Identification of novel genes expressed during mouse molar tooth development by microarray gene expression analysis
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE7164 | GEO | 2007/07/31
SECONDARY ACCESSION(S): PRJNA98171
REPOSITORIES: GEO
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Project description:To identify genes heretofore undiscovered as critical players in the biogenesis of teeth, we have used microarray gene expression analysis of the developing mouse molar tooth (DMT) between 1 and 10 days postnatal to identify genes differentially expressed when compared to 16 control tissues (GEO accession # GSE1986). Of the top 100 genes exhibiting increased expression in the DMT, 29 were found to have been previously associated with tooth development. Differential expression of the remaining 71 genes not previously associated with tooth development was confirmed by qRT-PCR analysis. Further analysis of seven of the latter genes by mRNA in situ hybridization found that five were specific to the developing tooth in the craniofacial region (Rspo4, Papln, Amtn, Gja1, Maf). Of the remaining two, one was found to be more widely expressed (Sp7) and the other was found to be specific to the nasal serous gland, which is close to, but distinct from, the developing tooth (Vrm). Experiment Overall Design: mRNA from molar teeth extracted from Swiss Webster mouse pups between 1 and 10 days post-natal was pooled, labeled, and hybridized in quadruplicate to Affymetrix Mouse Genome Expression 430 2.0 microarrays. This data was compared to that of 16 control tissues (GEO accession # GSE1986) to identify genes differentially expressed in the DMT mRNA.
2008-06-15 | E-GEOD-7164 | biostudies-arrayexpress
Project description:The dataset aims at comparing gene expression in the developing lower and upper first molars of two mouse strains: DUHi and FVB. We studied molar tooth germ an early cap stage, looking for differences in activation-inhibition mechanisms that promote tooth formation. 19202 genes are in common between FVB and reference strain C57B6 and have a MGI annotation. Out of these genes, 2234 genes (11.6%) presented a significant difference of expression between the mapping on the reference strain C57B6 and the mapping on FVB strain (DESeq2, adjusted P value < 0.05, considering the mapping effect that is with 12 replicates). This is presumably a mapping artifact, due to the sequence divergence between mouse strains. These genes were removed, and the remaining 16,968 genes were retained for further analysis. 3619 genes were found to be differentially expressed between the two strains in the lower and upper molar (jaw+strain)
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Project description:One of the key questions in developmental biology is how from universally shared molecular mechanisms and pathways, is it possible to generate organs displaying similar or complementary functions, with a wide range of different shapes or tissue organization? The dentition represents a valuable system to address the issues of differential molecular signatures generating specific tooth types. We performed a comparative transcriptomic analysis of developing murine lower incisors, mandibular molars and maxillary molars at the developmental cap stage (E14.5) prior to recognizable tooth shape and cusp pattern. We compared gene expression profiles in developing murine lower incisor and molars, as well as between the lower and upper (mandibular and maxillary) first molars
2013-03-31 | E-GEOD-43144 | biostudies-arrayexpress
Project description:One of the key questions in developmental biology is how from universally shared molecular mechanisms and pathways, is it possible to generate organs displaying similar or complementary functions, with a wide range of different shapes or tissue organization? The dentition represents a valuable system to address the issues of differential molecular signatures generating specific tooth types. We performed a comparative transcriptomic analysis of developing murine lower incisors, mandibular molars and maxillary molars at the developmental cap stage (E14.5) prior to recognizable tooth shape and cusp pattern.
