Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA197373 | ENA |
REPOSITORIES: ENA
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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
Project description:Gene expression profiling of anterior and posterior palatal tissue from Tgfbr2 mutant mouse models
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Project description:Gene expression profiling of the tongue in Tgfbr2 mutant mouse models
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Project description:Gene expression profiling of Tgfbr2 mutant mouse models of cleft palate
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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.
2013-10-01 | GSE46150 | GEO
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in palate development in order to discover candidate therapeutics for preventing and treating congenital birth defects. Here, we conducted gene expression profiling of embryonic palatal tissue 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 formation. To investigate the mechanism of cleft palate resulting from mutations in TGFBR2, we analyzed neural crest specific conditional inactivation of Tgfbr2 in mice (Tgfbr2fl/fl;Wnt1-Cre). We performed microarray analyses using the palatal tissue of Tgfbr2fl/fl;Wnt1-Cre mice at embryonic day E13.5 (prior to palatal fusion, n=6 per genotype) and E14.5 (during palatal fusion, n=5 per genotype) to examine the genes regulated by Tgf-beta during palate formation.
2011-11-29 | E-GEOD-22989 | biostudies-arrayexpress
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:Palatogenesis is a complex developmental process requiring coordinated growth, elevation, and fusion of the palatal shelves. Disruption of these events results in cleft palate, one of the most common congenital craniofacial anomalies. p130Crk-associated substrate (p130Cas) is an adaptor protein involved in integrin-mediated signaling and cytoskeletal regulation; however, its roles in late embryonic development remain poorly understood because global p130Cas-deficiency leads to early embryonic lethality. In this study, we used tamoxifen-inducible conditional knockout mice to investigate the function of p130Cas during palatal development. Conditional deletion of p130Cas resulted in cleft palate characterized by impaired horizontal growth of the palatal shelves. Reduced mesenchymal cell proliferation within the palatal shelves was confirmed by Ki-67 immunostaining and EdU incorporation. Consistently, primary mouse embryonic palatal mesenchymal (MEPM) cells derived from p130Cas-deficient embryos exhibited impaired proliferation and migration in vitro. In contrast, epithelial-specific deletion of p130Cas did not result in cleft palate, indicating that p130Cas function in the palatal mesenchyme is critical for normal palatal development. Together, these findings identify p130Cas as an important regulator of palatal mesenchymal expansion during secondary palatogenesis. Impaired proliferative growth of palatal mesenchyme likely underlies the developmental basis of cleft palate in this model.
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