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Mus musculus

ABSTRACT: H3K27me3 enrichment in the supraorbital cranial mesenchyme with ectoderm upon the deletion of β-catenin

PROVIDER: PRJNA379968 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5364367.fastq.gz	Fastqsanger.gz
	SRR5364368.fastq.gz	Fastqsanger.gz
	SRR5364369.fastq.gz	Fastqsanger.gz

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H3K27me3 enrichment in the supraorbital cranial mesenchyme with ectoderm upon the deletion of β-catenin

Project description:H3K27me3 enrichment in the supraorbital cranial mesenchyme with ectoderm upon the deletion of β-catenin

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Supraorbital cranial mesenchyme with ectoderm upon the deletion of β-catenin

Project description:Supraorbital cranial mesenchyme with ectoderm upon the deletion of β-catenin

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Project description:Gene expression changes in the supraorbital cranial mesenchyme after beta-catenin deletion in vivo

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Nonclassical beta catenin signaling regulate skeletal cell fate determination

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Transcription profiling of mouse intestinal crypts upon deletion of beta-catenin

Project description:The Wnt signaling pathway is deregulated in over 90% of human colorectal cancers. Î² Catenin, the central signal transducer of the Wnt pathway, can directly modulate gene expression by interacting with transcription factors of the TCF/LEF-family. In the present study we investigate the role of Wnt signaling in the homeostasis of intestinal epithelium using tissue-specific, inducible beta-catenin gene ablation in adult mice. Block of Wnt/beta-catenin signaling resulted in rapid loss of transient-amplifying cells and crypt structures. Importantly, intestinal stem cells were induced to terminally differentiate upon deletion of beta-catenin resulting in a complete block of intestinal homeostasis and fatal loss of intestinal function. Transcriptional profiling of mutant crypt mRNA isolated by laser capture micro dissection confirmed those observations and allowed to identify genes potentially responsible for the functional preservation of intestinal stem cells. Experiment Overall Design: laser capture microdissection of intestinal crypts, control vs. beta-catenin mutant (2days after induction of deletion by tamoxifen), two rounds of amplification of mRNA

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PRDM proteins control Wnt/β-catenin activity to regulate craniofacial chondrocyte differentiation

Project description:Cranial neural crest (NCC)-derived chondrocyte precursors undergo a dynamic differentiation and maturation process to establish a scaffold for subsequent bone formation, alterations in which contribute to congenital birth defects. Here, we demonstrate that transcription factor and histone methyltransferase proteins Prdm3 and Prdm16 control the differentiation switch of cranial NCCs to craniofacial cartilage. Loss of either results in hypoplastic and unorganized chondrocytes due to impaired cellular orientation and polarity. We show that PRDMs regulate cartilage differentiation by controlling the timing of Wnt/β-catenin activity in strikingly different ways: prdm3 represses while prdm16 activates global gene expression, though both by regulating Wnt enhanceosome activity and chromatin accessibility. Finally, we show that manipulating Wnt/β-catenin signaling pharmacologically or generating prdm3-/-;prdm16-/- double mutants rescues craniofacial cartilage defects. Our findings reveal upstream regulatory roles for Prdm3 and Prdm16 in cranial NCCs to control Wnt/β-catenin transcriptional activity during chondrocyte differentiation to ensure proper development of the craniofacial skeleton.

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Project description:Ectoderm and mesenchyme gene expression in the developing mouse face

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Gene bivalency at Polycomb domains regulates cranial neural crest positional identity [ATAC-seq]

Project description:The cranial neural crest cells are pluripotent cells that provide head skeletogenic mesenchyme and are crucial for craniofacial patterning. Here, we analyzed the in vivo chromatin landscapes of mouse cranial neural crest subpopulations. Early postmigratory neural crest subpopulations contributing to distinct mouse craniofacial structures displayed similar chromatin accessibility patterns, yet differed transcriptionally. Accessible promoters and enhancers of differentially silenced genes carried H3K27me3/H3K4me2 bivalent chromatin marks embedded in large Ezh2-dependent Polycomb domains, indicating transcriptional poising. These postmigratory bivalent regions were already present in neural crest premigratory progenitors. At Polycomb domains, H3K27me3 antagonized H3K4me2 deposition, which was restricted to accessible sites. Thus, bivalent Polycomb domains provide a chromatin template for the regulation of cranial neural crest cell positional identity in vivo contributing novel insights into the epigenetic regulation of face morphogenesis.

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