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RNA sequencing of Foxd1Cre;Smo(flox/-) mutant kidneys

ABSTRACT: Purpose: To analyze the mRNA content of Foxd1Cre;Smo(flox/-) mutant kidneys. Methods: We collected E13.5 wildtype and Foxd1Cre;Smo(flox/-) mutant kidneys and isolated RNA to do RNA-Seq. Results: Identified differentially expressed transcripts in Foxd1Cre;Smo(flox/-) mutant kidneys compared to wildtype controls. Conclusions: Our work provides novel insight into how Hedgehog signaling from stromal cells influences renal development.

ORGANISM(S): Mus musculus

PROVIDER: GSE103923 | GEO | 2018/06/26

REPOSITORIES: GEO

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Mus musculus

Project description:RNA sequencing of Foxd1Cre;Smo(flox/-) mutant kidneys

| PRJNA407570 | ENA

Mouse embryonic kidneys (E13.5): mutant (UB HDAC1,2-/-) vs. wild type

Project description:Transcriptional profiling of mouse embryonic kidneys (E13.5) comparing UB HDAC1,2-/- kidneys with wild type kidneys. Studies in our lab showed that histone deacetylase 1 (HDAC1) and 2 (HDAC2) perform redundant, yet essential functions in the developing mouse ureteric bud (UB) tissue. Double deletion of HDAC1 and HDAC2 in the UB results in impaired UB branching morphogenesis, followed by severe kidney dysgenesis. The goal of the microarray analysis was to identify the genetic pathways controlled by HDAC1 and 2 in the UB. Two-condition experiment: E13.5 mutant kidneys (UB HDAC1,2-/-) vs. E13.5 wild type kidneys . Biological replicates: 4 control replicates, 4 UB HDAC1,2-/- replicates. Two-color Agilent 4x44k chips with dye-swaps on 2 of 4 arrays.

2012-01-31 | E-GEOD-35432 | biostudies-arrayexpress

Transcriptome analysis of Yap mutant kidneys

Project description:Microarrays were used to examine gene expression changes between control and mutant (YapCM-/-) kidneys to investigate molecular changes responsible for abnormal nephrogenesis seen in Yap mutants. This work identifies a list of potential genes regulated by Yap during nephron development. Total RNA obtained from three mutants and three controls kidneys at embryonic day E13.5 were used for the expression profiling analysis.

2014-07-01 | E-GEOD-39550 | biostudies-arrayexpress

SMO variants explain the majority of drug resistance in basal cell carcinoma [Target Sequencing]

Project description:Advanced basal cell carcinomas (BCCs) frequently acquire resistance to Smoothened (SMO) inhibitors through unknown mechanisms, providing a unique opportunity to study human tumor evolution. Here, we identify SMO mutations in 50% (22/44) of resistant BCCs compared with 5.6% (2/36) of untreated BCCs (p<0.0001), and show that these mutations maintain Hedgehog signaling in the presence of SMO inhibitors. Alterations include four ligand binding pocket (LBP) mutations that define sites of inhibitor binding and four variants that confer constitutive activity and inhibitor resistance, thus defining pivotal residues of SMO that ensure receptor autoinhibition. Finally, we show that both classes of SMO variants respond to the aPKC-ι/λ inhibitor PSI and GLI2 antagonist ATO that operate downstream of SMO

2015-03-16 | GSE58376 | GEO

SMO variants explain the majority of drug resistance in basal cell carcinoma [RNA-Seq]

2015-03-16 | GSE58375 | GEO

SMO variants explain the majority of drug resistance in basal cell carcinoma [exome-seq]

2015-03-16 | GSE58374 | GEO

Genome-wide analysis of gene expression in normal and fibrotic mouse kidneys with and without Twist1 or with and without Snai1(Snail) expression in proximal tubular epithelial cells

Project description:In this study mice were engineered to specifically delete Twist1 or Snail expression in proximal tubular epithelial cells of the kidney (ggt-cre+;Twist flox/flox and ggt-cre+;Snail flox/flox ). These mice and control mice (ggtcre-;Twist flox/flox: these express Twist1, and ggtcre-;Snail flox/flox:these express Snail) were subjected to unilaterial ureteric obstruction. This experiment allows for the collection and analysis of expression in contralateral healthy (HK) kidney adn obstructed disease (DK) kidney. Total RNA was isolated from the contralateral healthy (HK) and obstructed disease (DK) kidneys of 3 mice with ggt-cre-;Twist flox/flox genotype (Wildtype like) and 4 mice with ggt-cre+;Twist flox/flox genotype (loss of Twist1 in proximal tubular epithelial cells), 3 mice with ggt-cre-;Snail flox/flox genotype (Wildtype like) and 3 mice with ggt-cre+;Snail flox/flox genotype (loss of Snail in proximal tubular epithelial cells). Total RNA was also isolated from kidneys of completely healthy mice: 3 mice ggt-cre-;WT, 3 mice ggt-cre+;WT, 3 mice ggt-cre+;Twist flox/flox and 3 ggt-cre+;Snail flox/flox

2015-08-03 | E-GEOD-60685 | biostudies-arrayexpress

Essential roles of mitochondria biogenesis regulator Nrf1 in retina development and homeostasis

Project description:Purpose: RNA-seq analysis for E13.5 wildtype vs. Nrf1-flox/flox:Six3-Cre retinas

2018-07-18 | GSE101550 | GEO

Parathyroid tissue transcriptome over 24h of PTHcre;Bmal1 flox/flox mice and of Bmal1 flox/flox mice

Project description:The objective is to elucidate the role of the circadian clock in the parathyroid glands. We investigate the parathyroid transcriptome of wildtype mice (Bmal1 flox/flox) and of mice with parathyroid-specific excision of the circadian clock gene Bmal1 (PTHcre;Bmal1 flox/flox) harvested at 4 hour interval for 24 hours. Rhythmic genes were identified by JTK_CYCLE analysis and revealed 1455 rhythmic genes of the Bmal1 flox/flox and 1055 rhythmic genes of the PTHcre;Bmal1 flox/flox. We found global damepning of circadian clock genes with abolished rhythmicity of Cry1, Cry2, Clock, Npas2, Rorc, and Usp2. We used GSEA analysis to investigate differential expression at each timepount and found downregulation of genes involved in ATP synthesis in PTHcre;Bmal1 flox/flox mice at 4 consecutive timepoints during the active period of the mouse.

2021-12-23 | GSE191264 | GEO

Mouse embryonic kidneys (E13.5): HDAC inhibitor (HDACi) treated vs. Control

Project description:Transcriptional profiling of cultured CD1 mouse embryonic kidneys (E13.5) comparing HDACi-treated kidneys with control drug-treated kidneys. Studies in our lab showed that pharmacological inhibition of HDAC activity in ex-vivo cultured metanephroi results in extensive defects in kidney development, including impaired UB branching, tubulogenesis, and glomerulogenesis, accompanied by cell cycle arrest and apoptosis.The goal of the microarray analysis was to elucidate the morphogenetic pathways affected by HDACi. Two-condition experiment, HDACi-treated E13.5 kidneys (Scriptaid 2.0 μg/ml x 6hrs) vs. Control drug-treated E13.5 kidneys (Nullscript 2.0 μg/ml x 6hrs). Biological replicates: 3 control replicates, 3 HDACi-treated replicates. Two-color Agilent 4x44k chips with dye-swap on 2 of 4 arrays.

2010-08-01 | E-GEOD-19581 | biostudies-arrayexpress

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