ATAC-seq of wildtype and Meis2 mutant in the developing palate
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA602085 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10913279_1.fastq.gz | Fastqsanger.gz | |||
| SRR10913279_2.fastq.gz | Fastqsanger.gz | |||
| SRR10913280_1.fastq.gz | Fastqsanger.gz | |||
| SRR10913280_2.fastq.gz | Fastqsanger.gz | |||
| SRR10913281.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:We use ATAC-seq to identify chromatin accessibility in the palatal mesenchyme of wildtype and Wnt1Cre;Meis2f/f mice at E12.5. Haploinsufficiency of MEIS2 is associated with cleft palate in humans and Meis2 inactivation leads to abnormal palate development in mice, implicating an essential role for Meis2 in palate development. However, its functional mechanisms remain unknown. In this study, we found widespread Meis2 expression in the developing palate in mice. Meis2 inactivation by Wnt1Cre in cranial neural crest cells led to the cleft of the secondary palate. Importantly, about half of Wnt1Cre;Meis2f/f mice exhibited submucous cleft, providing an excellent model for studying palatal bone formation and patterning. Consistent with a complete absence of the palatal bones, integrative analyses of Meis2 ChIP-seq, RNA-seq, and ATAC-seq results identified key osteogenic genes that are regulated directly by Meis2, indicating the fundamental role of Meis2 in palatal osteogenesis. De novo motif analysis discovered that the Meis2-bound regions possess highly enriched binding motifs of several key osteogenic transcription factors particularly Shox2. Comparison of Meis2 and Shox2 ChIP-seq analyses further revealed a genome-wide co-occupancy, in addition to their co-localization in the developing palate and physical interaction, suggesting that Shox2 and Meis2 act as partners. However, while Shox2 is required for proper palatal bone formation and is a direct downstream target of Meis2, Shox2 overexpression failed to rescue the palatal bone defects in Meis2 mutant background. These results, together with the facts that Meis2 expression is associated with high osteogenic potential and is required for the chromatin accessibility of osteogenic genes, support a vital function of Meis2 in setting up the ground state for palatal osteogenesis.
2020-03-23 | GSE143910 | GEO
Project description:We use RNA-sequencing to profile the different expression genes in the palatal mesenchyme of wildtype and Wnt1Cre;Meis2f/f mice at E12.5. Haploinsufficiency of MEIS2 is associated with cleft palate in humans and Meis2 inactivation leads to abnormal palate development in mice, implicating an essential role for Meis2 in palate development. However, its functional mechanisms remain unknown. In this study, we found widespread Meis2 expression in the developing palate in mice. Meis2 inactivation by Wnt1Cre in cranial neural crest cells led to the cleft of the secondary palate. Importantly, about half of Wnt1Cre;Meis2f/f mice exhibited submucous cleft, providing an excellent model for studying palatal bone formation and patterning. Consistent with a complete absence of the palatal bones, integrative analyses of Meis2 ChIP-seq, RNA-seq, and ATAC-seq results identified key osteogenic genes that are regulated directly by Meis2, indicating the fundamental role of Meis2 in palatal osteogenesis. De novo motif analysis discovered that the Meis2-bound regions possess highly enriched binding motifs of several key osteogenic transcription factors particularly Shox2. Comparison of Meis2 and Shox2 ChIP-seq analyses further revealed a genome-wide co-occupancy, in addition to their co-localization in the developing palate and physical interaction, suggesting that Shox2 and Meis2 act as partners. However, while Shox2 is required for proper palatal bone formation and is a direct downstream target of Meis2, Shox2 overexpression failed to rescue the palatal bone defects in Meis2 mutant background. These results, together with the facts that Meis2 expression is associated with high osteogenic potential and is required for the chromatin accessibility of osteogenic genes, support a vital function of Meis2 in setting up the ground state for palatal osteogenesis.
2020-03-23 | GSE143912 | GEO
Project description:Transcriptome of wildtype and Meis2 mutant in the developing palate
| PRJNA602083 | ENA
Project description:ChIP-Sequencing on Meis2-HA in E12.5 palate, to identify Meis2 binding chromatin regions and target genes. Haploinsufficiency of MEIS2 is associated with cleft palate in humans and Meis2 inactivation leads to abnormal palate development in mice, implicating an essential role for Meis2 in palate development. However, its functional mechanisms remain unknown. In this study, we found widespread Meis2 expression in the developing palate in mice. Meis2 inactivation by Wnt1Cre in cranial neural crest cells led to the cleft of the secondary palate. Importantly, about half of Wnt1Cre;Meis2f/f mice exhibited submucous cleft, providing an excellent model for studying palatal bone formation and patterning. Consistent with a complete absence of the palatal bones, integrative analyses of Meis2 ChIP-seq, RNA-seq, and ATAC-seq results identified key osteogenic genes that are regulated directly by Meis2, indicating the fundamental role of Meis2 in palatal osteogenesis. De novo motif analysis discovered that the Meis2-bound regions possess highly enriched binding motifs of several key osteogenic transcription factors particularly Shox2. Comparison of Meis2 and Shox2 ChIP-seq analyses further revealed a genome-wide co-occupancy, in addition to their co-localization in the developing palate and physical interaction, suggesting that Shox2 and Meis2 act as partners. However, while Shox2 is required for proper palatal bone formation and is a direct downstream target of Meis2, Shox2 overexpression failed to rescue the palatal bone defects in Meis2 mutant background. These results, together with the facts that Meis2 expression is associated with high osteogenic potential and is required for the chromatin accessibility of osteogenic genes, support a vital function of Meis2 in setting up the ground state for palatal osteogenesis.
