assessed the role of G9a enzymatic inhibitors (UNC0642) in the differentiation of human naïve T-cells under different stimulation conditions.

2022-12-31 | GSE196903 | GEO

The impact of G9a-inhibitors in T-cell and Treg differentiation [RNA-Seq]

2022-12-31 | GSE196226 | GEO

G9a target gene screening: H3K9 methyltransferase G9a negatively regulates UHRF1 transcription during leukemia cell differentiation

Project description:A genome-wide analysis identified a subset of G9a target genes including UHRF1

2015-04-01 | GSE61610 | GEO

G9a selectively represses a class of late-replicating genes at the nuclear periphery (Expression)

Project description:We have investigated the role of the histone methyltransferase G9a in the establishment of silent nuclear compartments. Following conditional knockout of the G9a methyltransferase in mouse ESCs, 167 genes were significantly up-regulated, and no genes were strongly down-regulated. A partially overlapping set of 119 genes were up-regulated after differentiation of G9a-depleted cells to neural precursors. Promoters of these G9a-repressed genes were AT rich and H3K9me2 enriched but H3K4me3 depleted and were not highly DNA methylated. Representative genes were found to be close to the nuclear periphery, which was significantly enriched for G9a-dependent H3K9me2. Strikingly, although 73% of total genes were early replicating, more than 71% of G9a-repressed genes were late replicating, and a strong correlation was found between H3K9me2 and late replication. However, G9a loss did not significantly affect subnuclear position or replication timing of any non-pericentric regions of the genome, nor did it affect programmed changes in replication timing that accompany differentiation. We conclude that G9a is a gatekeeper for a specific set of genes localized within the late replicating nuclear periphery. 4 cell states each in duplicate (i.e. a total of 8 individual replicates)

2010-06-20 | E-GEOD-18076 | biostudies-arrayexpress

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