Gene expression profile of FACS sorted cranial neural crest cells from E12.5-E13.5 mouse embryonic head
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE262468 | GEO | 2024/10/29
REPOSITORIES: GEO
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Project description:Cranial neural crest (NCC)-derived chondrocyte precursors undergo a dynamic differentiation and maturation process to establish a scaffold for subsequent bone formation, alterations in which contribute to congenital birth defects. Here, we demonstrate that transcription factor and histone methyltransferase proteins Prdm3 and Prdm16 control the differentiation switch of cranial NCCs to craniofacial cartilage. Loss of either results in hypoplastic and unorganized chondrocytes due to impaired cellular orientation and polarity. We show that PRDMs regulate cartilage differentiation by controlling the timing of Wnt/β-catenin activity in strikingly different ways: prdm3 represses while prdm16 activates global gene expression, though both by regulating Wnt enhanceosome activity and chromatin accessibility. Finally, we show that manipulating Wnt/β-catenin signaling pharmacologically or generating prdm3-/-;prdm16-/- double mutants rescues craniofacial cartilage defects. Our findings reveal upstream regulatory roles for Prdm3 and Prdm16 in cranial NCCs to control Wnt/β-catenin transcriptional activity during chondrocyte differentiation to ensure proper development of the craniofacial skeleton.
2022-02-08 | GSE175767 | GEO
Project description:The introduction and widespread adoption of induced pluripotent stem cell (iPSC) technology has opened new avenues for craniofacial regenerative medicine. Neural crest cells (NCCs) are the precursor population to many craniofacial structures, including dental and periodontal structures, and iPSC-derived NCCs may, in the near future, offer an unlimited supply of patient-specific cells for craniofacial repair interventions. Here, we used an established protocol involving simultaneous Wnt signaling activation and TGF-β signaling inhibition to differentiate three human iPSC lines to cranial NCCs. We then derived a putative craniofacial mesenchymal progenitor (PCMP) population with chondrogenic and osteogenic potential from cranial NCCs and investigated their similarity to widely studied human postnatal dental or periodontal stem/progenitor cells. PCMPs were quite distinct from both their precursor cells (NCCs) and bone-marrow mesenchymal stromal cells, a stromal population of mesodermal origin. Despite their similarity with dental stem/progenitor cells, PCMPS were clearly differentiated by a core set of 66 genes, including ACKR3 (CXCR7), whose expression (both at transcript and protein level) appear to be peculiar to PCMPs. Altogether, our data demonstrate the feasibility of craniofacial mesenchymal progenitor derivation from human iPSCs through a neural crest-intermediate and set the foundation for future studies regarding their full differentiation repertoire and their in vivo existence.
2018-10-22 | GSE113297 | GEO
Project description:Specialized chromatin-binding proteins are required for DNA-based processes during development. We recently established PWWP2A as a direct histone variant H2A.Z interactor involved in mitosis and craniofacial development. Here, we identify the H2A.Z/PWWP2A-associated protein HMG20A as part of several chromatin-modifying complexes, including NuRD, andshow that it localizes to distinct genomic regulatory regions. Hmg20a depletion causes severe head and heart developmental defects in Xenopus laevis. Our data indicate that craniofacial malformations are caused by defects in neural crest cell (NCC) migration and cartilage formation. These developmental failures are phenocopied in Hmg20a-depleted mESCs, which show inefficient differentiation into NCCs and cardiomyocytes (CM). Consequently, loss of HMG20A, which marks open promoters and enhancers, results in chromatin accessibility changes and a striking deregulation of transcription programs involved in epithelial-mesenchymal transition (EMT) and differentiation processes. Collectively, our findings implicate HMG20A as part of the H2A.Z/PWWP2A/NuRD-axis and reveal it as a key modulator of intricate developmental transcription programs that guide the differentiation of NCCs and CMs.
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Project description:In this study, we investigate the miRNA expression profile of cardiac neural crest cells (NCCs) and non-NCCs. Rosa-mT-mG reporter mice, which possess loxP sites on either side of a membrane-targeted tdTomato (mT) cassette and express strong red fluorescence in all tissues and cell types, were applied in this study. The presence of Wnt1-Cre leads to the deletion of the mT cassette and the expression of the membrane-targeted EGFP (mG) cassette located just downstream in NCCs. E10.5 Rosa-mT-mG/Wnt1-Cre EGFP positive embryos were collected. The 3rd, 4th and 6th pharyngeal arches and outflow tract were dissected out, digested and sorted for both EGFP+ cranial NCCs and EGFP- control cells by FACS sorting. Total RNAs were prepared for microRNA microarray from cardiac NCCs and non-NCCs.
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Project description:Transgenic mice expressing constitutively activated BMP type 1 receptor (caAcvr1) in neural crest cells (NCCs)(P0-Cre;caAcvr1 mice, hereafter, caAcvr1 mut mice) develop ectopic cartilage in the face but not in trunk region despite both facial and trunk region composed of NCCs. This study was aimed to identify genes that expressions are changed only in cranial NCCs by BMP signaling, but not in trunk NCCs. The genes were candidate genes involved in BMP-induced ectopic cartilage formation in the face.
