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Gene expression comparison of E14.5 Foxd1 null and wild type kidneys

ABSTRACT: Forkhead transcription factors are essential for diverse processes in early embryonic development and organogenesis. Foxd1 is required during kidney development and its inactivation results in failure of nephron progenitor cell differentiation. Foxd1 is expressed in interstitial cells adjacent to nephron progenitor cells, suggesting an essential role for the progenitor cell niche in nephrogenesis. To better understand how cortical interstitial cells in general, and FOXD1 in particular, influence the progenitor cell niche, we examined the differentiation states of two progenitor cell subtypes in Foxd1-/- tissue. We found that while nephron progenitor cells are retained in a primitive CITED1-expressing compartment, cortical interstitial cells prematurely differentiate. To identify pathways regulated by FOXD1, we used microarray analysis and screened for target genes by comparison of Foxd1 null and wild type tissues. We chose the E14.5 timepoint because at this stage nephron differentiation is present in wild type kidneys but absent from Foxd1 null kidneys. We examined genes that were upregulated or downregulated in the Foxd1 null compared to wild type.

ORGANISM(S): Mus musculus

PROVIDER: GSE52354 | GEO | 2013/11/14

SECONDARY ACCESSION(S): PRJNA227461

REPOSITORIES: GEO

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Gene expression comparison of E14.5 Foxd1 null and wild type kidneys

Project description:Forkhead transcription factors are essential for diverse processes in early embryonic development and organogenesis. Foxd1 is required during kidney development and its inactivation results in failure of nephron progenitor cell differentiation. Foxd1 is expressed in interstitial cells adjacent to nephron progenitor cells, suggesting an essential role for the progenitor cell niche in nephrogenesis. To better understand how cortical interstitial cells in general, and FOXD1 in particular, influence the progenitor cell niche, we examined the differentiation states of two progenitor cell subtypes in Foxd1-/- tissue. We found that while nephron progenitor cells are retained in a primitive CITED1-expressing compartment, cortical interstitial cells prematurely differentiate. To identify pathways regulated by FOXD1, we used microarray analysis and screened for target genes by comparison of Foxd1 null and wild type tissues. We chose the E14.5 timepoint because at this stage nephron differentiation is present in wild type kidneys but absent from Foxd1 null kidneys. We examined genes that were upregulated or downregulated in the Foxd1 null compared to wild type. Embryonic kidneys were harvested from Foxd1-/- and wild type littermates from three E14.5 litters. Three biological replicates were generated per genotype, each containing two non-littermate kidney pairs. Sex of embryos was not determined.

2013-11-14 | E-GEOD-52354 | biostudies-arrayexpress

Repression of interstitial cell identity in nephron progenitor cells by Pax2 establishes the nephron-interstitium lineage boundary throughout mammalian kidney development

Project description:The kidney contains the functional units, the nephrons, surrounded by the renal interstitium. Previously, we discovered that, once Six2-expressing nephron progenitor cells and Foxd1-expressing renal interstitial progenitor cells form at the onset of kidney development, descendant cells from these populations contribute exclusively to the main body of nephrons and renal interstitial tissues, respectively, indicating a lineage boundary between the nephron and renal interstitial compartments. Currently, it is unclear how lineages are regulated during kidney organogenesis. We demonstrate that nephron progenitor cells lacking Pax2 activity failed to differentiate into nephron cells, but can switch fates into renal interstitium cell types. These data suggest that Pax2 function maintains nephron progenitor cells by repressing transdifferentiation into renal interstitial cell states. Thus, the lineage boundary between the nephron and renal interstitial compartments is maintained by the Pax2 activity in nephron progenitor cells during kidney organogenesis.

