Ontology highlight
ABSTRACT:
PROVIDER: PRJNA997077 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25376500_1.fastq.gz | Fastqsanger.gz | |||
| SRR25376500_2.fastq.gz | Fastqsanger.gz | |||
| SRR25376501_1.fastq.gz | Fastqsanger.gz | |||
| SRR25376501_2.fastq.gz | Fastqsanger.gz | |||
| SRR25376502_1.fastq.gz | Fastqsanger.gz |
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Project description:The mandible of the jawed vertebrate is derived from the mandibular process of the first pharyngeal arch of the early embryo. The first pharyngeal arch consists of cells from all three germ layers, with the neural crest giving rise to all the skeletal elements of the mandible. The correct patterning of the neural crest cells by spatially and temporally controlled expression of various transcription factors during mandible development is crucial for the proper morphogenesis of the lower jaw. Msx family genes encode transcription factors which contain the conserved homeodomain. Among the three members of Msx genes, Msx1 and Msx2 are expressed in the neural crest and epithelium of distal mandibular process during early embryonic development with partially overlapped expression patterns. Msx1-/- mouse embryos develop multiple craniofacial developmental defects including tooth agenesis, cleft palate, and hypoplastic mandible. Although no jaw defects were observed in Msx2-/- mouse embryos, Msx1-/-Msx2-/- mouse embryos exhibit significantly severer mandibular defects compared to Msx1-/- mouse embryos, suggesting a partial functional redundancy between the two genes in mandible development. Besides the direct roles of Msx1 and Msx2 in the development of the mandibular neural crest, the phenotypes of Msx1-/-Msx2-/- may also contributed by secondary impacts from defective pre-migrative neural crest and non-neural crest tissues. Here we performed the gene expression profiling by RNA-seq in the distal mandibular processes of Msx1f/f;Msx2f/f;Hand2-Cre and Msx1f/+;Msx2f/f;Hand2-Cre embryos at E10.75, the former developed distally truncated mandible at later stages while the latter served as morphologically normal littermate control. Comparing the gene expression profiles of the two will give us insight into the functions of Msx1 and Msx2 expressed in mandibular neural crest cells in the development of the mandible.
2024-01-10 | GSE222566 | GEO
Project description:Craniofacial development requires intricate cooperation of multiple transcription factors and signaling pathways. Six1 is a critical transcription factor regulating craniofacial development. However, the exact function of Six1 during craniofacial development remains elusive. In this study, we investigated the function of Six1 in mandible development using a Six1 knockout mouse model (Six1-/-) and a cranial neural crest-specific, Six1 conditional knockout mouse model (Six1f/f; Wnt1-Cre). The Six1-/- mice exhibited multiple craniofacial deformities, including severe microsomia, high-arched palate, and uvula deformity. Importantly, the Six1f/f; Wnt1-Cre mice recapitulate the microsomia phenotype of Six1-/- mice, thus demonstrating that the expression of Six1 in ectomesenchyme is critical for mandible development. We further showed that the knockout of Six1 led to abnormal expression of osteogenic genes within the mandible. Moreover, the knockdown of Six1 in C3H10 T1/2 cells reduced their osteogenic capacity in vitro. Using RNA-seq, we showed that both the loss of Six1 in the E18.5 mandible and the Six1 knockdown in C3H10 T1/2 led to the dysregulation of genes involved in embryonal skeletal development. In particular, we showed that Six1 binds to the promoter of Bmp4, Fat4, Fgf18, and Fgfr2, and promotes their transcription. Collectively, our results suggest that Six1 plays a critical role in the regulation of mandibular skeleton formation during mouse embryogenesis.
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Project description:Craniofacial development requires intricate cooperation of multiple transcription factors and signaling pathways. Six1 is a critical transcription factor regulating craniofacial development. However, the exact function of Six1 during craniofacial development remains elusive. In this study, we investigated the function of Six1 in mandible development using a Six1 knockout mouse model (Six1-/-) and a cranial neural crest-specific, Six1 conditional knockout mouse model (Six1f/f; Wnt1-Cre). The Six1-/- mice exhibited multiple craniofacial deformities, including severe microsomia, high-arched palate, and uvula deformity. Importantly, the Six1f/f; Wnt1-Cre mice recapitulate the microsomia phenotype of Six1-/- mice, thus demonstrating that the expression of Six1 in ectomesenchyme is critical for mandible development. We further showed that the knockout of Six1 led to abnormal expression of osteogenic genes within the mandible. Moreover, the knockdown of Six1 in C3H10 T1/2 cells reduced their osteogenic capacity in vitro. Using RNA-seq, we showed that both the loss of Six1 in the E18.5 mandible and the Six1 knockdown in C3H10 T1/2 led to the dysregulation of genes involved in embryonal skeletal development. In particular, we showed that Six1 binds to the promoter of Bmp4, Fat4, Fgf18, and Fgfr2, and promotes their transcription. Collectively, our results suggest that Six1 plays a critical role in the regulation of mandibular skeleton formation during mouse embryogenesis.
