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ERK signalling orchestrates neural differentiation by promoting the polycomb repressive complex.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE181015 | GEO | 2022/09/16

REPOSITORIES: GEO

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ERK signalling orchestrates neural differentiation by promoting the polycomb repressive complex [dataset 3]

Project description:mRNAseq was examined in human embryonic stem cells (H9) and neuromesodermal progenitors differentiated from these cells in vitro

2022-09-16 | GSE196774 | GEO

ERK signalling orchestrates neural differentiation by promoting the polycomb repressive complex [dataset 1]

Project description:In this experiment patterns of chromatin accessibility were compared in (H9) human ES cell derived neuromesodermal progenitors (NMP-L)s and derived neural progenitors (NP)s at different days during the neural differentiation procedure (day 5, day 6 and day 8) and also in NPs at day 5 and 6 exposed to carrier control with DMSO or the MEK inhibitor PD184352.

2022-09-16 | GSE121126 | GEO

ERK signalling orchestrates neural differentiation by promoting the polycomb repressive complex [dataset 2]

Project description:In this experiment, Ring1b occupancy was examined in human neuromesodermal progenitors derived from embryonic stem cells (H9)

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ERK signalling orchestrates neural differentiation by promoting the polycomb repressive complex.

Project description:ERK signalling orchestrates neural differentiation by promoting the polycomb repressive complex.

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ERK signalling orchestrates neural differentiation by promoting the polycomb repressive complex [dataset 1]

Project description:ERK signalling orchestrates neural differentiation by promoting the polycomb repressive complex [dataset 1]

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ERK signalling orchestrates neural differentiation by promoting the polycomb repressive complex [dataset 3]

Project description:ERK signalling orchestrates neural differentiation by promoting the polycomb repressive complex [dataset 3]

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ERK signalling orchestrates neural differentiation by promoting the polycomb repressive complex [dataset 2]

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ERK1/2 signalling dynamics promote neural differentiation by regulating chromatin accessibility and the polycomb repressive complex.

Project description:Fibroblast growth factor (FGF) is a neural inducer in many vertebrate embryos, but how it regulates chromatin organization to coordinate the activation of neural genes is unclear. Moreover, for differentiation to progress, FGF signalling must decline. Why these signalling dynamics are required has not been determined. Here, we show that dephosphorylation of the FGF effector kinase ERK1/2 rapidly increases chromatin accessibility at neural genes in mouse embryos, and, using ATAC-seq in human embryonic stem cell derived spinal cord precursors, we demonstrate that this occurs genome-wide across neural genes. Importantly, ERK1/2 inhibition induces precocious neural gene transcription, and this involves dissociation of the polycomb repressive complex from key gene loci. This takes place independently of subsequent loss of the repressive histone mark H3K27me3 and transcriptional onset. Transient ERK1/2 inhibition is sufficient for the dissociation of the repressive complex, and this is not reversed on resumption of ERK1/2 signalling. Moreover, genomic footprinting of sites identified by ATAC-seq together with ChIP-seq for polycomb protein Ring1B revealed that ERK1/2 inhibition promotes the occupancy of neural transcription factors (TFs) at non-polycomb as well as polycomb associated sites. Together, these findings indicate that ERK1/2 signalling decline promotes global changes in chromatin accessibility and TF binding at neural genes by directing polycomb and other regulators and appears to serve as a gating mechanism that provides directionality to the process of differentiation.

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Polycomb Repressive Complex 2 regulates lineage fidelity during embryonic stem cell differentiation.

Project description:Polycomb Repressive Complex 2 (PRC2) catalyzes histone H3 lysine 27 tri-methylation (H3K27me3), an epigenetic modification associated with gene repression. H3K27me3 is enriched at the promoters of a large cohort of developmental genes in embryonic stem cells (ESCs). Loss of H3K27me3 leads to a failure of ESCs to properly differentiate, making it difficult to determine the precise roles of PRC2 during lineage commitment. Moreover, while studies suggest that PRC2 prevents DNA methylation, how these two epigenetic regulators coordinate to regulate lineage programs is poorly understood. Using several PRC2 mutant ESC lines that maintain varying levels of H3K27me3, we found that partial maintenance of H3K27me3 allowed for proper temporal activation of lineage genes during directed differentiation of ESCs to spinal motor neurons (SMNs). In contrast, genes that function to specify other lineages failed to be repressed in these cells, suggesting that PRC2 is also necessary for lineage fidelity. We also found that loss of H3K27me3 leads to a modest gain in DNA methylation at PRC2 target regions in both ESCs and in SMNs. Our study demonstrates a critical role for PRC2 in safeguarding lineage decisions and in protecting genes against inappropriate DNA methylation.

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Polycomb repressive complex 2 shields naive human pluripotent cells from trophectoderm differentiation.

Project description:The first lineage choice in human embryo development separates trophectoderm from the inner cell mass. Naïve human embryonic stem cells are derived from the inner cell mass and offer possibilities to explore how lineage integrity is maintained. Here, we discover that polycomb repressive complex 2 (PRC2) maintains naïve pluripotency and restricts differentiation to trophectoderm and mesoderm lineages. Through quantitative epigenome profiling, we found that a broad gain of histone H3 lysine 27 trimethylation (H3K27me3) is a distinct feature of naïve pluripotency. We define shared and naïve-specific bivalent promoters featuring PRC2-mediated H3K27me3 concomitant with H3K4me3. Naïve bivalency maintains key trophectoderm and mesoderm transcription factors in a transcriptionally poised state. Inhibition of PRC2 forces naïve human embryonic stem cells into an 'activated' state, characterized by co-expression of pluripotency and lineage-specific transcription factors, followed by differentiation into either trophectoderm or mesoderm lineages. In summary, PRC2-mediated repression provides a highly adaptive mechanism to restrict lineage potential during early human development.

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