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Canonical Wnt signaling regulates soft palatal development through mediating ciliary homeostasis

ABSTRACT: The goal of this study is to compare transcriptome profiling (RNA-seq) of soft palatal tissue at E14.0 between control and Osr2-Cre;b-cateninfl/fl mice

ORGANISM(S): Mus musculus

PROVIDER: GSE208619 | GEO | 2023/02/23

REPOSITORIES: GEO

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Canonical Wnt signaling regulates soft palatal development through mediating ciliary homeostasis

Project description:Canonical Wnt signaling regulates soft palatal development through mediating ciliary homeostasis

| PRJNA860346 | ENA

Canonical Wnt signaling regulates soft palate development by mediating ciliary homeostasis.

Project description:Craniofacial morphogenesis requires complex interactions involving different tissues, signaling pathways, secreted factors and organelles. The details of these interactions remain elusive. In this study, we have analyzed the molecular mechanisms and homeostatic cellular activities governing soft palate development to improve regenerative strategies for individuals with cleft palate. We have identified canonical Wnt signaling as a key signaling pathway primarily active in cranial neural crest (CNC)-derived mesenchymal cells surrounding soft palatal myogenic cells. Using Osr2-Cre;β-cateninfl/fl mice, we show that Wnt signaling is indispensable for mesenchymal cell proliferation and subsequently for myogenesis through mediating ciliogenesis. Specifically, we have identified that Wnt signaling directly regulates expression of the ciliary gene Ttll3. Impaired ciliary disassembly leads to differentiation defects in mesenchymal cells and indirectly disrupts myogenesis through decreased expression of Dlk1, a mesenchymal cell-derived pro-myogenesis factor. Moreover, we show that siRNA-mediated reduction of Ttll3 expression partly rescues mesenchymal cell proliferation and myogenesis in the palatal explant cultures from Osr2-Cre;β-cateninfl/fl embryos. This study highlights the role of Wnt signaling in palatogenesis through the control of ciliary homeostasis, which establishes a new mechanism for Wnt-regulated craniofacial morphogenesis.

| S-EPMC10108707 | biostudies-literature

RNAseq Analysis of Transcriptome expression profiles in E12.5 and E13.5 FACS sorted Osr2RFP/- (mutant)and Osr2RFP/+ (control) palatal mesenchymal cells

Project description:Purpose: The purpose of this study is to compare the transcriptome expression profiles of E12.5 and E13.5 Osr2RFP/- and Osr2RFP/+ palatal mesenchyme by using RNA-seq analysis. Methods: Osr2RFP/+ male mice were crossed with Osr2+/- female mice. The embryos were harvested at E12.5 and E13.5. The pair of palatal shelves were dissected from each Osr2-RFP positive embryo. The RFP+ palatal mesenchyme cells were isolated by using fluorescence-activated cell sorting (FACS). RNA-seq analysis was carried out using the FACS-isolated palatal mesenchyme from Osr2RFP/- and Osr2RFP/+ embryos, respectively.

2018-02-13 | GSE95638 | GEO

Gene expression profiling of anterior and posterior palatal tissue from Tgfbr2 mutant mouse models

Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in epithelial cells as it pertains to the orientation of muscle fibers in the soft palate during embryogenesis. Here, we first conducted gene expression profiling of the anterior and posterior portions of the palate from wild-type mice. In addition, we also conducted gene expression profiling of the posterior palate in mutant mice with an epithelium-specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of submucosal cleft palate, which is a congenital birth defect commonly observed in many syndromic conditions. To investigate the adverse effects of dysfunctional TGF-Beta signaling on tissue-tissue interaction between the palatal epithelium and myofibers during palatogenesis, we analyzed mice with an epithelial cell-specific conditional inactivation of Tgfbr2 (Tgfbr2fl/fl;K14-Cre). We performed microarray analyses of anterior palatal tissue and posterior palatal tissue of E15.5 Tgfbr2fl/fl control mice (n=5, each region), and posterior palatal tissue of Tgfbr2fl/fl;K14-Cre mutant mice, collected at embryonic day 15.5 (n=5). Control samples and mutant samples are from separate litters.

