Ontology highlight
ABSTRACT:
PROVIDER: PRJNA741731 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14929000_1.fastq.gz | Fastqsanger.gz | |||
| SRR14929000_2.fastq.gz | Fastqsanger.gz | |||
| SRR14929001_1.fastq.gz | Fastqsanger.gz | |||
| SRR14929001_2.fastq.gz | Fastqsanger.gz | |||
| SRR14929002_1.fastq.gz | Fastqsanger.gz |
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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:Distinct shaping of the upper versus lower facial skeleton is essential for function of the vertebrate jaw and middle ear, yet the cellular mechanisms by which this occurs have remained unclear. Here, we show that Endothelin1 (Edn1) signaling accelerates mesenchymal condensation and subsequent cartilage formation in the lower face through antagonism of Jagged-Notch signaling and Prrx1 transcription factors. A genomic analysis of facial skeletal precursors in mutants and overexpression embryos reveals that Jagged-Notch signaling represses genes that are strongly induced as pharyngeal arch neural crest-derived cells begin skeletal differentiation. In wild types, initial Jagged-Notch repression dorsally ensures that barx1+ condensations and cartilage differentiation occur first in ventral-intermediate zones of the pharyngeal arches. Reduced Jagged-Notch signaling results in an expansion of pre-cartilage condensations in the upper face, with loss of barx1 partially restoring dorsal cartilage shapes in jag1b mutants. Further, by studying new mutants for zebrafish prrx1a and prrx1b, we find that Prrx1 genes function in parallel to Jagged-Notch signaling to restrict the formation of dorsal barx1+ pre-cartilage condensations. Consistently, combined losses of jag1b and prrx1a/b robustly rescue ventral barx1+ condensations and lower facial cartilage development in edn1 mutants. Together, our work suggests that Edn1 works through parallel inhibition of Jagged-Notch and Prrx1 pathways to promote an earlier and more extensive establishment of cartilage condensations in the lower face. We performed RNAseq on FACS-sorted neural crest-derived pharyngeal arch cells (fli1a:GFP; sox10:DsRed double positive) from wild-type embryos at 3 different stages (20, 28, and 36 hours post fertilization) and embryos with altered levels of Edn1 and Notch signaling (edn1 mutants and hsp70I:Gal4; UAS:Edn1 transgenics; jag1b mutants, dibenzazepine-treated embryos, and hsp70I:Gal4; UAS:NICD transgenics. We also sequenced RNA from heat-shocked UAS:Edn1+ and hsp70I:Gal4+ transgenics and jag1b+/+ controls.
2016-03-23 | E-GEOD-72985 | biostudies-arrayexpress
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.
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Project description:Despite even large phenotypic differences among vertebrate groups, dentitions and jaws fit and function together, yet the genetic processes that orchestrate cranial and dental morphogenesis remain poorly understood. In the p63-/- mouse mutant, teeth but not jaws fail to form. This edentate mouse is a model with which to tease out genes important for odontogenesis but not jaw morphogenesis, and which may thus allow dentitions to change during development and evolution without necessarily affecting the jaw skeleton. With the working hypothesis that tooth and jaw development are autonomously controlled by discreet gene regulatory networks, we probed for genes crucial for tooth development only. Using gene expression microarray assays validated by quantitative reverse-transcription PCR, we contrasted expression in mandibular prominences at embryonic days (E) 10-13 among mice with normal lower jaw development and either normal (p63+/-, p63+/+) or arrested (p63-/-) tooth development. We predicted that expression of a suite of genes specific to odontogenesis would differ in the edentate mice. The p63-/- mice showed significantly different expression (fold change ≥1.5, ≤-1.5; p≤0.05) of several genes, some of which are already reported to help regulate odontogenesis (e.g., p63, Osr2, Cldn3/4) and/or to be targets of p63 (e.g., Jag1/2, Fgfr2), others of which have no previously reported roles in odontogenesis or the p63 pathway (e.g, Fermt1, Cbln1, Pltp, Cxcl14, Krt8, and additional keratin and claudin family members). As expected, from E10-E13 few genes known to regulate mandible morphogenesis differed in expression between mouse strains. Thus this study links for the first time several genes to odontogenesis and/or the p63 signaling network. We propose that these genes act in a novel odontogenic network that is exclusive of lower jaw morphogenesis, and posit that this network evolved in oral, not pharyngeal, teeth.
2016-12-23 | GSE92769 | GEO
Project description:Distinct shaping of the upper versus lower facial skeleton is essential for function of the vertebrate jaw and middle ear, yet the cellular mechanisms by which this occurs have remained unclear. Here, we show that Endothelin1 (Edn1) signaling accelerates mesenchymal condensation and subsequent cartilage formation in the lower face through antagonism of Jagged-Notch signaling and Prrx1 transcription factors. A genomic analysis of facial skeletal precursors in mutants and overexpression embryos reveals that Jagged-Notch signaling represses genes that are strongly induced as pharyngeal arch neural crest-derived cells begin skeletal differentiation. In wild types, initial Jagged-Notch repression dorsally ensures that barx1+ condensations and cartilage differentiation occur first in ventral-intermediate zones of the pharyngeal arches. Reduced Jagged-Notch signaling results in an expansion of pre-cartilage condensations in the upper face, with loss of barx1 partially restoring dorsal cartilage shapes in jag1b mutants. Further, by studying new mutants for zebrafish prrx1a and prrx1b, we find that Prrx1 genes function in parallel to Jagged-Notch signaling to restrict the formation of dorsal barx1+ pre-cartilage condensations. Consistently, combined losses of jag1b and prrx1a/b robustly rescue ventral barx1+ condensations and lower facial cartilage development in edn1 mutants. Together, our work suggests that Edn1 works through parallel inhibition of Jagged-Notch and Prrx1 pathways to promote an earlier and more extensive establishment of cartilage condensations in the lower face.
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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.
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