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Mus musculus

ABSTRACT: Brg1 Modulates Enhancer Activation and Polycomb-mediated Repression in Mesoderm Differentiation [ChIP-exo]

PROVIDER: PRJNA269676 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1698120.fastq.gz	Fastqsanger.gz
	SRR1698121.fastq.gz	Fastqsanger.gz
	SRR1698122.fastq.gz	Fastqsanger.gz
	SRR1698119.fastq.gz	Fastqsanger.gz

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Project description:Brg1 Modulates Enhancer Activation and Polycomb-mediated Repression in Mesoderm Differentiation

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Brg1 Modulates Enhancer Activation and Polycomb-mediated Repression in Mesoderm Differentiation [ChIP-exo]

Project description:We investigated the genome-wide occupancy changes in normal and Brg1-deleted mesoderm differentiation of mouse embryonic stem cells of chromatin regulators and histone modifications. ChIP exo for BRG1 in 2 conditions: Day4 THF (Control) and Day4 4OHT (Brg1-deleted). 1-2 replicates per condition.

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Chromatin remodeler Brahma safeguards labile canalization of cardiac mesoderm differentiation

Project description:Differentiation proceeds along a continuum of increasingly fate-restricted intermediates, referred to as canalization. Canalization is essential for stabilizing cell fate, but mechanisms underlying robust canalization are unclear. Here we show that the BRG1/BRM-associated factor (BAF) chromatin remodeling complex ATPase gene Brm safeguards cell identity during directed cardiogenesis of mouse embryonic stem cells. Despite establishment of well-differentiated precardiac mesoderm, Brm-null cells predominantly became neural precursors, violating germ layer assignment. Trajectory inference showed sudden acquisition of non-mesodermal identity in Brm-null cells, consistent with a new transition state referred to as a saddle-node bifurcation. Mechanistically, loss of Brm prevented de novo accessibility of cardiac enhancers while increasing expression of neurogenic factor POU3F1, preventing expression of neural suppressor REST, and disrupting composition of BRG1 complexes. Brm mutant identity switch was overcome by increasing BMP4 levels during mesoderm induction. Mathematical modeling supports all our observations. In the mouse embryo, Brm deletion exacerbated mesoderm-deleted Brg1 mutant phenotypes, severely compromising cardiogenesis, unmasking an in vivo role for Brm. Our results reveal Brm as a compensable safeguard of the fidelity of mesoderm chromatin states, and support a model in which developmental canalization is not a rigid irreversible path, but a highly plastic trajectory.

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Dynamic BRG1 Recruitment During T Helper Differentiation And Activation Reveals Distal Regulatory Elements

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Project description:Polycomb complexes are essential regulators of stem cell identity, yet very little is known about their molecular mechanisms during cell differentiation. Pcgf proteins (Pcgf1/2/3/4/5/6) are core subunits of the Polycomb repressive complex 1 (PRC1). It has been recently proposed that specific Pcgf proteins are associated to particular PRC1 complexes, yet the molecular and biological functions of different Pcgf proteins remains largely elusive. Using specific differentiation protocols, we have elucidated a role for Pcgf2/Mel18 in specifically regulating mesoderm differentiation. Mechanistically, during early cardiac mesoderm differentiation, Pcgf2/Mel18 functions as a classical Polycomb protein by repressing pluripotency, lineage specification, late cardiac differentiation and negative regulators of the BMP pathway, yet Pcgf2/Mel18 also positively regulates the expression of key mesoderm transcription factors, revealing a novel function of Pcgf2/Mel18 in gene activation during cardiac differentiation. Mel18 depletion results in an unbalance of pathways that positively and negatively regulate cardiac differentiation. We propose that Mel18 is a novel epigenetic factor that controls mesoderm differentiation by opposing molecular mechanisms. List of ChIPseq samples: Mel18 in ESCs and MES, Ring1b, RYBP and Cbx2 in MES, IgG in MESs. List of RNAseq experiments: Mel18 KD, Ring1b KO and CTR in ESCs, Mel18 KD and CTR in MES, Mel18 KD and CTR in CMs.

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