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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE196774 | GEO | 2022/09/16

REPOSITORIES: GEO

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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)

2022-09-16 | GSE181014 | 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.

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

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

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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]

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

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

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Polycomb repressive complex 2 regulates skeletal growth by suppressing Wnt and TGF-β signalling.

Project description:Polycomb repressive complex 2 (PRC2) controls maintenance and lineage determination of stem cells by suppressing genes that regulate cellular differentiation and tissue development. However, the role of PRC2 in lineage-committed somatic cells is mostly unknown. Here we show that Eed deficiency in chondrocytes causes severe kyphosis and a growth defect with decreased chondrocyte proliferation, accelerated hypertrophic differentiation and cell death with reduced Hif1a expression. Eed deficiency also causes induction of multiple signalling pathways in chondrocytes. Wnt signalling overactivation is responsible for the accelerated hypertrophic differentiation and kyphosis, whereas the overactivation of TGF-β signalling is responsible for the reduced proliferation and growth defect. Thus, our study demonstrates that PRC2 has an important regulatory role in lineage-committed tissue cells by suppressing overactivation of multiple signalling pathways.

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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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Molecular architecture of polycomb repressive complexes.

Project description:The polycomb group (PcG) proteins are a large and diverse family that epigenetically repress the transcription of key developmental genes. They form three broad groups of polycomb repressive complexes (PRCs) known as PRC1, PRC2 and Polycomb Repressive DeUBiquitinase, each of which modifies and/or remodels chromatin by distinct mechanisms that are tuned by having variable compositions of core and accessory subunits. Until recently, relatively little was known about how the various PcG proteins assemble to form the PRCs; however, studies by several groups have now allowed us to start piecing together the PcG puzzle. Here, we discuss some highlights of recent PcG structures and the insights they have given us into how these complexes regulate transcription through chromatin.

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