Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA290376 | ENA |
REPOSITORIES: ENA
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Project description:We are characterizing global expression in the whole kidney at developmental stage E18.5, where we have used three Cre strains that result in knock out Wt1 in different cell types during renal development. Here the purpose is to identify the developmental stage at which the loss of Wt1 impacts kidney development, specifically in the context of a degree of disruption capable of ending in pediatric kidney cancers. Total RNA was isolated from whole kidneys of E18.5 mouse embryos following a variety of conditional knockouts of Wt1, plus appropriate control animals.
2015-07-27 | E-GEOD-70892 | biostudies-arrayexpress
Project description:Wt1 is required for renal development and homozyogus knockout mice show renal agenesis caused by apoptosis of the metanepric mesnchyme. To identify genes regulated by WT1, we performed comparative gene expression profiling on kidney rudmients of Wt1 heterozygous and homozygous mutant E10.25 embryos. To identify deregulated genes, timed matings were performed and embryos isolated at E10.25, a time point before the onset of apoptosis in Wt1 mutants. The region containing the metanephric mesenchyme was microdissected, RNA isolated and after labeling, hybridized to Mouse Genome Survey Microarrays. Deregulated genes were identified using GeneSpring (GSX) software.
2014-06-01 | E-GEOD-58073 | biostudies-arrayexpress
Project description:The Wilms tumor protein Wt1 is a transcription factor known to play an important role in urogenital development. Mutations in the human Wt1 encoding gene (WT1) lead to several syndromes associated with defective renal and sexual development, namely WAGR-, Denys-Drash-, and Frasier-syndrome. During mammalian embryogenesis, urogenital development starts with formation of the urogenital ridges, consisting of the embryonic kidneys, called mesonephroi, and the gonads. In Wt1 knockout mice, these ridges start to form, degenerate, however, during further embryonic development . Although WT1 and the syndromes associated with its mutation are known for several years, it is still unclear which genes, regulated by Wt1, mediate the whole variety of Wt1's function in gonad and mesonephros development. To obtain a comprehensive view on Wt1-dependent gene activity in developing urogenital ridges, we employed microarray analysis. Comparison of gene expression in Wt1 wild-type and knockout mice, led to the identification of almost 150 genes with differences in expression levels higher than factor three. Keywords: wild-type and knockout comparison
2007-06-01 | GSE6700 | GEO
Project description:In developing mammalian kidney, nephron progenitor cells (NPC) give rise to all cells in mature nephrons. Several transcription factors, including Six2, Hoxd11, Osr1 and Wt1, are expressed in NPC and are essential for its maintenance and/or specification. In order to understand the regulatory functions of these factors, we mapped binding sites of Six2, Hoxd11 and Osr1 in NPC using a novel transgenic strategy, and of Wt1 in wild-type developing kidney.
2018-01-18 | GSE90016 | GEO
Project description:Wt1 is required for renal development and homozyogus knockout mice show renal agenesis caused by apoptosis of the metanepric mesnchyme. To identify genes regulated by WT1, we performed comparative gene expression profiling on kidney rudmients of Wt1 heterozygous and homozygous mutant E10.25 embryos.
2014-06-01 | GSE58073 | GEO
Project description:Absence of WT1 during kidney organoid development from human induced pluripotent stem cells (iPSCs) induces hallmarks of Wilms tumorigenesis. To define underlying transcriptional alterations and similarities to human patients, we performed timecourse RNA-seq of kidney organoid development from control iPSCs (control, not edited) and in the absence of WT1. Two timepoints for knockout (KO) of WT1 were investigated: In iPSCs (KO in iPSCs), and between day 4 and day 7 of organoid formation (KO d4-7).
2021-08-01 | E-MTAB-9957 | biostudies-arrayexpress
Project description:We report the the identification of chrosomal regions bound by the Wilms' tumor suppressor gene WT1 during embryonic mouse kidney development. Two indepednent ChIP-Seq experiments on microdissected E18.5 developing mouse kidneys were carried out using either WT1-specific or IgG-antibodies as a negative control.
2014-06-15 | E-GEOD-58179 | biostudies-arrayexpress
Project description:Activity-dependent transcription influences neuronal connectivity, but the roles and mechanisms of inactivation of activity-dependent genes have remained poorly understood. Genome-wide analyses in the mouse cerebellum revealed that the nucleosome remodeling and deacetylase (NuRD) complex deposits the histone variant H2A.z at promoters of activity-dependent genes, thereby triggering their inactivation. Purification of translating mRNAs from synchronously developing granule neurons (Sync-TRAP) showed that conditional knockout of the core NuRD subunit Chd4 impairs inactivation of activity-dependent genes when neurons undergo dendrite pruning. Chd4 knockout or expression of NuRD-regulated activity genes impairs dendrite pruning. Imaging of behaving mice revealed hyperresponsivity of granule neurons to sensorimotor stimuli upon Chd4 knockout. Our findings define an epigenetic mechanism that inactivates activity-dependent transcription and regulates dendrite patterning and sensorimotor encoding in the brain.
2016-07-18 | GSE83253 | GEO
Project description:Activity-dependent transcription influences neuronal connectivity, but the roles and mechanisms of inactivation of activity-dependent genes have remained poorly understood. Genome-wide analyses in the mouse cerebellum revealed that the nucleosome remodeling and deacetylase (NuRD) complex deposits the histone variant H2A.z at promoters of activity-dependent genes, thereby triggering their inactivation. Purification of translating mRNAs from synchronously developing granule neurons (Sync-TRAP) showed that conditional knockout of the core NuRD subunit Chd4 impairs inactivation of activity-dependent genes when neurons undergo dendrite pruning. Chd4 knockout or expression of NuRD-regulated activity genes impairs dendrite pruning. Imaging of behaving mice revealed hyperresponsivity of granule neurons to sensorimotor stimuli upon Chd4 knockout. Our findings define an epigenetic mechanism that inactivates activity-dependent transcription and regulates dendrite patterning and sensorimotor encoding in the brain. One or two replicates of the histone modifications (H3K27me3 and H2A.z), total histone proteins (H2A.z and H3), and ATPase Chd4 using postnatal day 22 cerebella from wild type (WT) or Chd4 conditional knockout (cKO) mice were examined using libraries prepared with the Illumina ChIP-Seq DNA Sample Prep Kit. Four replicates of total RNA were extracted from postnatal day 27-28 cerebella from rotarod-trained or control homecage mice, or Chd4 cKO or WT mice using Trizol and reverse-transcribed with oligo-dT priming. Three replicates of immunoprecipitated Sync-TRAP RNA or the input control using postnatal day 12 Chd4 cKO or WT cerebella were purified and amplified with Ovation RNA-Seq System V2 (NuGEN). All samples were sequenced on the Illumina HiSeq 2000 platform.
2016-07-18 | E-GEOD-83253 | biostudies-arrayexpress