Canonical Wnt signaling regulates soft palatal development through mediating ciliary homeostasis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA860346 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20324817.fastq.gz | Fastqsanger.gz | |||
| SRR20324818.fastq.gz | Fastqsanger.gz | |||
| SRR20324819.fastq.gz | Fastqsanger.gz | |||
| SRR20324820.fastq.gz | Fastqsanger.gz | |||
| SRR20324821.fastq.gz | Fastqsanger.gz |
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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
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
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.
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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.
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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.
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Project description:How soft corona i.e., the protein corona’s outer layer contributes to “biological” identity of nanomaterials (NMs) is largely unknown due to a longstanding challenge in capturing protein composition of the soft corona in situ. We herein develop an in situ “Fishing” method that can monitor the dynamic formation of protein corona on ultra-small chiral Cu2S nanoparticles (NPs) allowing us to directly separate and identify their protein composition. This method can detect spatiotemporal processes in the evolution of hard and soft coronas on chiral NPs, revealing subtle differences in their composition even within several minutes. This study highlights the importance of in situ and dynamic analysis of soft/hard corona composition, provides detailed insights into the roles of protein corona composition in mediating the biological responses of NPs, and offers a universal strategy to characterize the soft corona that will serve as a powerful tool for rational design of biomedical NMs.
2022-10-13 | PXD033976 | Pride
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.
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Project description:We identify a role for two evolutionarily related, secreted metalloproteases of the ADAMTS family (A disintegrin-like and metalloprotease domain with thrombospondin type-1 motif), ADAMTS20 and ADAMTS9, in palatogenesis. Adamts20 mutations cause the mouse white spotting mutant belted (bt), whereas Adamts9 is essential for survival beyond 7.5 days of gestation (E7.5). Functional overlap of Adamts9 with Adamts20 was established in bt/bt:Adamts9+/- mice, which have increased white spotting relative to bt mice, as previously reported, and a fully penetrant cleft palate. Palatal closure was delayed, although eventually completed, in both bt/+;Adamts9+/- and bt/bt mice, demonstrating a cooperative role of these related genes. Adamts9 and Adamts20 are both expressed in palatal mesenchyme, with Adamts9 expressed exclusively in microvascular endothelial cells. Palatal shelves from bt/bt:Adamts9+/- mice fused in culture, suggesting an intact TGF signaling pathway in palatal epithelium, and indicating a temporally specific delay in palatal shelf elevation and growth toward the midline. Palatal shelf mesenchymal cells showed a statistically significant decrease of cell proliferation at E13.5 and E14.5, as well as decreased processing of versican, an ADAMTS substrate, at these stages. Vcan haploinsufficiency led to a greater penetrance of cleft palate in bt mice, and impaired proliferation was also seen in palatal mesenchymal cells of these mice, suggesting a role for ADAMTS-mediated versican proteolysis in palatal closure. In a parallel with recent work identifying a role for a bioactive ADAMTS-generated versican fragment in regulating apoptosis during interdigital web regression, we propose that versican proteolysis may influence palatal mesenchymal cell proliferation. Palatal shelves were dissected from four E13.75 Adamts9+/-:bt/bt embyos (correspond to the 4 samples: Palate_Adamts9+/-:bt/bt_Rep1, Palate_Adamts9+/-:bt/bt_Rep2, Palate_Adamts9+/-:bt/bt_Rep3 and Palate_Adamts9+/-:bt/bt_Rep4) and age-matched 3 wild-type C57Bl/6 embryos (correspond to the 3 samples: Palate_WT_Rep1, Palate_WT_Rep2, and Palate_WT_Rep3) that were used as the controls
2010-06-30 | E-GEOD-21358 | biostudies-arrayexpress
Project description:This study is the first to investigate the process of osteoclast differentiation, its potential functions, and the associated mRNA and signaling pathway during embryonic palatal bone. Our findings suggest that osteoclasts may be involved in bone remodeling, bone marrow cavity formation, and blood vessel formation in embryonic palatal bone. We observed Trap-positive osteoclasts at E16.5, E17.5, and E18.5 at the palatal process of the palate (PPP), Posterior and anterior part of the palatal process of the maxilla (PPMXP, and PPMXA), respectively, with osteoclast differentiation starting 2 days prior to TRAP positivity. By comparing the key periods of osteoclast differentiation between PPMX and PPP (E14.5, E15.5, and E16.5) using RNA-seq data of the palates, we found that the PI3K-AKT and MAPK signaling pathways were sequentially enriched, which may play critical roles in osteoclast survival and differentiation. Csf1r, Tnfrsff11a, Ctsk, Fos, Tyrobp, Fcgr3, and Spi1 were significantly upregulated in both PPMX and PPP, while Pik3r3, Tgfbr1, and Mapk3k7 were significantly downregulated in both. Interestingly, Tnfrsff11b was upregulated in PPMX but downregulated in PPP, which may regulate the timing of osteoclast appearance. These results contribute to the limited knowledge regarding mRNA specific steps in OLCs differentiation in the embryonic palatal bone.
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