Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA136271 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Little is known about the role of cell-cell adhesion in the development of mineralized tissues. Here we report that PERP, a tetraspan membrane protein essential for epithelial integrity, is a critical regulator of enamel formation. Perp is necessary for proper cell attachment and gene expression during tooth development, and its expression is controlled by P63, a master regulator of stratified epithelial development. During enamel formation, PERP is localized to the interface between the enamel-producing ameloblasts and the stratum intermedium (SI), a layer of cells subjacent to the ameloblasts. Perp-null mice display dramatic enamel defects, which are caused, in part, by the detachment of ameloblasts from the SI. Microarray analysis comparing gene expression in teeth of wild-type and Perp-null mice identified several differentially expressed genes during enamel formation. Analysis of these genes in ameloblast-derived LS8 cells upon knock down of PERP confirmed the role for PERP in the regulation of gene expression. Together, our data show that PERP is necessary for the integrity of the ameloblast-SI interface and that the lack of Perp causes downregulation of genes that are critical for proper enamel formation. Two-condition experiment, RNA isolated from WT vs. Perp-null lower 1st molars. Biological replicates: 3 control replicates, 3 mutant replicates.
2011-01-22 | E-GEOD-26796 | biostudies-arrayexpress
Project description:We performed mRNA transcriptional profiling of mouse retina in the wild-type and Nrl-null context to determine Nrl-dependent gene expression We sequenced cDNA libraries made from polyA+ selected RNA from retinas of litter-matched WT and Nrl-/- adult mice at postnatal day 21 (P21) (WT vs Nrl-/-, n=5 and n= 6 resp.)
2020-01-08 | GSE136564 | GEO
Project description:Nogo-A is a major regulator of neural development and regeneration in the central nervous system, but its role in tooth innervation remains largely unknown. Neurons of the trigeminal ganglion innervate the teeth. We showed that Nogo-A is expressed in the trigeminal ganglion and tooth-related nerve fibres. Nogo-A deletion in mice leads to a less complex neuronal network when compared to wild-type animals. Bulk RNA sequencing on the trigeminal ganglia of Nogo-A KO and wild-type mice revealed gene expression changes associated with alterations in neurotrophin signalling and neuronal synaptic formation during the development and maturation of the trigeminal neurons.
2024-12-04 | GSE283391 | GEO
Project description:Transcriptional profiling of M. tuberculosis CDC1551 wild type vs aprABC null, aprBC null, aprC null and phoP transposon mutants.
| PRJNA128063 | ENA
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:Transcriptional profiling of Embryonic Day 14.5 mouse kidneys comparing the infuence of gestational high salt stress on gene expression remolding of BdkrB2 receptor null mice with that of BdkrB2 receptor wild type mice. The BdkrB2 receptor has been shown to be playing a role in renal vascular tone, kidney secretion and reabsorption function, normal kidney development, while impaired BdkrB2 receptor in kidney shown being associated with renal agenesis and renal dysplasia. Goal was to determine the effects of BdkrB2 receptor knockout together with gestational high salt stress on renal gene expression pattern. Two-condition experiment, BdkrB2 null mouse kidney vs. BdkrB2 WT mosue kidney with both on gestational high salt stress . Biological replicates: 3 BdkrB2 null/WT replicates, 3 BdkrB2 WT/null replicates, all 6 replicates were duplicated.
2011-01-19 | E-GEOD-26681 | biostudies-arrayexpress
Project description:We previously reported LATS2 null mice (Yabuta et al., 2007). LATS2 known as a tumor suppressor protein. However, the LATS2 mediated transcriptional regulation remains largely unknown. To investigate potential signaling pathways, we performed the expression profiling by using primary MEFs derived from wild type and LATS2 null mice.
2016-10-16 | GSE25536 | GEO