2020-03-23 | GSE143911 | GEO
Project description:We use single cell RNA-sequencing to profile palatal mesenchyme cells from Shox2Cre/+;R26RmTmG at E13.5. Haploinsufficiency of MEIS2 is associated with cleft palate in humans and Meis2 inactivation leads to abnormal palate development in mice, implicating an essential role for Meis2 in palate development. However, its functional mechanisms remain unknown. In this study, we found widespread Meis2 expression in the developing palate in mice. Meis2 inactivation by Wnt1Cre in cranial neural crest cells led to the cleft of the secondary palate. Importantly, about half of Wnt1Cre;Meis2f/f mice exhibited submucous cleft, providing an excellent model for studying palatal bone formation and patterning. Consistent with a complete absence of the palatal bones, integrative analyses of Meis2 ChIP-seq, RNA-seq, and ATAC-seq results identified key osteogenic genes that are regulated directly by Meis2, indicating the fundamental role of Meis2 in palatal osteogenesis. De novo motif analysis discovered that the Meis2-bound regions possess highly enriched binding motifs of several key osteogenic transcription factors particularly Shox2. Comparison of Meis2 and Shox2 ChIP-seq analyses further revealed a genome-wide co-occupancy, in addition to their co-localization in the developing palate and physical interaction, suggesting that Shox2 and Meis2 act as partners. However, while Shox2 is required for proper palatal bone formation and is a direct downstream target of Meis2, Shox2 overexpression failed to rescue the palatal bone defects in Meis2 mutant background. These results, together with the facts that Meis2 expression is associated with high osteogenic potential and is required for the chromatin accessibility of osteogenic genes, support a vital function of Meis2 in setting up the ground state for palatal osteogenesis.
2020-03-23 | GSE143913 | GEO
Project description:The homeodomain protein Meis1 is essential for definitive hematopoiesis and vascular patterning in the mouse embryo. Meis2, another member of the same family, shares 82% protein identities with Meis1. Our present study suggested Meis2 exerts two distinguishable effects in differentiating ES cells. First, it increases the numbers of hematopoietic progenitors and extends their persistence in culture. Second, Meis2 skews hematopoietic differentiation by suppressing erythroid while enhancing megakaryocytic progenitor differentiation. To identify the underlying transcriptional bases of these actions, we carried out microarray analysis to compare the various populations of cells developing in ES differentiation cultures in the presence and absence of Meis2 induction. ES cells with dox-inducible Meis2 (A2lox.Meis2) were differentiated as embryoid bodies (EBs) for 6 days before plating on OP9-GFP cell monolayers and cytokines, and treated with (+) or without (-) doxycycline (dox). Cells were purified by cell sorting on day 7 or 8 into various populations based on levels of CD41 expression: GFP-CD41-, GFP-CD41+ (day 7) and GFP-CD41-,GFP-CD41int, and GFP-CD41hi (day 8). Gene expression of these purified populations was determined by microarray analysis.
2012-08-02 | E-GEOD-34541 | biostudies-arrayexpress
Project description:The homeodomain protein Meis1 is essential for definitive hematopoiesis and vascular patterning in the mouse embryo. Meis2, another member of the same family, shares 82% protein identities with Meis1. Our present study suggested Meis2 exerts two distinguishable effects in differentiating ES cells. First, it increases the numbers of hematopoietic progenitors and extends their persistence in culture. Second, Meis2 skews hematopoietic differentiation by suppressing erythroid while enhancing megakaryocytic progenitor differentiation. To identify the underlying transcriptional bases of these actions, we carried out microarray analysis to compare the various populations of cells developing in ES differentiation cultures in the presence and absence of Meis2 induction.
2012-08-03 | GSE34541 | GEO
Project description:Tamoxifen (TAM), a widely-used drug in treating breast cancer, has been reported to be associated with craniofacial defects including micrognathia and cleft palate in humans. However, the exact effects of TAM on the developing palate remain unclear. In the present study, we conclude that excess TAM exposure causes cleft palate defect in mice by regulating MAPK pathways, which implicates the importance of tightly regulated MAPK signaling in palate development and provides a basis for further exploration of the molecular etiology of cleft palate defects caused by environmental factors.
2022-11-22 | GSE140836 | GEO
Project description:Background: The FACEBASE consortium was established in part to create a central resource for craniofacial researchers. One purpose is to provide a molecular anatomy of craniofacial development. To this end we have used a combination of laser capture microdissection and RNA-Seq to define the gene expression programs driving development of the murine palate. Results: We focused on the E14.5 palate, soon after medial fusion of the two palatal shelves. The palate was divided into multiple compartments, including medial and lateral, as well as oral and nasal, for both the anterior and posterior domains. A total of 25 RNA-Seq datasets were generated. The results provide a comprehensive view of the region specific expression of all transcription factors, growth factors and receptors. Paracrine interactions can be inferred from flanking compartment growth factor/receptor expression patterns. The results are validated primarily through very high concordance with extensive previously published gene expression data for the developing palate. In addition selected immunostain validations were carried out. Conclusions: This report provides an RNA-Seq based atlas of gene expression patterns driving palate development at microanatomic resolution. This FACEBASE resource is designed to fuel discovery by the craniofacial research community. Laser capture microdissection and RNA-seq were used to generate gene expression profiles of different compartments of the mouse E14.5 developing palate
2015-04-03 | E-GEOD-67525 | biostudies-arrayexpress