Expression data at 24 hours after the blocking of Shh signaling in tooth germs at embryonic day 14
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE27429 | GEO | 2011/02/22
SECONDARY ACCESSION(S): PRJNA137219
REPOSITORIES: GEO
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Project description:The genetic mechanism governing the spatial patterning of teeth still remains to be elucidated. Sonic hedgehog (Shh) is one of key signaling molecules involved in the spatial patterning of teeth. By utilizing maternal transfer of 5E1 (an IgG1 monoclonal antibody against Shh protein) through the placenta to block Shh signaling, we investigated the changes in tooth patterning and in gene expression. We used microarrays to detect specific genes related with Shh signaling in tooth germs and identified some specific genes up- or down-regulated after blocking of Shh signaling activity. Gene-chip expression analysis was performed with RNA from mandibular tooth germs from embryos of pregnant mice at one day after injection of 5E1 (an IgG1 monoclonal antibody against Shh protein; number of replicates =2), 40-1a (an IgG1 monoclonal antibody against β-galactosidase; number of replicates=2), cyclopamine (a specific Smo antagonist; number of replicates=2) or PBS (Phosphate buffered saline; number of replicates=2), using a Affymetrix mouse gene microarray.
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Project description:miRNAs are not well known their expression and function in tooth development. To identify the miRNAs expression during tooth development, tooth germs were dissected from the initiation bud, cap and bell stages. miRNA-chip expression analysis was performed with RNAs of the molar tooth germs from embryos of pregnant mice at emrbryonic day 11, 12, 14, and 16, using Agilent's miRNA microarray.
2014-01-09 | E-GEOD-53903 | biostudies-arrayexpress
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Project description:Embryologically the tooth is derived from both the ectoderm and neural crest (ectomesenchyme). It is often used as a model to study how epithelialmesenchymal interactions can control differentiation and morphogenesis. During early development organs of ectodermal origin share both a set of signalling molecules and exhibit common morphological features, subsequently proceeding along separate developmental programs.<br><br>Tooth development is a continuous process that can be divided into the initiation -, bud -, cap -, and bell-stages. In mice, tooth development begins at embryonic day 11.5 (E11.5), by thickening of the dental epithelium, while mineralization of enamel and dentin in first molar starts at postnatal day 0 (P0) (5). A multistep and complex process of the gene expression are involved in the early stage of tooth development. So far expression of more than 1300 genes and/or proteins have been detected during tooth germ development by microarrays/immunocytochemistry/in situ hybridization. Studies with mutant mice have identified a number of genes that regulate tooth development and morphology. For example, deficiency of Lef-1 or P63 arrests tooth development at early stages. Deficiency of Msx1 or Pax9 results in arrest of tooth development at the bud stage , while deficiency of Runx2/Cbfa1 or Sp3 inhibits cyto-differentiation of ameloblasts and/or odontoblasts. Shh is required for normal growth and morphogenesis, but is not essential for cyto-differentiation of the ameloblast and odontoblast populations. Ameloblastin and amelogenin knock-out mice develop severe enamel hypoplasia with abnormal ameloblast differentiation. <br><br>Recently, new connections between retinoid metabolism and PPAR responses have been identified. It has also been shown that endogenous retinoic acid is necessary for the initiation of odontogenesis , and that some of the genes that catalyze the oxidation of retinaldehyde into retinoic acid, exhibit distinct patterns of expression in developing murine teeth. Little is known about functions of PPAR-a as regards tooth germs or mature teeth. It is, however, likely that mitochondrial oxidative metabolism well as fatty acid metabolism is enhanced in late odontogenesis. These are metabolic activities which in other tissues are stimulated by PPAR-a agonists.<br><br>For this reason it was of interest to carry out comparative gene expression profiling of the first molar tooth germs of PPAR-a knock-out mouse and of the corresponding wild-type mice. The results suggest marked differences in gene expression, parts of which may be associated with an observed hypomineralization of enamel in the mature PPAR-a knock-out murine tooth.
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Project description:Previous studies have suggested that Bmp4 is a key Msx1-dependent mesenchymal odontogenic signal for driving tooth morphogenesis through the bud-to-cap transition. Whereas the bud stage tooth developmental arrest in Msx1-/- mutant mice was accompanied by reduction in mesenchymal Bmp4 mRNA expression, we show that depleting functional Bmp4 mRNAs in the tooth mesenchyme, through neural crest-specific gene inactivation in Bmp4f/f;Wnt1Cre mice, caused mandibular molar developmental arrest at the bud stage but allowed maxillary molars and incisors to develop to mineralized teeth. We show that the Wnt inhibitors Dkk2 and Wif1 were much more abundantly expressed in the mandibular than maxillary molar mesenchyme in wildtype embryos and that Dkk2 expression was significantly unregulated in the tooth mesenchyme in Bmp4f/f;Wnt1Cre embryos. In addition, expression of Osr2, which encodes a zinc finger protein that antagonizes Msx1-mediated activation of odontogenic mesenchyme, is significantly upregulated in the molar mesenchyme in Bmp4f/f;Wnt1Cre embryos. Msx1 heterozygosity enhanced maxillary molar developmental defects whereas Osr2 heterozygosity rescued mandibular first molar morphogenesis in Bmp4f/f;Wnt1Cre mice. Moreover, in contrast to complete lack of supernumerary tooth initiation in Msx1-/-Osr2-/- mutant mice, Osr2-/-Bmp4f/f;Wnt1Cre compound mutant mice exhibit formation and subsequent arrest of supernumerary tooth germs that correlated with down regulation of Msx1 expression in the tooth mesenchyme. Taken together, our data indicate that, while reduction in mesenchymal Bmp4 expression alone could not account for the tooth bud arrest phenotype in Msx1-/- mutant mice, Bmp4 signaling synergizes with Msx1 and antagonizes Osr2 to activate mesenchymal odontogenic activity to drive tooth morphogenesis and sequential tooth formation. E13.5 mouse embryos tooth germs were microdissected by laser capture microdissection (LCM), and the mandibular molar and maxillary molar were separated. 3 pairs of control and mutant samples were pooled for the RNA extraction.
