Terminal B cell differentiation
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ABSTRACT:
PROVIDER: PRJNA564227 | ENA |
REPOSITORIES: ENA
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Project description:Expression profiling of terminal B cell differentiation [RNA-Seq]
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Project description:Chromatin accessibility profiling of terminal B cell differentiation [ATAC-Seq]
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Project description:The terminal differentiation of B cells into antibody-secreting cells (ASCs) is a critical component of adaptive immune responses. Using our in vitro differentiation system, we combined RNA sequencing with ATAC-seq to characterize genomic events driving the ASC differentiation of human primary naive B cells. After an initial response to IL-4, cells that committed to an ASC fate downregulated the CD23 marker and IL-4 signaling, whereas cells that maintained IL-4 signaling did not differentiate. As demonstrated in the mouse, downregulation of the human ubiquitin ligase CBLB was required to free IRF4 from proteasomal degradation and produce levels needed for ASC differentiation. Our results evidenced two previously undocumented mechanisms driving human terminal B cell differentiation. Lastly, we showed that CD23-negative cells (i) carried the imprint of their previous activated B-cell status, (ii) were precursors of plasmablasts, and (iii) had a similar phenotype to in vivo pre-plasmablasts.
2020-11-08 | GSE136989 | GEO
Project description:The histone 3 lysine 9 (H3K9)-specific methyltransferase (KMT) Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on Setdb1 role(s) in these mutually exclusive processes, we used mouse skeletal myoblasts as a model of terminal differentiation. Ex vivo studies on isolated single myofibres showed that Setdb1 is required for muscle adult stem cells expansion following activation and in vitro studies on skeletal myoblasts confirmed that Setdb1 suppresses terminal myoblast differentiation. We used genome-wide analyses to identify Setdb1 direct target genes in myoblasts and observed a release of Setdb1 from the promoter of selected target genes upon myoblast terminal differentiation, concomitant to a nuclear export of Setdb1 to the cytoplasm. We demonstrated that both genomic release and cytoplasmic Setdb1 relocalisation during differentiation were dependent on canonical Wnt signalling. Taken together, our findings uncover a functional link between Setdb1 and canonical Wnt signalling in skeletal muscle cells, which affects the expression of a subset of Setdb1 target genes. We revealed Wnt-dependent subcellular relocalisation of Setdb1 as a novel mechanism regulating Setdb1 functions. ChIP-seq of Setdb1 and H3K9me3 in Myoblast cells (C2C12)
2016-02-01 | E-GEOD-65493 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE22322: Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and their denucleation [lens tissue] GSE25168: Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and their denucleation [eyeball tissue] Refer to individual Series
2011-01-01 | E-GEOD-25169 | biostudies-arrayexpress
Project description:The terminal differentiation of B cells into antibody-secreting cells (ASCs) is a critical component of adaptive immune responses. Using our in vitro differentiation system, we combined RNA sequencing with ATAC-seq to characterize genomic events driving the ASC differentiation of human primary naive B cells. After an initial response to IL-4, cells that committed to an ASC fate downregulated the CD23 marker and IL-4 signaling, whereas cells that maintained IL-4 signaling did not differentiate. As demonstrated in the mouse, downregulation of the human ubiquitin ligase CBLB was required to free IRF4 from proteasomal degradation and produce levels needed for ASC differentiation. Our results evidenced two previously undocumented mechanisms driving human terminal B cell differentiation. Lastly, we showed that CD23-negative cells (i) carried the imprint of their previous activated B-cell status, (ii) were precursors of plasmablasts, and (iii) had a similar phenotype to in vivo pre-plasmablasts.
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Project description:Global Transcriptome Analyses of Mammalian Terminal Erythroid Differentiation
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Project description:The histone 3 lysine 9 methyltransferase Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on Setdb1 roles in these mutually exclusive processes, we used mouse skeletal myoblasts as a model of terminal differentiation. Ex vivo studies on isolated single myofibres showed that Setdb1 is required for adult muscle stem cells expansion following activation. In vitro studies in skeletal myoblasts confirmed that Setdb1 suppresses terminal differentiation. Genomic binding analyses showed a release of Setdb1 from selected target genes upon myoblast terminal differentiation, concomitant to a nuclear export of Setdb1 to the cytoplasm. Both genomic release and cytoplasmic Setdb1 relocalisation during differentiation were dependent on canonical Wnt signalling. Transcriptomic assays in myoblasts unravelled a significant overlap between Setdb1 and Wnt3a regulated genetic programs. Together, our findings revealed Wnt-dependent subcellular relocalisation of Setdb1 as a novel mechanism regulating Setdb1 functions and myogenesis. This SuperSeries is composed of the SubSeries listed below.
2016-02-01 | GSE70070 | GEO
Project description:The histone 3 lysine 9 (H3K9)-specific methyltransferase (KMT) Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on Setdb1 role(s) in these mutually exclusive processes, we used mouse skeletal myoblasts as a model of terminal differentiation. Ex vivo studies on isolated single myofibres showed that Setdb1 is required for muscle adult stem cells expansion following activation and in vitro studies on skeletal myoblasts confirmed that Setdb1 suppresses terminal myoblast differentiation. We used genome-wide analyses to identify Setdb1 direct target genes in myoblasts and observed a release of Setdb1 from the promoter of selected target genes upon myoblast terminal differentiation, concomitant to a nuclear export of Setdb1 to the cytoplasm. We demonstrated that both genomic release and cytoplasmic Setdb1 relocalisation during differentiation were dependent on canonical Wnt signalling. Taken together, our findings uncover a functional link between Setdb1 and canonical Wnt signalling in skeletal muscle cells, which affects the expression of a subset of Setdb1 target genes. We revealed Wnt-dependent subcellular relocalisation of Setdb1 as a novel mechanism regulating Setdb1 functions.
2016-02-01 | GSE65493 | GEO