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Increased FGF8 Signaling Promotes Chondrogenic Rather Than Osteogenic Development in the Embryonic Skull

ABSTRACT: RNA-seq of RNA isolated from E14.5 mouse embryos- wildtype cranial base tissue, Msx2-Cre;CAGFgf8 mutant cranial vault, and wildtype cranial vault; 3 replicates of each group.

ORGANISM(S): Mus musculus

PROVIDER: GSE112413 | GEO | 2018/05/23

REPOSITORIES: GEO

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Increased FGF8 signaling promotes chondrogenic rather than osteogenic development in the embryonic skull.

Project description: Not available

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FGFR3 is a positive regulator of osteoblast expansion and differentiation during zebrafish skull vault development

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Increased FGF8 Signaling Promotes Chondrogenic Rather Than Osteogenic Development in the Embryonic Skull

Project description:Increased FGF8 Signaling Promotes Chondrogenic Rather Than Osteogenic Development in the Embryonic Skull

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Fgf8 signaling alters the osteogenic cell fate in anterior hard palate

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.

2018-05-23 | GSE101909 | GEO

Gene Expression Changes Between Patent and Fused Cranial Sutures in a Nonsyndromic Craniosynostosis Population

Project description:Assaying gene expression in sutural bone fragments from patients diagnosed with non-syndromic craniosynostosis. Sutural fragments were collected from both the fused and patent cranial suture of infants during cranial vault reconstruction. Gene expression was compared between the patent and fused sutures using the paired t-test. The aim was to identify thoses genes significantly differentially expressed in fused suture relative to patent. Total RNA isolated from patent and fused human cranial sutures was assayed. Expression in synostosed suture was compared to patent suture.

2013-09-12 | E-GEOD-50796 | biostudies-arrayexpress

Gene Expression Changes Between Patent and Fused Cranial Sutures in a Nonsyndromic Craniosynostosis Population

2013-09-12 | GSE50796 | GEO

FGF8 Signaling Alters the Osteogenic Cell Fate in the Hard Palate.

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Whole-transcriptome analysis of hematopoietic progenitors in the cranial dura, femur, and skull

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Transcription profiling of gonads from E14.5 megalin+/+ and megalin-/- embryos

Project description:Presently, genes regulated by steroid hormones during induced regression of the CSL (cranial suspensory ligament) are unknown. To identify such genes and to evaluate their expression levels in megalin-deficient mice, we performed global gene expression profiling on gonads from E14.5 megalin+/+ and megalin-/- embryos.

2005-06-30 | E-MEXP-352 | biostudies-arrayexpress

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Project description:The homeoprotein Msx1 and Msx2 involved in normal skeletal muscle development and also contribute to muscle defects if altered during development. Deciphering the downstream signaling networks of Msx1 and Msx2 in myoblasts differentiation will help us to understand the molecular events that contribute to muscle defects. The objective of this study was to evaluate the proteomics characteristics in Msx1 and Msx2 mediated myoblasts differentiation, using isobaric tags for the relative and absolute quantification labelling technique (iTRAQ). The results showed that 1535 proteins with quantitative information were obtained. Volcano plots illustrated, in undifferentiated stage, 32 common downstream regulatory proteins for Msx1 and Msx2, 39 specific regulatory proteins for Msx1, and 13 specific for Msx2. While, in differentiated stage, 17 common downstream regulatory proteins for Msx1 and Msx2, 10 specific regulatory proteins for Msx1, and 21 specific for Msx2. Gene ontology, KEGG pathway and protein-protein interaction networks analyses revealed these proteins primarily associated with Arginine and proline metabolism, Glycolysis/Gluconeogenesis, Fatty acid degradation, Metabolism of xenobiotics by cytochrome P450 and Apoptosis. In addition, our data shows Acta1 was probably a core of the downstream regulatory networks of Msx1 and Msx2 in skeletal muscle development. The findings will help us to understand the molecular roles of Msx1 and Msx2 during muscle development as well as regeneration, and to understand the molecular events that contribute to muscle defects.

2023-07-20 | PXD026944 | Pride

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