Jaw-D pTCP4::mTCP4:GR_Cycloheximide + Dexamethasone microarray
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ABSTRACT:
PROVIDER: PRJNA731150 | ENA |
REPOSITORIES: ENA
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Project description:9-day-old jaw-D;pTCP4::mTCP4:GR treated with Cycloheximide (CHX, control) and the combination of Cycloheximide and Dexamethasone (CHX DEX, treated).
2021-05-20 | GSE174702 | GEO
Project description:Analysis of gene expression in activation-tagged jaw-d mutant plants. Total RNA was extracted from the aerial parts of two weeks old jaw-d and control plants. Keywords: other
2003-07-09 | GSE518 | GEO
Project description:The jaws are complementary in form and function but develop asymmetrically, as the lower but not upper jaw bone forms around a prominent cartilage template. How such differences in skeletal composition are patterned is unclear. Here, we identify four Nuclear receptor 2f genes, nr2f1a, nr2f1b, nr2f2, and nr2f5, as enriched in zebrafish upper jaw precursors. Whereas loss of Nr2f genes results in expansion of upper jaw cartilage to resemble that of the lower jaw, Nr2f5 misexpression inhibits lower jaw cartilage formation. Genome-wide analyses show that Nr2f genes prevent expansion of lower jaw-associated gene expression into the upper jaw territory. Further, restriction of Nr2f expression by Endothelin1 signaling is critical for lower jaw development, as reducing Nr2f dosage fully restores lower jaw development in edn1 mutants. We propose that Nr2f genes drive jaw asymmetry by limiting early cartilage differentiation in the upper jaw to preserve more precursors for later osteogenesis.
2018-01-18 | GSE101719 | GEO
Project description:Exposure to environmental contaminants can disrupt normal development of the early vertebrate skeleton. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs craniofacial skeletal development across many vertebrate species and its effects are especially prominent in early life stages of fish. TCDD activates the aryl hydrocarbon receptor (AHR), a transcription factor that mediates most if not all TCDD responses. We investigated the transcriptional response in the developing zebrafish jaw following TCDD exposure using DNA microarrays. Zebrafish larvae were exposed to TCDD at 96 h postfertilization (hpf) and jaw cartilage tissue was harvested for microarray analysis at 1, 2, 4 and 12 h postexposure (hpe). Numerous chondrogenic transcripts were misregulated by TCDD in the jaw. Comparison of transcripts altered by TCDD in jaw with transcripts altered in embryonic heart showed that the transcriptional responses in the jaw and the heart were strikingly different. Sox9b, a critical chondrogenic transcription factor, was the most significantly reduced transcript in the jaw. We hypothesized that the TCDD reduction of sox9b expression plays an integral role in affecting formation of the embryonic jaw. Morpholino knock down of sox9b expression demonstrated that partial reduction of sox9b expression alone was sufficient to produce a TCDD-like jaw phenotype. Heterozygous sox9b deletion mutant embryos were sensitized to TCDD. Lastly, embryos injected with sox9b mRNA and then exposed to TCDD blocked TCDD-induced jaw toxicity in approximately 14% of sox9b-injected embryos. These results suggest that reduced sox9b expression in TCDD-exposed zebrafish embryos contributes to jaw malformation. Keywords: Time course
2008-11-01 | GSE11893 | GEO
Project description:Craniofacial and jaw bones have unique physiological specificities when compared to axial and appendicular bones. However, the molecular profile of the jaw osteoblast (OB) remains incomplete. The purpose of this study was to decipher the bone site-specific profile of transcription factors (TF) expressed in jaw osteoblasts in vivo. We accomplished this by performing RNA-seq analysis on flow-sorted osteoblasts isolated from jaw and tibial bones of 9-day-old (P9) transgenic Col1a1*2,3-GFP mice. This study demonstrated the feasibility of a new method to isolate pure OB populations and map their gene expression signature in the context of OB physiological environment, avoiding in vitro culture and its associated biases. Our results provided insights into the site-specific developmental pathways governing OB and identify new major OB regulators of bone physiology.
2022-02-14 | GSE186535 | GEO
Project description:Analysis of gene expression in activation-tagged jaw-d mutant plants. Total RNA was extracted from the aerial parts of two weeks old jaw-d and control plants.