2013-03-31 | GSE43144 | GEO
Project description:In this study, whole-genome ChIP-seq analysis was performed to identify Sp6 regulatory targets from postnatal mouse molars. Enriched sequence reads (peaks) from Sp6 immunoprecipitations were located predominately adjacent to transcriptional start sites. Notably enriched for Sp6 peaks were genes highly-expressed in the tooth. Bioinformatic analysis of two pools of 1400 Sp6 enriched sequences identified a consensus nine-nucleotide DNA pulldown sequence of CTg/aTAATTA from mesenchyme and the nearly identical sequence, CTa/gTAATTA, from epithelium. Sp6 AT-rich interaction sequences are nearly identical to the ChIP-seq enriched sequences reported for Sp7 and Sp9. ChIP-seq analysis indicates Sp6 regulates a significant number of genes expressed in the tooth. GSE145909 is the original submission. GSE151391 is also from the same study. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE151391
2021-11-23 | GSE145909 | GEO
Project description:Transcriptional profiling of mouse E14 tooth molar germ comparing E11, 12, 16, 18 tooth molar germ. Goal was to identify unknown genes involved in tooth development,
2020-11-20 | GSE161851 | GEO
Project description:The tooth is derived from both the ectoderm and the neural crest (ectomesenchyme). It is often used as a model for studies of the basic mechanisms of organ development, including differentiation, cellular interaction, morphogenesis, and mineralization of extracellular matrices. In mouse, tooth development begins at embryonic day 11.5 (E11.5) by thickening of the dental epithelium, whereas mineralization of enamel and dentin in first molars starts at postnatal day 0 (P0). Tooth development entails a multistep and complex process of gene expression. Studies with genetically modified mice have contributed substantially to our understanding of genes that regulate tooth development and morphology. MicroRNAs (miRNA) are a class of non-coding RNAs that regulate gene expression at a post-transcriptional level, and are considered as important regulatory molecules during foetal development. By binding to target mRNAs, miRNA induce mRNA decay or translation repression. Recent bioinformatic predictions of miRNA targets in vertebrates indicate that hundreds of miRNAs are responsible for regulation of expression of up to 30% of the human protein-coding genes. Recent experiments has verified that miRNAs can regulate expression of hundreds of mRNAs in cultured cells. Previous study has also shown that microarrays can be used to detect physiologically relevant effects of miRNAs on expression of mRNAs in vertebrates; miRNAs have been shown to alter expression of a greater number of transcripts than previously appreciated, primarily through interaction with 3M-4UTRs. Understanding the biological function of miRNAs require knowledge of their mRNA targets. Bioinformatic approaches have been used to predict mRNA targets, among which both transcription factors and pro-apoptopic genes were prominent candidates. The precise molecular function of miRNAs remains largely unknown and a better understanding may require loss-of-function studies in vivo. It has been shown that intravenous administration of a novel class of chemically engineered oligonucleotides termed M-^SantagomirsM-^T resulted in a marked reduction of corresponding miRNA levels in most tissues. This resulted in upregulated expression of hundreds of genes predicted to be repressed by miR-122 because these genes had a miR-122 recognition motif in their 3M-4UTR region. Paradoxically, antagomir treatment also revealed a significant number of downregulated genes that may be activated by miR-122. The mechanism by which miRNAs may activate gene expression in vivo is unknown. However, it may involve an indirect effect (the suppression of a transcriptional repressor), or alternatively, miRNA may have a direct effect on gene activation (e.g. chromatin remodeling). Studies of microRNA expression profiles of the developing murine molar tooth germ have shown these to be highly dynamic, some miRNAs being abundantly expressed during the early development of the molar tooth germ, while others are highly expressed only at later developmental stages. A recent study also suggested that miRNAs modulate tooth morphogenesis and ameloblast differentiation, perhaps largely by fine tuning conserved signaling networks. The function of microRNA-214 (miR-214) is unknown, however, it has been related to normal growth and skeletal development in mice. In tooth germs miR-214 is more highly expressed during later developmental stages. It was selected as a target for silencing using anti-miR-214. Here we report effects from injections of 1-100 pmol of anti-miR-214 close to developing first mandibular molar in newborn mice. At 24 hrs, or more, after injection significant changes in gene expression, and in levels of several correspondingly encoded proteins, were found in the tooth germ.
2011-08-31 | E-MTAB-357 | biostudies-arrayexpress
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.
2009-08-06 | E-MTAB-42 | biostudies-arrayexpress
Project description:Purpose: the goals of this study are to explore the effect of loss of Ptip in Sp7 positive dental progenitor cells on CD45- Ter119- Tie2- dental progenitor cells Methods: CD45- Ter119- Tie2- dental progenitor cells were sorted by FACs in lower incisors from Ptipf/f and Ptipf/f;Sp7-cre mice and performed RNAseq Our finding reveals that Ptip as crucial regulator in tooth homeostasis, functioning to safeguard the Sp7+ progenitor cells epigenome from a breach in lineage confinement that triggers irreversible tooth defects. Conclusions: loss of Ptip unregulate dental development and active Wnt signal pathway
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Project description:Tooth is a good model for studying stem cell driving epithelial and mesenchymal cells development and differentiation. Identifying key factors and pathways governing tooth development will help elucidate the physiological and pathological processes including genetic defects. To investigate the time-dependent proteomic changes of tooth development, label-free quantitative proteomics were conducted for human deciduous molars collected from post conception week (PCW) 12, 15 and 18, encompassing cap to early bell stage. The proteomic profiles reveal dynamic changes of driving proteins and canonical signaling pathways governing tooth development. The proteins with different expression patterns were identified and the protein-protein interaction networks were constructed. Besides, a series of proteins that were potential or novel drivers of tooth morphogenesis had been screened. The polarized expression patterns in odontogenic mesenchymal cell and muscle cell development and the bipolar expression pattern in odontogenic epithelial cell development were revealed. Three candidate proteins (GJA1, PAX9 and KRT15) with different expression patterns were validated by immunohistochemistry. Our study provides an invaluable resource for further mechanistic studies and suggests core factors regulating tooth development.
2023-02-09 | PXD039974 | iProX