SW480 cells undergoes postmitotic neuron-like differentiation in response to EZH2 knockdown
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PROVIDER: PRJNA486167 | ENA |
REPOSITORIES: ENA
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Project description:Formerly we found that combined inhibition of class I HDACs, DNMTs, EZH2 and LSD1 with chemical inhibitors in a variety of cancer cells caused neuronal differentiation. Our recent study demonstrated that functional knockdown of EZH2 alone in SW480 cells can also lead to significant neuronal differentiation. We used microarray to analyze global gene expression change in SW480 cells after neuronal differentiation induced by EZH2 knockdown.
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Project description:EZH2 plays an important role in stem cell renewal and maintenance by inducing gene silencing via its histone methyltransferase activity. Previously, we showed EZH2 downregulation markedly enhances neuron differentiation of human mesenchymal stem cells (hMSCs). To understand how EZH2 regulates neuron differentiation of hMSCs, we wanted to identify the target genes of EZH2. For this reasons we performed ChIP-on-chip experiments using specific EZH2 antibodies followed by a human promoter array for the whole human genome. The 3A6-hMSCs were differentiated into neuron for 5 days, and then 109 cells were harvested for the ChIP-on-chip assay. The procedure was based on the manufacturer's instructions (NimbleGen).
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Project description:ChIP-on-chip tilling array comparing untreated human SW480 cells vs SW480 cells treated with 2mM H2O2 for 30min. Exposing cells to the reactive oxygen species, hydrogen peroxide, recruits DNA methyltransferase 1 (DNMT1) to damaged chromatin. DNMT1 becomes part of a complex(es) containing DNMT3B and members of Polycomb Repressive Complex 4. The goal was to determine the effect of hydrogen peroxide treatment on chromatin, including changes in histone modifications and binding patterns of chromatin-associated proteins. [Agilent-014706]: Two-condition: untreated SW480 cells (U) vs H2O2 treated SW480 cells (T). Five-mark: SIRT1, gamma-HA2X, DNMT1, DNMT3B, and EZH2. [Agilent-014707]: Two-condition: untreated SW480 cells (U) vs H2O2 treated SW480 cells (T). Five-mark: SIRT1, gamma-HA2X, DNMT1, DNMT3B, and EZH2. [Agilent-026595]: Two-condition: untreated SW480 cells (U) vs H2O2 treated SW480 cells (T). Five-mark: SIRT1, gamma-HA2X, DNMT1, DNMT3B, and H3. [Agilent-027811]: Two-condition: untreated SW480 cells (U) vs H2O2 treated SW480 cells (T). Four-mark: H3, 3MeK4H3, AcK16H4, and 3MeK27H3.
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Project description:EZH2 plays an important role in stem cell renewal and maintenance by inducing gene silencing via its histone methyltransferase activity. Previously, we showed EZH2 downregulation markedly enhances neuron differentiation of human mesenchymal stem cells (hMSCs). To understand how EZH2 regulates neuron differentiation of hMSCs, we wanted to identify the target genes of EZH2. For this reasons we performed ChIP-on-chip experiments using specific EZH2 antibodies followed by a human promoter array for the whole human genome.
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Project description:The functional and transcriptional maturation of neurons is a prolonged process that extends well beyond mitotic exit and terminal fate commitment of progenitors. The differentiation of cerebellar granule neurons (CGNs) in the postnatal mouse cerebellum provides a useful model to identify chromatin mechanisms that orchestrate temporal changes in transcription as postmitotic CGNs mature. Here we report that CGN maturation is associated with dynamic changes in the genomic distribution of histone H3 lysine 27 trimethylation (H3K27me3), a modification best known for its role in repressing alternative fates during cell specification. H3K27me3 is gained rapidly in newly postmitotic CGNs at progenitor-expressed genes that are repressed in neurons. H3K27me3 is lost more gradually at the promoters of a subset of neuronal genes that are transcriptionally induced upon CGN maturation. The loss of H3K27me3 is facilitated by the lysine demethylase KDM6B, and genes that are induced in maturing CGNs show impaired expression in the cerebellum of conditional KDM6B knockout mice. Genes that lose H3K27me3 gain H3K27 acetylation and binding of the pro-maturation ZIC1/2 transcription factors, suggesting that developmental loss of H3K27me3 may be required to permit the onset of transcriptional maturation. Interestingly, pharmacological inhibition of the H3K27 methyltransferase EZH2 in early postmitotic CGNs not only blocked the repression of progenitor genes but also impaired the induction of mature CGN genes. These data show that regulation of H3K27me3 functions in developing postmitotic neurons beyond the period of cell fate commitment to regulate the dynamics of gene expression programs that underlie functional neuronal maturation.
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Project description:The functional and transcriptional maturation of neurons is a prolonged process that extends well beyond mitotic exit and terminal fate commitment of progenitors. The differentiation of cerebellar granule neurons (CGNs) in the postnatal mouse cerebellum provides a useful model to identify chromatin mechanisms that orchestrate temporal changes in transcription as postmitotic CGNs mature. Here we report that CGN maturation is associated with dynamic changes in the genomic distribution of histone H3 lysine 27 trimethylation (H3K27me3), a modification best known for its role in repressing alternative fates during cell specification. H3K27me3 is gained rapidly in newly postmitotic CGNs at progenitor-expressed genes that are repressed in neurons. H3K27me3 is lost more gradually at the promoters of a subset of neuronal genes that are transcriptionally induced upon CGN maturation. The loss of H3K27me3 is facilitated by the lysine demethylase KDM6B, and genes that are induced in maturing CGNs show impaired expression in the cerebellum of conditional KDM6B knockout mice. Genes that lose H3K27me3 gain H3K27 acetylation and binding of the pro-maturation ZIC1/2 transcription factors, suggesting that developmental loss of H3K27me3 may be required to permit the onset of transcriptional maturation. Interestingly, pharmacological inhibition of the H3K27 methyltransferase EZH2 in early postmitotic CGNs not only blocked the repression of progenitor genes but also impaired the induction of mature CGN genes. These data show that regulation of H3K27me3 functions in developing postmitotic neurons beyond the period of cell fate commitment to regulate the dynamics of gene expression programs that underlie functional neuronal maturation.
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