2008-06-13 | E-GEOD-518 | biostudies-arrayexpress
Project description:Exposure to environmental contaminants can disrupt normal development of the early vertebrate skeleton. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs craniofacial skeletal development across many vertebrate species and its effects are especially prominent in early life stages of fish. TCDD activates the aryl hydrocarbon receptor (AHR), a transcription factor that mediates most if not all TCDD responses. We investigated the transcriptional response in the developing zebrafish jaw following TCDD exposure using DNA microarrays. Zebrafish larvae were exposed to TCDD at 96 h postfertilization (hpf) and jaw cartilage tissue was harvested for microarray analysis at 1, 2, 4 and 12 h postexposure (hpe). Numerous chondrogenic transcripts were misregulated by TCDD in the jaw. Comparison of transcripts altered by TCDD in jaw with transcripts altered in embryonic heart showed that the transcriptional responses in the jaw and the heart were strikingly different. Sox9b, a critical chondrogenic transcription factor, was the most significantly reduced transcript in the jaw. We hypothesized that the TCDD reduction of sox9b expression plays an integral role in affecting formation of the embryonic jaw. Morpholino knock down of sox9b expression demonstrated that partial reduction of sox9b expression alone was sufficient to produce a TCDD-like jaw phenotype. Heterozygous sox9b deletion mutant embryos were sensitized to TCDD. Lastly, embryos injected with sox9b mRNA and then exposed to TCDD blocked TCDD-induced jaw toxicity in approximately 14% of sox9b-injected embryos. These results suggest that reduced sox9b expression in TCDD-exposed zebrafish embryos contributes to jaw malformation. Experiment Overall Design: Three independent replicate microarray time course experiments were performed comparing transcript levels between TCDD-exposed and control zebrafish. For each experiment, zebrafish were exposed to TCDD for 1 h starting at 96 hpf as described above. For each time point (97, 98, 100 and 108 hpf) and treatment jaw samples were pooled from 10 dissections for RNA isolation and hybridization with Affymetrix zebrafish arrays (Affymetrix, Santa Clara, CA). Each microarray contains roughly 14,900 probes corresponding to approximately 30% of the zebrafish genome. For each array, total RNA (1 µg) was isolated from 10 jaw microdissections with the QIAGEN RNeasy Mini kit following the manufacturerâs protocol (QIAGEN, Valencia, CA). The One-Cycle Target Labeling and Control Reagents kit was used to synthesize cDNA and biotinylated cRNA following the manufacturerâs protocol (Affymetrix, Santa Clara, CA). Biotin-labeled cRNA (15 µg) was fragmented and hybridized onto Affymetrix Zebrafish Genechip Arrays following the protocol in the Affymetrix Genechip Expression Analysis Technical Manual. Following hybdrization, the arrays were washed and stained with streptavidin-phycoerythrin on an Affymetrix Fluidics Station 400 using the protocol EukGE WS2v4. Arrays were scanned with an Agilent Gene Array Scanner.
2008-11-13 | E-GEOD-11893 | biostudies-arrayexpress
Project description:The association between T2 DM and BMSCs osteogenic differentiation has been documented in experimental settings. We examine miRNA expression specific for BMSCs from human jaw in Type 2 diabetics.
2021-03-06 | GSE168327 | GEO
Project description:Development of the vertebrate jaw apparatus depends on highly conserved signaling pathways. Patterning of the lower jaw is driven by Endothelin receptor type A (Ednra) and secreted ligand Endothelin 1 (Edn1). The Ednra signaling pathway establishes the identity of lower jaw progenitors by regulating expression of numerous patterning genes, but the intracellular signaling mechanisms linking receptor activation to gene regulation remains poorly understood. As a first step towards addressing this question, we examined the function of the Gq/11 family of Gα subunits in zebrafish using pharmacological and genetic ablation of Gq/11 activity and transgenic induction of a constitutively active Gq protein in edn1-/- embryos. Loss of Gq/11 activity fully recapitulated the edn1-/- phenotype, with genes encoding for G11 being most essential. Furthermore, inducing Gq activity in edn1-/- embryos not only restored Ednra-dependent jaw structures and gene expression signatures but also caused homeosis of the upper jaw structures into a lower jaw-like structure. These results indicate that Gq/11 is necessary and sufficient to mediate the lower jaw patterning mechanism for Ednra.
2024-09-19 | GSE275013 | GEO
Project description:The functional jaw is composed of multiple connective tissues including skeletal components (bone, cartilage, and teeth), tendon, ligament, and musculature. Cranial neural crest-derived mesenchyme of the mandibular arch give rise to diverse tissue types within the lower jaw. To understand how the specification of diverse cell types with spatial and temporal precision is achieved, we profile multi-omic chromatin accessibility (snATACseq) and transcriptome (snRNAseq) of jaw mesenchyme at single-cell resolution from the developing zebrafish jaw.
2023-02-13 | GSE210251 | GEO