Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA215228 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mouse embryonic kidneys (E13.5): mutant (UB HDAC1,2-/-) vs. wild type
| PRJNA152771 | ENA
Project description:We wanted to compare the transcriptional profile of wild-type and p53 null mouse embryonic stem cells at day 3 of differentiation in N2B27 media.
2024-01-01 | E-MTAB-13589 | biostudies-arrayexpress
Project description:p53 limits the self-renewing ability of a variety of stem cells. Here, contrary to its classical role in restraining cell proliferation, we demonstrate a divergent function of p53 in maintenance of self-renewal of the nephron progenitor population in the embryonic mouse kidney. p53-null nephron progenitor cells (NPC) exhibit progressive loss of the self-renewing progenitor niche in the cap mesenchyme, identified by Cited1 and Six2 expression, and loss of cap integrity. Nephron endowment is regulated by NPC availability and their differentiation to nephrons. Quantitatively, the Six2p53-/- cap has 30% fewer Six2GFP+ cells. While the apoptotic index is unchanged the proliferation index is significantly lower, in accordance with cell cycle analysis data showing less mutant Six2p53-/-;GFP+ cells in S and G2/M phases in comparison to Six2p53+/+;GFP+ cells. The mutant kidneys also show nephron deficit and decreased Fgf8 expression. To investigate the underlying changes in gene expression in the cap mesenchyme that contribute to the Six2p53-/- phenotype, we utilized RNA-Seq for transcriptome comparison. Top biological processes affected by p53 loss are development and morphogenesis, cell adhesion/migration, cell survival and metabolism. Cells from the mutant CM showed increased cellular ROS levels as well as deregulated expression of energy metabolism and mitochondrial genes suggesting metabolic dysfunction. Adhesion defects are visualized by decreased immunostaining of adhesion marker NCAM, and may possibly contribute to the differentiation defect as well. Altogether our data suggest a novel role for p53 in enabling self-renewal of the NPC and preservation of the progenitor niche, and thus regulating nephron endowment. mRNA profiles of wild-type (WT) and conditional p53 knockout (KO) of Six2+ mouse nephron progenitor cells (NPC) at embryonic day 15.5
2015-02-16 | E-GEOD-56253 | biostudies-arrayexpress
Project description:Gestational high salt stressed Embryonic Day 14.5 BdkrB2 Null Mouse Kidney vs. BdkrB2 Wild Type Mouse Kidney
| PRJNA136585 | ENA
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:To investigate how pleiotropic the impact of p53 loss is on cellular function, generated isogenic, polyclonal wild-type (sgNTC) and p53-null (sgp53) E1A;HrasG12V mouse embryonic fibroblast cell lines using CRISPR/Cas9. Here we show gene expression analysis on p53 wild-type (sgNTC) and p53null (sgp53) E1A;HrasG12V MEFs grown under physiological oxygen conditions (5% oxygen).
2020-08-07 | GSE136355 | GEO
Project description:Gene expression microarray analysis was performed on E15.5 p53+/+ and p53-/- litter-matched kidneys. We have previously shown that p53 is expressed in both UB and MM lineages in the kidney, and that p53-null embryos on C57B6L background exhibit a range of congenital abnormalities of the kidney and urinary tract such as duplicated ureters, reduced nephron numbers, and compromised nephron progenitor renewal and differentiation. Here our goal was to reveal the p53 transcriptome in mouse embryonic kidneys at E15.5.
2013-09-05 | GSE49878 | GEO
Project description:Whole C57BL/6 mouse esophagus: embryonic day 15.5 (E15.5) vs. postnatal day 2 (P2)
| PRJNA243635 | ENA
Project description:Autosomal dominant polycystic kidney disease (ADPKD) is characterized by cyst formation throughout the kidney parenchyma. It is caused by mutations in either of two genes, PKD1 and PKD2. Mice that lack functional Pkd1 (Pkd1null/null), develop rapidly progressive cystic disease during embryogenesis, and serve as a model to study human ADPKD. We examined the molecular pathways that modulate renal cyst growth in the Pkd1null/null model by performing global gene-expression profiling in embryonic kidneys at day 14 and 17. Gene Ontology and gene set enrichment analysis were used to identify overrepresented signaling pathways in Pkd1null/null kidneys. We found dysregulation of developmental, metabolic, and signaling pathways (e.g. Wnt, calcium, TGF-b and MAPK) in Pkd1null/null kidneys. Total RNA were obtained from kidneys of wild-type and Pkd1null/null animals at embryonic ages 14.5 and 17.5.
2011-04-30 | E-GEOD-24352 | biostudies-arrayexpress