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Effect of depletion of MED23 on gene expression during primary mouse OPC differentiation [RNA-seq]

ABSTRACT: Effect of depletion of MED23 on gene expression during primary mouse OPC differentiation [RNA-seq]

PROVIDER: PRJNA938769 | ENA |

REPOSITORIES: ENA

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Effect of depletion of MED23 on gene expression during primary mouse OPC differentiation [RNA-seq]

Project description:To determine the role played by Med23 in OPC differentiation, OPCs were isolated from the Med23cKO (i.e., Med23-/-OPCs) or control mice (i.e., Med23+/+OPCs) and induced to differentiate in vitro. We then performed gene expression profiling analysis using data obtained from RNA-seq of Med23+/+iOLs and Med23-/-iOLs .

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Effect of depletion of MED23 on H3K27AC histone modifications during mouse OPC differentiation [ChIP-seq]

Project description:Effect of depletion of MED23 on H3K27AC histone modifications during mouse OPC differentiation [ChIP-seq]

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Effect of depletion of MED23 on H3K27AC histone modifications during mouse OPC differentiation [ChIP-seq]

Project description:To determine the role played by Med23 in the genome wide H3K27AC histone modifications.

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Effect of depletion of MED23 on genome-wide occupancy of Sp1 and P300 during mouse OPC differentiation [cut&tag]

Project description:To determine the role played by Med23 in the cooperation between Sp1 and P300.

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Effect of depletion of MED23 on genome-wide occupancy of Sp1 and P300 during mouse OPC differentiation [cut&tag]

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Mediator Med23-deficiency Enhances Neural Differentiation of Embryonic Stem Cells through Modulating BMP Signaling

Project description:Unraveling the mechanisms underlying early neural differentiation of ESCs is crucial to the cell-based therapies of neurodegenerate diseases. Neural fate acquisition is proposed to be controlled by a âdefaultâ mechanism, for which the molecular regulation is not well understood. In this study, we investigated the functional roles of Mediator Med23 in pluripotency and lineage commitment of embryonic stem cells (ESCs). Unexpectedly we found that, despite the largely unchanged pluripotency and self-renewal of ESCs, Med23-depletion rendered the cells prone to neural differentiation in different differentiation assays. Knockdown of other Mediator subunit, Med1 or Med15, did not alter the neural differentiation of ESCs; and Med15 knockdown selectively inhibited endoderm differentiation, suggesting the specificity of cell fate control by distinctive Mediator subunits. Gene profiling revealed that Med23-depletion attenuated the BMP signaling in ESCs. Mechanistically, MED23 modulated Bmp4 expression by controlling the activity of ETS1 that is involved in the Bmp4 promoter-enhancer communication. Interestingly, Med23 knockdown in zebrafish embryos also enhanced the neural development at early embryogenesis, which could be reversible by coinjection of bmp4 mRNA. Taken together, our study reveals an intrinsic, restrictive role of MED23 in early neural development, thus providing new molecular insights for neural fate determination. We used microarrays to detail the global gene expression after MED23 knockout We examined the gene expression level in WT and MED23 knockout ES cells in steady culture condition.

2015-03-05 | E-GEOD-64500 | biostudies-arrayexpress

Mediator Med23-deficiency Enhances Neural Differentiation of Embryonic Stem Cells through Modulating BMP Signaling

Project description:Unraveling the mechanisms underlying early neural differentiation of ESCs is crucial to the cell-based therapies of neurodegenerate diseases. Neural fate acquisition is proposed to be controlled by a “default” mechanism, for which the molecular regulation is not well understood. In this study, we investigated the functional roles of Mediator Med23 in pluripotency and lineage commitment of embryonic stem cells (ESCs). Unexpectedly we found that, despite the largely unchanged pluripotency and self-renewal of ESCs, Med23-depletion rendered the cells prone to neural differentiation in different differentiation assays. Knockdown of other Mediator subunit, Med1 or Med15, did not alter the neural differentiation of ESCs; and Med15 knockdown selectively inhibited endoderm differentiation, suggesting the specificity of cell fate control by distinctive Mediator subunits. Gene profiling revealed that Med23-depletion attenuated the BMP signaling in ESCs. Mechanistically, MED23 modulated Bmp4 expression by controlling the activity of ETS1 that is involved in the Bmp4 promoter-enhancer communication. Interestingly, Med23 knockdown in zebrafish embryos also enhanced the neural development at early embryogenesis, which could be reversible by coinjection of bmp4 mRNA. Taken together, our study reveals an intrinsic, restrictive role of MED23 in early neural development, thus providing new molecular insights for neural fate determination. We used microarrays to detail the global gene expression after MED23 knockout

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