2013-10-01 | E-GEOD-46211 | biostudies-arrayexpress

RNAseq Analysis of Transcriptome expression profiles in E13.5 Foxf2-/-Osr2RFP/+ and control palatal mesenchymal cells

Project description:Purpose: The purpose of this study is to compare the transcriptome expression profiles of E13.5 Foxf2-/-;Osr2RFP/+ and control palatal mesenchyme by using RNA-seq analysis. Methods: Foxf2+/- female mice were crossed with Foxf2+/-;Osr2RFP/+ male mice.The embryos were harvested at E13.5. The pair of palatal shelves were dissected from each Osr2-RFP+ embryo. The RFP+ palatal mesenchyme cells were isolated by using fluorescence-activated cell sorting (FACS). RNA-seq analysis was carried out using the FACS-isolated palatal mesenchyme from Foxf2-/-;Osr2RFP/+, Foxf2+/-;Osr2RFP/+ and Osr2RFP/+embryos, respectively.

2015-12-28 | GSE67015 | GEO

Gene expression profiling of primary mouse embryonic palatal mesenchymal cells in Tgfbr2 mutant mouse models

Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in regulating the cellular metabolism of cranial neural crest (CNC) cells during palate development. Here, we conducted gene expression profiling of primary mouse embryonic palatal mesenchymal (MEPM) cells from wild type mice as well as those with a neural crest specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of cleft palate, which is among the most common congenital birth defects and observed in many syndromic conditions. To investigate the adverse effects of dysfunctional TGF-Beta signaling on the cellular metabolism of palatal mesenchyme during palatogenesis, we analyzed mice with a neural crest cell-specific conditional inactivation of Tgfbr2 (Tgfbr2fl/fl;Wnt1-Cre). We performed microarray analyses of primary mouse embryonic palatal mesenchymal cells of Tgfbr2fl/fl;Wnt1-Cre mutant mice and Tgfbr2fl/fl control mice, collected at embryonic day 13.5 (n=4 per genotype) and cultured with standard media (DMEM with supplements). Cells were collected after 2 passages.

2013-10-01 | E-GEOD-46150 | biostudies-arrayexpress

Ectopic Hedgehog signalling causes cleft palate and defective osteogenesis

Project description:In this study, we have investigated the molecular basis of Shh signalling during development of the secondary palate and how CNCC patterning and fate is influenced by the Shh signalling network. Using a gain-of-function mouse model to activate Smoothened (R26SmoM2) signalling in the palatal mesenchyme (Osr2-IresCre), we demonstrate ectopic Hh-Smo signalling results in fully penetrant cleft palate, disrupted oral-nasal patterning and defective palatine bone formation. We show that a series of Fox transcription factors, including the novel direct target Foxl1, function downstream of Hh signalling in the secondary palate. Furthermore, we demonstrate that Wnt/BMP antagonists, in particular Sostdc1, are positively regulated by Hh signalling, concomitant with down-regulation of key regulators of osteogenesis and BMP signalling effectors. Microarray analysis was performed on excised palatal shelves from Osr2-IresCre+/- (wild-type) and Osr2-IresCre;Smo+/M2 (mutant) embryos at embryonic day (E)13.5. Osr2-IresCre (PMID:17941042) and R26SmoM2 (PMID:15107405) mice have been described previously.

2018-10-02 | E-MTAB-5518 | biostudies-arrayexpress

Primary mouse embryonic palatal mesenchyme LC-MS/MS

Project description:To identify proteins phosphorylated by Akt downstream of PI3K-mediated PDGFRalpha signaling, we immunoprecipitated Akt phosphorylation substrates from PDGF-AA-treated primary mouse embryonic palatal mesenchyme (MEPM) lysates and analyzed the peptides by nano LC-MS/MS.

2019-06-04 | PXD000779 | Pride

ATAC-seq profile of mouse palatal epithelium at E14.5

Project description:To profile nucleosome free regions of moust palatal epithelium at E14.5, we performed ATAC-seq for isolated palatal epithelium and mesenchyme cells.

2019-11-06 | GSE139945 | GEO

Expression data from Tbx1 knockout (KO) palatal shlelves

Project description:Deletion of Tbx1, a member of the T-box transcription factor gene family, results in abnormal epithelial fusion between the palatal shelves and the mandible, which induces cleft palate by inhibiting elevation of the palatal shelves. We used microarrays to determine the downstream genes of Tbx1 during palatogenesis and identified distinct classes of dysregulated genes.

2016-04-20 | GSE79514 | GEO

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