2023-03-10 | GSE216759 | GEO
Project description:To determine if there are differences between osteoclasts from the mandible and femur of 1-year-old mice we evaluated gene expression and differentiation potential of osteoclast precursors. Osteoclasts from the mandible of 1-year-old mice were larger in size compared to those in the femur, but significantly less in number. The differentially regulated genes with increased expression in the mandible are associated with osteoclast lineage commitment, proliferation, and inflammation; similar to those in the 2-month old mice. Bulk RNA sequencing demonstrated that the mandible had more upregulated genes compared to the femur, and the pathways enriched in the mandible were distinct from those in the femur. Changes in osteoclast precursors due to again may be regulated by different mechanisms in the craniofacial and appendicular regions of the skeleton.
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Project description:Mutations within FGFR2 are causative for various craniosynostosis syndromes. The mandibular dysmorphogenesis in these syndromes has rarely been quantitatively characterized prenatally and the cellular and molecular mechanism involved is unclear. To investigate the effects of FGFR2 mutations on development of the mandible, micro-computed tomography (μCT) images were acquired using newborn mice of three Fgfr2-mutant lines associated with Apert and Crouzon craniosynostosis syndromes. Euclidean Distance Matrix Analysis and analysis of relative bone mineral density (BMD) of 3D μCT images revealed differences in mandible morphology and BMD between the mice carrying the Fgfr2 mutations and their unaffected littermates. We further investigated the mechanism for mandibular dysgenesis in the Fgfr2+/S252W (Fgfr2S252W) mouse model that showed the most severe phenotypes. At E16.5, Fgfr2S252W embryos showed an increase in the size of the osteogenic anlagen and Meckel’s cartilage (MC) and altered microarchitecture and mineralization in the mandible relative to unaffected littermates. Laser capture microdissection and RNA-Seq analysis revealed transcriptomic changes in the mandibular bone, highlighting increased expression of genes undergoing osteoclast differentiation and dysregulated genes active in bone mineralization. Increased osteoclastic activity in the mandible of Fgfr2S252W embryos was confirmed and elevated inorganic pyrophosphate concentration was identified due to upregulated expression of Enpp1 and Ank. In contrast, increased proliferation in MC was observed at E12.5. These findings provide evidence that gain-of-function mutations in FGFRs differentially affect intramembranous ossification of dermal bone and cartilage formation contributing to mandibular dysmorphogenesis in craniosynostosis syndromes.
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Project description:Previous analysis of Myf5-/-:MyoD-/- mouse fetuses lacking skeletal muscle demonstrated the importance of muscle contraction and static loading in mouse skeletogenesis. Previous analysis of Myf5-/-:MyoD-/- mouse fetuses lacking skeletal muscle demonstrated the importance of muscle contraction and static loading in mouse skeletogenesis. Among abnormal skeletal features, micrognathia (mandibular hypoplasia) was detected: small, bent and posteriorly displaced mandible. As an example of Waddingtonian epigenetics, we suggest that muscle, in addition to acting via mechanochemical signal transduction pathways, networks and promoters, also exerts secretory stimuli on skeleton. Our goal is to identify candidate molecules at that muscle-mandible interface. By employing Systematic Subtractive Microarray Analysis approach, we compared gene expression between mandibles of amyogenic and wild type mouse fetuses. We identified a set of candidate genes with involvement in mandibulardevelopment: Cacna1s, Ckm, Des, Mir300, Myog and Tnnc1. We also performed mouse-to-human translational experiments and found analogies. In the light of our findings we discuss various players in mandibular morphogenesis and make an argument for the need to consider mandibular development as a consequence of reciprocal epigenetic interactions of both skeletal and non-skeletal compartments.
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Project description:Acquisition of the lower jaw (mandible) was evolutionarily important for jawed vertebrates. In humans, syndromic craniofacial malformations often accompany jaw anomalies. Hand2 is involved in coordinating the developmental network of mandibles and the oral apparatus through Hand2-downstream genes and is therefore a major determinant of jaw identity. We used microarrays to detail the global programme of gene expression involved in mandible specification and identified distinct classes of up-regulated genes during this process. Wild-type and Hand2 mutant (Hand2 CAT/+; Wnt1-Cre) embryos were collected at Embryonic day (E) 11.5 or E12.5 for RNA extraction and hybridization on Affymetrix microarrays.
2015-12-15 | E-GEOD-75805 | biostudies-arrayexpress
Project description:Acquisition of the lower jaw (mandible) was evolutionarily important for jawed vertebrates. In humans, syndromic craniofacial malformations often accompany jaw anomalies. Hand2 is involved in coordinating the developmental network of mandibles and the oral apparatus through Hand2-downstream genes and is therefore a major determinant of jaw identity. We used microarrays to detail the global programme of gene expression involved in mandible specification and identified distinct classes of up-regulated genes during this process.
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