2013-01-22 | E-GEOD-39918 | biostudies-arrayexpress
Project description:Numerous genes that play important regulative roles during tooth development in mice have been identified. However, very little is known about gene expression and function in human odontogenesis. We used microarrays to detail the global programme of gene expression underlying tooth development and identified distinct classes of up-regulated genes during in the tooth germs. Tooth germs of molar, incisor, and canine at the cap stage were dissected, respectively, from 12-week-old human embryonic oral cavity for RNA extraction and hybridization on Affymetrix microarrays. We sought to screen for the genes that are strongly expressed in the dental tissues and analysis if these genes related to mammalian tooth development and tooth abnormalities.
2015-04-01 | E-GEOD-48150 | biostudies-arrayexpress
Project description:Dioxins are ubiquitous environmental poisons that are developmentally toxic. Exposure of mouse E14 tooth germs to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to reduced tooth size and deformation of cuspal morphology implying the induction of a variety of biological responses on both cellular and molecular levels. To verify such responses at the gene level, mouse embryonic cap staged tooth germs were cultured for 24 h with/without 1 µM TCDD. Experiment Overall Design: Organ culture: Mandibular molar tooth regions from E14 mouse embryos (NMRI X NMRI; the day of vaginal plug = E0) were dissected under a stereomicroscope and transferred to an organ culture. The tissue explants were supported by polycarbonate Nuclepore filters [pore size, 0.1 µm; Corning Inc., New York] placed on a stainless steel grid. The basal culture medium was Dulbeccoâs modified Eagleâs medium (DMEM) containing Glutamax-1 (Gibco BRL, Paisley, Scotland) supplemented with 10% fetal calf serum (FCS; Gibco BRL). TCDD (from the Department of Chemistry, University of Jyväskylä, Jyväskylä, Finland) was dissolved in dimethylsulfoxide (DMSO) at a concentration of 50 µg/ml. TCDD at the concentration of 1 µM, or DMSO, was added to the basal culture medium from the start of culture. The culture dishes were kept in a humidified incubator at 37 ºC in an atmosphere of 5% CO2. The tissue explants were cultured for 24 hours, after which they were snap frozen in liquid nitrogen. Explants from several experiments were collected and kept in liquid nitrogen. In a single experiment, 15â29 explants were included in each experimental group. Experiment Overall Design: Microarray analysis: Experiment Overall Design: Three separate experiments were combined for each replicate sample. About 60 explants each were pooled and homogenized while still frozen in liquid nitrogen. Total RNA was isolated using the RNeasy Mini Kit (Qiagen). cDNA was synthesized from the total RNA by using a GeneChip T7-Oligo(dT)24 Promoter Primer Kit (Affymetrix) and Superscript II Choice System (Invitrogen Life Sciences). The double stranded cDNA was cleaned-up with the GeneChip Sample Cleanup Module (Affymetrix). Biotin-labelled cRNA was synthesized by in vitro transcription usin a RNA labelling kit from Enzo Life Sciences, Inc. The labelling time was 5 h in 37ºC waterbath. All syntheses were done according to the manufacturers instructions. Unincorporated NTPs were removed with the GeneChip Sample Cleanup kit and the concentration of the labelled cRNA was mesured by spectrophotometric analysis and quantificated. 15 or 16 µg of labelled cRNA was fragmented by incubation at 94 ºC for 35 min in the fragmentation buffer supplied in the GeneChip Sample Cleanup kit. The cRNA was hybridized to a murine U74v2A array (Affymetrix) for 16 h at 45 ºC, washed and stained with streptavidine-phycoerythrin. The arrays were scanned in a Genechip System confocal scanner (Aligent) and Affymetrix Microarray Suite 5.0 was used to scan and analyze the relative abundance of each gene. The target signal scaling was set to 100.
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Project description:Numerous genes that play important regulative roles during tooth development in mice have been identified. However, very little is known about gene expression and function in human odontogenesis. We used microarrays to detail the global programme of gene expression underlying tooth development and identified distinct classes of up-regulated genes during in the tooth germs.
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