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GRHL2 and AP2a coordinate early surface ectoderm lineage commitment and craniofacial development [H9_d7_HiChIP_AP2KO]

ABSTRACT: Cohesin HiChIP of AP2a KO hESCs treated with RA/BMP4 for 7 days

ORGANISM(S): Homo sapiens

PROVIDER: GSE225922 | GEO | 2023/02/24

REPOSITORIES: GEO

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GRHL2 and AP2a coordinate early surface ectoderm lineage commitment and craniofacial development (ChIP-Seq)

Project description:ChIP-seq for GRHL2 or AP2a in hESCs treated with RA/BMP4 for 7 days

2023-02-24 | GSE197911 | GEO

GRHL2 and AP2a coordinate early surface ectoderm lineage commitment and craniofacial development (ATAC-Seq)

Project description:ATAC-seq in GRHL2 or AP2a KO hESCs treated with RA/BMP4 for 7 days

2023-02-24 | GSE197910 | GEO

GRHL2 and AP2a coordinate early surface ectoderm lineage commitment and craniofacial development (Multiome)

Project description:scRNA and scATAC in WT and GRHL2 KO hESCs after 7 days of RA/BMP4 (10x multiome)

2023-02-24 | GSE197912 | GEO

GRHL2 and AP2a coordinate early surface ectoderm lineage commitment and craniofacial development (RNA-Seq)

Project description:RNA-seq in GRHL2 KO hESCs treated with RA/BMP4 for 7 days, or GRHL2 over-expression for 7 days.

2023-02-24 | GSE197913 | GEO

UMI-4C in wild-type and p63-null surface ectoderm cells

Project description:Purpose: Validate HiChIP-identified long-range chromatin interactions at the TFAP2C locus, in a viewpoint-specific manner. Methods: UMI-4C libraries targeting 3 individual viewpoints at the TFAP2C locus were generated in duplicate, in surface ectoderm cells with and without p63. Replicates were sequenced on Illumina NextSeq sequencer, and reads were aligned and filtered for valid long-range interactions using HiCPro. Results: Dynamic long-range interactions at the TFAP2C locus were detected with and without p63 in surface ectoderm cells. Conclusion: Long-range interactions detected via HiChIP were confirmed in the surface ectoderm by this technique, validating the HiChIP method through an orthogonal approach.

2018-11-06 | GSE114846 | GEO

Spinal neural tube closure depends on regulation of surface ectoderm identity and biomechanics by Grhl2.

Project description:Lack or excess expression of the surface ectoderm-expressed transcription factor Grainyhead-like2 (Grhl2), each prevent spinal neural tube closure. Here we investigate the causative mechanisms and find reciprocal dysregulation of epithelial genes, cell junction components and actomyosin properties in Grhl2 null and over-expressing embryos. Grhl2 null surface ectoderm shows a shift from epithelial to neuroepithelial identity (with ectopic expression of N-cadherin and Sox2), actomyosin disorganisation, cell shape changes and diminished resistance to neural fold recoil upon ablation of the closure point. In contrast, excessive abundance of Grhl2 generates a super-epithelial surface ectoderm, in which up-regulation of cell-cell junction proteins is associated with an actomyosin-dependent increase in local mechanical stress. This is compatible with apposition of the neural folds but not with progression of closure, unless myosin activity is inhibited. Overall, our findings suggest that Grhl2 plays a crucial role in regulating biomechanical properties of the surface ectoderm that are essential for spinal neurulation.

| S-EPMC6554357 | biostudies-literature

Cohesin HiChIP datasets of pluripotent and surface ectoderm cells with and without p63

Project description:Purpose: Assess changes in the three-dimensional (3D) chromatin architecture during surface ectoderm commitment and evaluate changes in 3D chromatin architecture in human embryonic stem cells and surface ectoderm cells with and without p63. Methods: Cohesin HiChIP profiles for human embryonic stem cells and surface ectoderm cells with and without p63 were generated in triplicate with deep sequencing on the Illumina HiSeq 4000 sequencer. Using HiC-Pro, paired end reads were aligned to hg19, duplicate reads were removed, and then were assigned to MboI restriction fragments, filtered for valid interactions, and used to generate binned interaction matrices of 10 kb resolution. Contacts were called using FitHiC and filtered for counts >= 10 and FDR < 0.001. Results: The greatest change in 3D chromatin architecture was observed between human embryonic stem cells and surface ectoderm cells, while moderate changes were observed in human embryonic stem cells with and without p63, and limited changes were observed in surface ectoderm cells with and without p63. Conclusion: Both p63 and the surface ectoderm morphogens direct changes in chromatin folding to establish the 3D chromatin landscape in the surface ectoderm.

2018-11-06 | GSE120294 | GEO

Early commitment genes drive fast, irreversible commitment to human embryonic stem cell differentiation [scRNA-seq]

Project description:The goal of this study was to characterise transcriptional changes in single hESCs grown in a colony and treated with BMP4 to induce differentiation The goal of this study was to characterise transcriptional changes in single GATA3-/- hESCs grown in a colony and treated with BMP4 to induce differentiation

2020-04-19 | GSE135253 | GEO

The TET-Sall4-BMP regulatory axis controls craniofacial cartilage development

Project description:Craniofacial microsomia (CFM) is a congenital defect that usually results from aberrant development of embryonic pharyngeal arches. However, the molecular basis of CFM pathogenesis is largely unknown. Here, we employ the zebrafish model to investigate mechanisms of CFM pathogenesis. In early embryos, tet2 and tet3 are essential for pharyngeal cartilage development. Single-cell RNA sequencing reveals that loss of Tet2/3 impairs chondrocyte differentiation due to insufficient BMP signaling. Moreover, biochemical and genetic evidence reveals that the sequence-specific 5mC/5hmC-binding protein, Sall4, binds the promoter of bmp4 to activate bmp4 expression and control pharyngeal cartilage development. Mechanistically, Sall4 directs co-phase separation of Tet2/3 with Sall4 to form condensates that mediate 5mC oxidation on the bmp4 promoter, thereby promoting bmp4 expression and enabling sufficient BMP signaling. These findings suggest the TET-BMP-Sall4 regulatory axis is critical for pharyngeal cartilage development. Collectively, our study provides insights into understanding craniofacial development and CFM pathogenesis.

2024-03-04 | GSE226184 | GEO

The TET-Sall4-BMP regulatory axis controls craniofacial cartilage development

Project description:Craniofacial microsomia (CFM) is a congenital defect that usually results from aberrant development of embryonic pharyngeal arches. However, the molecular basis of CFM pathogenesis is largely unknown. Here, we employ the zebrafish model to investigate mechanisms of CFM pathogenesis. In early embryos, tet2 and tet3 are essential for pharyngeal cartilage development. Single-cell RNA-sequencing reveals that loss of Tet2/3 impaired chondrocyte differentiation due to insufficient BMP signaling. Moreover, biochemical and genetic evidence reveals that the sequence-specific 5mC/5hmC-binding protein, Sall4, binds the promoter of bmp4 to activate bmp4 expression and control pharyngeal cartilage development. Mechanistically, Sall4 directs co-phase separation of Tet2/3 with Sall4 to form condensates that mediate 5mC oxidation on the bmp4 promoter, thereby promoting bmp4 expression and enabling sufficient BMP signaling. These findings suggest the TET-BMP-Sall4 regulatory axis is critical for pharyngeal cartilage development. Collectively, our study provides novel insights into understanding craniofacial development and CFM pathogenesis.

2024-02-02 | PXD049147 | iProX

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