Shox2 regulates osteogenesis and patterns the hard palate during palatogenesis
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ABSTRACT:
PROVIDER: PRJNA533289 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10258454.fastq.gz | Fastqsanger.gz | |||
| SRR10258455.fastq.gz | Fastqsanger.gz | |||
| SRR10258456.fastq.gz | Fastqsanger.gz | |||
| SRR10258457.fastq.gz | Fastqsanger.gz | |||
| SRR10258458.fastq.gz | Fastqsanger.gz |
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Project description:Being a transcription factor, Shox2 binds to specific DNA sites to regulate gene expression via modulating chromatin status. To investigate the impact of Shox2 on the chromatin accessible landscape in the anterior hard palate, we subjected FACS-sorted Shox2+ cells from the palate of E14.5 Shox2Cre/+;Nkx2.5F/F;R26RmTmG and Shox2Cre/-;Nkx2.5F/F;R26RmTmG mice to ATAC-Seq analysis.
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Project description:This SuperSeries is composed of the SubSeries listed below.
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Project description:To characterize the anterior palate-specific chromatin landscape of the distal Shox2-binding sites, we conducted Shox2 ChIP-Seq again in parallel with H3K27ac ChIP-Seq on the Shox2+ domain anterior palate and the Shox2- posterior palate. Integrative analysis of the Shox2 and H3K27ac ChIP-Seq datasets and aggregate plots of binding signals of H3K27ac in the anterior and posterior palate, respectively, versus the summits of Shox2 binding sites showed close association of Shox2 binding peak with enriched H3K27ac in the anterior palate but not the posterior palate, indicate that Shox2 occupancy is highly related to active enhancer elements.
2019-10-23 | GSE138721 | GEO
Project description:ChIP-Sequencing on Shox2-HA E12.5 and E13.5 Limb and Palate, as well as Pbx on E12.5 limb . Abstract: Vertebrate appendage patterning is programmed by Hox-TALE factors-bound regulatory elements. However, it remains enigmatic which cell lineages are commissioned by Hox-TALE factors to generate regional specific pattern and whether other Hox-TALE co-factors exist. In this study, we investigated the transcriptional mechanisms controlled by the Shox2 transcriptional regulator in limb patterning. Harnessing an osteogenic lineage-specific Shox2 inactivation approach we show that despite widespread Shox2 expression in multiple cell lineages, lack of the stylopod observed upon Shox2 deficiency is a specific result of Shox2 loss of function in the osteogenic lineage. ChIP-Seq revealed robust interaction of Shox2 with cis-regulatory enhancers clustering around skeletogenic genes that are also bound by Hox-TALE factors, supporting a lineage autonomous function of Shox2 in osteogenic lineage fate determination and skeleton patterning. Pbx ChIP-Seq further allowed the genome-wide identification of cis-regulatory modules exhibiting co-occupancy of Pbx, Meis, and Shox2 transcriptional regulators. Integrative analysis of ChIP-Seq and RNA-Seq data and transgenic enhancer assays indicate that Shox2 patterns the stylopod as a repressor via interaction with enhancers active in the proximal limb mesenchyme and antagonizes the repressive function of TALE factors in osteogenesis. Shox2/TALE For ChIP-Seq, the list of libraries below, including controls, were generated [listed in the format of (antibody)-target-tissue-stage]: (α-HA)-Shox2-Limb-E12.5, (α-HA)-Shox2-Limb-E13.5, (α-HA)-Shox2-Palate-E12.5, (α-HA)-Shox2-Limb/Palate-E12.5, (α-Pbx)-Pbx-Limb-E12.5, Input (control), (α-HA)-Mixed Limb/Palate from Shox2+/+ mice-E12.5 (control). *The attached signal tracks(*.bigwig) were generated by âbdgcmp (MACS2) to filter out background signal(by filtering against the signal track obtained from (α-HA)-Mixed Limb/Palate from Shox2+/+ mice-E12.5 (control)) and subsequently convert to bigwig for analysis and visualization.
2016-07-05 | E-GEOD-81897 | biostudies-arrayexpress
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:Perturbations in gene regulation during palatogenesis can lead to cleft palate, which is among the most common congenital birth defects. However, currently there is no comprehensive multiomics map of the developing secondary palate. Here, we perform single-cell multiome sequencing and profile chromatin accessibility and gene expression simultaneously within the same cells (n = 36,154) isolated from mouse secondary palate across embryonic days (E) 12.5, E13.5, E14.0, and E14.5. We construct five trajectories representing continuous differentiation of cranial neural crest-derived multipotent cells into distinct lineages. By linking open chromatin signals to gene expression changes, we characterize the underlying lineage-determining transcription factors. In silico perturbation analysis identifies transcription factors SHOX2 and MEOX2 as important regulators of the development of the anterior and posterior palate, respectively. In conclusion, our study chart epigenetic and transcriptional dynamics in palatogenesis, serving as a valuable resource for further cleft palate research.
2023-12-19 | GSE250247 | GEO
Project description:In order to profile genome-wide effect of Shox2 in regulating osteogenesis in the developing palate, we further performed RNA-Seq on the anterior palatal tissues from E14.5 Shox2Cre/-;Nkx2.5F/F embryos and controls, respectively.
2019-10-23 | GSE129821 | GEO
Project description:FGF signaling has been implicated in the regulation of osteogenesis in both intramembranous and endochondral ossification. In the developing palate, the anterior bony palate forms by direct differentiation of cranial neural crest-derived mesenchymal cells, but the signals that regulate osteogenic cell fate remains unclear. In the present study, we present evidence that locally activated FGF8 signaling in the anterior palate leads to complete bone loss of the palatine process of the maxilla (ma) and ectopic cartilage formation. This aberrant developmental process was accompanied by significantly elevated level of cell proliferation, which contributes to abnormally thickened ma, and complete inhibition of Osterix expression, which accounts for the lack of bone formation. Consistent with the phenotype, RNA-Sequencing (RNA-Seq) analysis further demonstrated that augmented FGF8 signaling downregulated genes involved in ossification, biomineral tissue development, and bone mineralization, but upregulated genes involved in cell proliferation, cartilage development, and cell fate commitment. Expression validation of selected genes supported the RNA-Seq results. We conclude that FGF signaling functions as a negative regulator of osteogenic fate but promotes chondrogenesis of cranial neural crest cell-derived mesenchyme in the hard palate, which will have implication in directed differentiation of precursor cells for clinical application.
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Project description:Perturbations in gene regulation during palatogenesis can lead to cleft palate, which is among the most common congenital birth defects. However, currently there is no comprehensive multiomics map of the developing secondary palate. Here, we perform single-cell multiome sequencing and profile chromatin accessibility and gene expression simultaneously within the same cells (n = 36,154) isolated from mouse secondary palate across embryonic days (E) 12.5, E13.5, E14.0, and E14.5. We construct five trajectories representing continuous differentiation of cranial neural crest-derived multipotent cells into distinct lineages. By linking open chromatin signals to gene expression changes, we characterize the underlying lineage-determining transcription factors. In silico perturbation analysis identifies transcription factors SHOX2 and MEOX2 as important regulators of the development of the anterior and posterior palate, respectively. In conclusion, our study chart epigenetic and transcriptional dynamics in palatogenesis, serving as a valuable resource for further cleft palate research.
2024-01-09 | GSE252592 | GEO
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