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Project description:Cardiac NCC were extracted by dissecting out Prdm6f/f; Wnt1-Cre2; ZsGreen1 embryos and their wildtype littermates (Prdm6+/+; Wnt1-Cre2; ZsGreen1) from mid otic placode to the posterior edge of the 4th somite. The ScRNA-seq was carried out using the 10X Genomics Chromium system. There was an average of 2,742 and 3,102 counts per cell or an average of 1,294 and 1,432 unique genes detected in respectively WT and KO conditions. In our models we show that the absence of Prdm6 tips the balance in favor of Wnt1 by reducing Bmp4 and increasing Wnt1 transcripts in several clusters, leading to impaired CNCC migration.
2022-01-30 | GSE195589 | GEO
Project description:To elucidate the molecular features of craniofacial versus trunk neural crest cells (NCCs), we utilized P0-Cre/Floxed-EGFP mice that specifically label NCCs (Yamauchi et al., 1999 (PMID 10419695)). Craniofacial and trunk regions were isolated from P0-Cre/Floxed-EGFP mouse embryos at embryonic day E12.5, and dissociated cells were analyzed by flow cytometory in regard to the intensity of EGFP. In this study, we performed at least duplicate experiments for each of the four groups (Craniofacial EGFP+, Trunk EGFP+, Craniofacial EGFP-, Trunk EGFP-). Total of 9 samples.
2014-08-01 | E-GEOD-39191 | biostudies-arrayexpress
Project description:TWIST1, a basic helix-loop-helix transcription factor is essential for the development of cranial mesoderm and cranial neural crest-derived craniofacial structures. Our previous work showed that, in the absence of TWIST1, some cells within the cranial mesoderm adopt an abnormal epithelial configuration. Here, we show by transcriptome analysis that loss of TWIST1 in the cranial mesoderm is accompanied by a reduction in the expression of genes that are associated with cell-extracellular matrix interactions and the acquisition of mesenchymal characteristics. By comparing the transcriptional profiles of cranial mesoderm-specific Twist1 loss-of-function mutant and control mouse embryos, we identified a set of genes that are both TWIST1-dependent and predominantly expressed in the mesoderm. By ChIP-seq in a cell line model of a TWIST1-dependent mesenchymal state, we identified, among the downstream genes, three direct transcriptional targets of TWIST1: Ddr2, Pcolce and Tgfbi. Our findings show that the mesenchymal properties of the cranial mesoderm is likely to be regulated by a network of TWIST1 targets genes that influence the extracellular matrix and cell-matrix interactions, and collectively they are required for the morphogenesis of the craniofacial structures. Cranial neural crest and cranial mesoderm cells were isolated by flow sorting of GFP reporter-labelled cells collected from heads of E9.5 mouse embryos. Three replicates were independently isolated and hybridized to Illumina mouse WG v 2.0 chips
2016-08-23 | E-GEOD-80335 | biostudies-arrayexpress
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tissue-tissue interactions between myogenic precursors of craniofacial muscles and cranial neural crest cells (CNCCs). Here, we conducted gene expression profiling of the tongue bud from mice at embryonic day E13.5 with a CNCC-specific conditional inactivation of the TGF-beta receptor type 1 gene Alk5. These mice provide a model of microglossia as well as disrupted extraocular and masticatory muscle development, which are congenital birth defects commonly observed in several syndromic conditions. To investigate the adverse effects of dysfunctional TGF-beta signaling on tissue-tissue interactions between CNCCs and myogenic precursors of craniofacial muscles, we analyzed tongue bud tissue of mice with a CNCC-specific conditional inactivation of Alk5 (Wnt1-Cre; Alk5 fl/fl). We performed microarray analyses of the tongue bud of Alk5 fl/fl control mice and Wnt1-Cre; Alk5 fl/fl mutant mice, collected at embryonic day E13.5 (n=4 per group).
2014-06-18 | E-GEOD-52358 | biostudies-arrayexpress
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tissue-tissue interactions between myogenic precursors of craniofacial muscles and cranial neural crest cells (CNCCs). Here, we conducted gene expression profiling of the mandibular arch from mice at embryonic day E11.5 with a CNCC-specific conditional inactivation of the TGF-beta receptor type 1 gene Alk5. These mice provide a model of microglossia as well as disrupted extraocular and masticatory muscle development, which are congenital birth defects commonly observed in several syndromic conditions. To investigate the adverse effects of dysfunctional TGF-beta signaling on tissue-tissue interactions between CNCCs and myogenic precursors of craniofacial muscles, we analyzed mandibular arch tissue of mice with a CNCC-specific conditional inactivation of Alk5 (Wnt1-Cre; Alk5 fl/fl). We performed microarray analyses of the mandibular arch of Alk5 fl/fl control mice and Wnt1-Cre; Alk5 fl/fl mutant mice, collected at embryonic day E11.5 (n=4 per group).
2014-06-18 | E-GEOD-52357 | biostudies-arrayexpress