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IER5 is required for Notch-mediated induction of squamous cell differentiation [ChIP-seq RBPJ & MAML1]

ABSTRACT: Conditional activation of Notch in squamous cells activates a context-specific gene expression program through lineage-specific regulatory elements. IER5 is a direct Notch-regulated gene and required for Notch-induced differentiation of squamous carcinoma cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE156486 | GEO | 2020/08/31

REPOSITORIES: GEO

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IER5 is required for Notch-mediated induction of squamous cell differentiation [RNA-seq]

Project description:Conditional activation of Notch in squamous cells activates a context-specific gene expression program through lineage-specific regulatory elements. IER5 is a direct Notch-regulated gene and required for Notch-induced differentiation of squamous carcinoma cells.

2020-08-31 | GSE156487 | GEO

IER5 is required for Notch-mediated induction of squamous cell differentiation [H3K27ac ChIP-seq]

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IER5 is required for Notch-mediated induction of squamous cell differentiation

Project description:IER5 is required for Notch-mediated induction of squamous cell differentiation

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IER5 is required for Notch-mediated induction of squamous cell differentiation [ChIP-seq RBPJ & MAML1]

Project description:IER5 is required for Notch-mediated induction of squamous cell differentiation [ChIP-seq RBPJ & MAML1]

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IER5 is required for Notch-mediated induction of squamous cell differentiation [RNA-seq]

Project description:IER5 is required for Notch-mediated induction of squamous cell differentiation [RNA-seq]

| PRJNA658112 | ENA

IER5 is required for Notch-mediated induction of squamous cell differentiation [H3K27ac ChIP-seq]

Project description:IER5 is required for Notch-mediated induction of squamous cell differentiation [H3K27ac ChIP-seq]

| PRJNA658110 | ENA

IER5, a DNA damage response gene, is required for Notch-mediated induction of squamous cell differentiation.

Project description:Notch signaling regulates squamous cell proliferation and differentiation and is frequently disrupted in squamous cell carcinomas, in which Notch is tumor suppressive. Here, we show that conditional activation of Notch in squamous cells activates a context-specific gene expression program through lineage-specific regulatory elements. Among direct Notch target genes are multiple DNA damage response genes, including IER5, which we show is required for Notch-induced differentiation of squamous carcinoma cells and TERT-immortalized keratinocytes. IER5 is epistatic to PPP2R2A, a gene that encodes the PP2A B55α subunit, which we show interacts with IER5 in cells and in purified systems. Thus, Notch and DNA-damage response pathways converge in squamous cells on common genes that promote differentiation, which may serve to eliminate damaged cells from the proliferative pool. We further propose that crosstalk involving Notch and PP2A enables tuning and integration of Notch signaling with other pathways that regulate squamous differentiation.

| S-EPMC7529455 | biostudies-literature

IER5 is required for Notch-mediated induction of squamous cell differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-31 | GSE156488 | GEO

RBPJ/CBF1 interacts with L3MBTL3/MBT1 to promote repression of Notch signaling via histone demethylase KDM1A/LSD1

Project description:Notch signaling is an evolutionarily conserved signal transduction pathway that is essential for metazoan development. At the molecular level, the key components of the Notch pathway are the NOTCH-family receptors, the ligands of the DSL (Delta, Serrate, Lag-2) family and the transcription factor CSL [CBF1/RBPJ, Su(H), Lag-1]. Upon ligand binding, the NOTCH Intra-Cellular Domain (NOTCH ICD) translocates into the nucleus and forms a complex with RBPJ to activate the transcription of target genes. In the absence of NOTCH ICD, RBPJ acts as a transcriptional repressor. Using a proteomic approach, we identified L3MBTL3 as a novel interactor of RBPJ. We discovered that L3MBTL3 competes with NOTCH ICD for binding to RBPJ. In the absence of NOTCH ICD, RBPJ recruits L3MBTL3 and its co-factor KDM1A [lysine (K)-specific demethylase 1A] to the promoters/enhancers of Notch target genes to promote H3K4me2 demethylation and transcriptional repression. In three distinct cell contexts in which Notch signaling governs cell fate, i.e., mature T-cells as well as brain and breast tumor cells, the loss of L3MBTL3 results in the de-repression of Notch target genes. Finally, the genetic analyses of the homologs of RBPJ and L3MBTL3 in Drosophila melanogaster and Caenorhabditis elegans demonstrate that the functional link between RBPJ/Su(H)/lag-1 and L3MBTL3/dL(3)mbt/lin-61 is evolutionarily conserved, thus identifying L3MBTL3 as a universal modulator of Notch signaling in metazoans.

2017-10-17 | PXD004196 | Pride

Dynamic binding of RBPJ is determined by Notch signalling status

Project description:Notch signalling plays crucial roles in mediating cell fate choices in all metazoans largely by specifying the transcriptional output of one cell in response to a neighbouring cell. The DNA-binding protein RBPJ is the principle effector of this pathway in mammals and together with the transcription factor moiety of Notch (NICD) it regulates the expression of target genes. The prevalent view presumes that RBPJ statically occupies consensus binding sites while exchanging repressors for activators in response to NICD. We present the first specific RBPJ chromatin immunoprecipitation and high-throughput sequencing study in mammalian cells. To dissect the mode of transcriptional regulation by RBPJ and identify its direct targets, whole genome binding profiles were generated for RBPJ, its coactivator p300, NICD and the histone H3 modifications H3K4me3, H3K4me1 and H3K27ac in myogenic cells under active or inhibitory Notch signalling conditions. Our results demonstrate dynamic binding of RBPJ in response to Notch activation at essentially all sites co-occupied by NICD. Additionally, we identify a distinct set of sites where RBPJ recruits neither NICD nor p300, and binds DNA statically, irrespective of Notch activity. These findings significantly modify our views on how RBPJ and Notch signalling mediate their activities and consequently impact on cell fate decisions. ChIP (chromatin immunoprecipitation) is followed by deep sequencing to generate genome-wide patterns of RBP-J binding in mouse C2C12 cells under various conditions. Cells were either Notch activated by exposure to immobilized ligand or by overexpression of NICDGFP, or Notch inhibited by treatment with DAPT. Notch activation and inhibition treatments were applied for 6h and 24h. In addition to RBP-J, p300 and NICDGFP were profiled by ChIP-Seq and gene expression was assessed by RNA-Seq.

2013-05-13 | E-GEOD-37184 | biostudies-arrayexpress

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