2017-03-11 | GSE79137 | GEO

p53 Enables Self Renewal of Nephron Progenitor Cells

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

Stromal Fat4 acts non-autonomously with Dachsous1/2 to restrict the nephron progenitor pool

Project description:Regulation of the balance between progenitor self-renewal and differentiation is critical to development. In the mammalian kidney, reciprocal signaling between three lineages (stromal, mesenchymal and ureteric) ensures correct nephron progenitor self-renewal and differentiation. Loss of either the atypical cadherin Fat4 or its ligand Dachsous1 (Dchs1) results in expansion of the mesenchymal nephron progenitor pool, called the condensing mesenchyme (CM). This has been proposed to be due to misregulation of the Hippo kinase pathway transcriptional co-activator YAP. Here, we use tissue-specific deletions to prove that Fat4 acts non-autonomously in the renal stroma to control nephron progenitors. We show that loss of Yap from the CM in a Fat4-null background does not reduce the expanded CM, indicating Fat4 regulates the CM independent of YAP. Analysis of Six2-/-;Fat4-/- double mutants demonstrates that excess progenitors in Fat4 mutants are dependent on Six2, a critical regulator of nephron progenitor self-renewal. Electron microscopy reveals that cell organization is disrupted in Fat4 mutants. Gene expression analysis demonstrates that the expression of Notch and FGF pathway components are altered in Fat4 mutants. Finally, we show that Dchs1, and its paralog Dchs2 function in a partially redundant fashion to regulate the number of nephron progenitors. Our data supports a model in which FAT4 in the stroma binds to DCHS1/2 in the CM to restrict progenitor self-renewal. A total of 3 Fat4-/- mutant embryos and 3 wildtype (Fat4+/+) control embryos were examined. Two kidneys from each embryo was used thereby yielding a total of 6 Fat4-/- mutant kidneys and 6 Fat4+/+ wildype kidneys. All kidneys examined were at E13.5.

2015-08-01 | E-GEOD-70452 | biostudies-arrayexpress

Gene expression of p53 null vs. p53 wild-type mouse kidneys at embryonic day 15.5

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

p53 Enables Self Renewal of Nephron Progenitor Cells

2015-02-16 | GSE56253 | GEO

Aberrant centrosome biogenesis disrupts nephron and collecting duct progenitor growth and fate resulting in fibrocystic kidney disease [P15]

Project description:Mutations that disrupt centrosome biogenesis or function cause congenital kidney developmental defects and fibrocystic pathologies. Yet, how centrosome dysfunction results in the kidney disease phenotypes remains unknown. Here, we examined the consequences of conditional knockout of the ciliopathy gene Cep120, essential for centrosome duplication, in the nephron and collecting duct progenitor niches of the mouse embryonic kidney. Cep120 loss led to reduced abundance of both cap mesenchyme and ureteric bud populations, due to a combination of delayed mitosis, increased apoptosis, and premature differentiation of progenitor cells. These defects resulted in dysplastic kidneys at birth, which rapidly formed cysts, displayed increased interstitial fibrosis, and decline in kidney function. RNA sequencing of embryonic and postnatal kidneys from Cep120-null mice identified changes in pathways essential for development, fibrosis, and cystogenesis. Our study defines the cellular and developmental defects caused by centrosome dysfunction during kidney morphogenesis, and identifies new therapeutic targets for patients with renal centrosomopathies.

2023-12-08 | GSE249689 | GEO

Aberrant centrosome biogenesis disrupts nephron and collecting duct progenitor growth and fate resulting in fibrocystic kidney disease

2023-12-08 | GSE249693 | GEO

Aberrant centrosome biogenesis disrupts nephron and collecting duct progenitor growth and fate resulting in fibrocystic kidney disease [Embryonic]

2023-12-08 | GSE249692 | GEO

mRNA-Seq profiling SIX2+ and Foxd1+ cells in mouse embryonic and SIX2+ and SIX2-/MEIS1+ cells human fetal kidney

Project description:To characterize the molecular features of human and mouse nephron progenitors and stromal cells we performed intracellular labeling for SIX2 and/or MEIS1 antibodies, FACS, and RNA-seq. Mouse interstitial progenitors were isolated by Foxd1-Tdt transgenic line, FACS, and RNA-seq

2018-02-14 | GSE102230 | GEO

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