Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA352225 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4836620.fastq.gz | Fastqsanger.gz | |||
| SRR4836630.fastq.gz | Fastqsanger.gz | |||
| SRR4836650.fastq.gz | Fastqsanger.gz | |||
| SRR4836670.fastq.gz | Fastqsanger.gz | |||
| SRR4836611.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 47 |
Similar Datasets
Project description:Gene bivalency at Polycomb domains regulates cranial neural crest positional identity
| PRJNA352213 | ENA
Project description:Gene bivalency at Polycomb domains regulates cranial neural crest positional identity [ATAC-seq]
| PRJNA352306 | ENA
Project description:Gene bivalency at Polycomb domains regulates cranial neural crest positional identity [ChIP-seq]
| PRJNA352221 | ENA
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.
2017-03-31 | GSE89436 | GEO
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.
2017-03-31 | GSE89435 | GEO
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.
2017-03-31 | GSE89434 | GEO
Project description:The neural crest is a highly plastic stem cell population that represents a notable exception to the germ layer theory. Despite being of ectodermal origin, these cells can differentiate into skeletal derivatives like cartilage and bone, tissues that are typically formed by mesoderm. The inductive program that endows the neural crest with these unique properties is still poorly understood. Here, we report that Smad2/3-mediated TGFβ signaling endows cranial neural crest cells with enhanced developmental potential. Our results show that TGFβ signaling modulates neural crest axial identity and directly activates the gene circuits that support skeletal differentiation. Cooperation between TGFβ and low levels of WNT-signaling in the embryonic head activates cranial-specific cis-regulatory elements of anterior genes. Activation of the TGFβ pathway allowed reprogramming of trunk neural crest cells to adopt an anterior identity and led to the development of an improved protocol for the generation of human cranial neural crest cells. Our findings indicate TGFβ signaling is required for the specification of cranial neural crest cells, endowing them with the potential to give rise to the craniofacial skeleton.
2025-01-19 | GSE175809 | GEO
Project description:The neural crest is a highly plastic stem cell population that represents a notable exception to the germ layer theory. Despite being of ectodermal origin, these cells can differentiate into skeletal derivatives like cartilage and bone, tissues that are typically formed by mesoderm. The inductive program that endows the neural crest with these unique properties is still poorly understood. Here, we report that Smad2/3-mediated TGFβ signaling endows cranial neural crest cells with enhanced developmental potential. Our results show that TGFβ signaling modulates neural crest axial identity and directly activates the gene circuits that support skeletal differentiation. Cooperation between TGFβ and low levels of WNT-signaling in the embryonic head activates cranial-specific cis-regulatory elements of anterior genes. Activation of the TGFβ pathway allowed reprogramming of trunk neural crest cells to adopt an anterior identity and led to the development of an improved protocol for the generation of human cranial neural crest cells. Our findings indicate TGFβ signaling is required for the specification of cranial neural crest cells, endowing them with the potential to give rise to the craniofacial skeleton.
2025-01-19 | GSE175808 | GEO
Project description:The neural crest is a highly plastic stem cell population that represents a notable exception to the germ layer theory. Despite being of ectodermal origin, these cells can differentiate into skeletal derivatives like cartilage and bone, tissues that are typically formed by mesoderm. The inductive program that endows the neural crest with these unique properties is still poorly understood. Here, we report that Smad2/3-mediated TGFβ signaling endows cranial neural crest cells with enhanced developmental potential. Our results show that TGFβ signaling modulates neural crest axial identity and directly activates the gene circuits that support skeletal differentiation. Cooperation between TGFβ and low levels of WNT-signaling in the embryonic head activates cranial-specific cis-regulatory elements of anterior genes. Activation of the TGFβ pathway allowed reprogramming of trunk neural crest cells to adopt an anterior identity and led to the development of an improved protocol for the generation of human cranial neural crest cells. Our findings indicate TGFβ signaling is required for the specification of cranial neural crest cells, endowing them with the potential to give rise to the craniofacial skeleton.
2025-01-19 | GSE278072 | GEO
Project description:The neural crest is a highly plastic stem cell population that represents a notable exception to the germ layer theory. Despite being of ectodermal origin, these cells can differentiate into skeletal derivatives like cartilage and bone, tissues that are typically formed by mesoderm. The inductive program that endows the neural crest with these unique properties is still poorly understood. Here, we report that Smad2/3-mediated TGFβ signaling endows cranial neural crest cells with enhanced developmental potential. Our results show that TGFβ signaling modulates neural crest axial identity and directly activates the gene circuits that support skeletal differentiation. Cooperation between TGFβ and low levels of WNT-signaling in the embryonic head activates cranial-specific cis-regulatory elements of anterior genes. Activation of the TGFβ pathway allowed reprogramming of trunk neural crest cells to adopt an anterior identity and led to the development of an improved protocol for the generation of human cranial neural crest cells. Our findings indicate TGFβ signaling is required for the specification of cranial neural crest cells, endowing them with the potential to give rise to the craniofacial skeleton.
2025-01-19 | GSE278071 | GEO