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Differential gene expression in nephron progenitors lacking miR-17~92

ABSTRACT: Purpose: The goal of this study is to compare the differential expression of transcripts in control kidneys compared to kidneys lacking the miR-17~92 cluster in nephron progenitors and their derivatives by RNA-seq to identify potential miRNA targets in the mutant kidneys.

ORGANISM(S): Mus musculus

PROVIDER: GSE52514 | GEO | 2014/03/07

SECONDARY ACCESSION(S): PRJNA229148

REPOSITORIES: GEO

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Differential gene expression in nephron progenitors lacking miR-17~92

Project description:Purpose: The goal of this study is to compare the differential expression of transcripts in control kidneys compared to kidneys lacking the miR-17~92 cluster in nephron progenitors and their derivatives by RNA-seq to identify potential miRNA targets in the mutant kidneys. mRNA profiles of control and mutant (=Six2-TGC; miR-17~92 flx/flx) embryonic day 16 kidneys were generated by deep sequencing, in triplicate, using Illumina HiSeq2000

2014-03-07 | E-GEOD-52514 | biostudies-arrayexpress

Whole transcriptome RNA sequencing of E16.5 Six2TGC and Six2TGC;miR-17~92fl/fl nephron progenitors

Project description:The goal of this study is to identify dysregulated mRNAs and lncRNAs in nephron progenitors as a consequence of a loss of miR-17~92 post-transcriptional regulation

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Loss of miR-17~92 results in dysregulation of Cftr in nephron progenitors.

Project description: Not available

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Oncogenic biogenesis of pri-miR-17~92

Project description:The microRNAs encoded by the miR-17~92 polycistron are commonly overexpressed in cancer and orchestrate a wide range of oncogenic functions. Here, we identify a novel mechanism for miR-17~92 oncogenic function through the disruption of endogenous miRNA processing. We show that upon oncogenic overexpression of the miR-17~92 primary transcript (pri-miR-17~92), the Microprocessor complex remains associated with partially processed intermediates that aberrantly accumulate. These intermediates reflect a series of hierarchical and conserved steps in the early processing of the pri-miR-17~92 transcript. Encumbrance of the Microprocessor by miR-17~92 intermediates leads to the broad, but selective, downregulation of co-expressed polycistronic miRNAs, including miRNAs derived from tumour suppressive miR-34b/c, and from the Dlk1-Dio3 polycistrons. We propose that the newly identified steps of polycistronic miR-17~92 biogenesis contribute to the oncogenic re-wiring of gene regulation networks. Our results reveal new functional paradigms for polycistronic miRNAs in cancer.

2019-05-20 | GSE130282 | GEO

Transcriptional response of cap mesenchyme (undifferentiated nephron progenitors) to Wnt activation

Project description:During mammalian kidney development, mesenchymal nephron progenitors (cap mesenchyme) differentiate into the epithelial cells that go on to form the nephron. Although differentiation of nephron progenitors is triggered by activation of Wnt/b-catenin signaling, constitutive activation of Wnt/b-catenin signaling blocks epithelialization of nephron progenitors. Full epithelialization of nephron progenitors requires transient activation of Wnt/b-catenin signaling. We performed transcriptional profiling of nephron progenitors responding to constitutive or transient activation of Wnt/b-catenin signaling. Nephron progenitors were FACS-isolated from BAC transgenic Six2GFPcre-positive embryonic kidneys at E16.5. Cells were aggregated by centrifugation at 850g for 5min and incubated in 10%FBS/DMEM containing either 4uM BIO or the equal volume of DMSO for 24hrs or 48hrs.

2012-09-11 | E-GEOD-39583 | biostudies-arrayexpress

Protein profiling upon miR-17-92 induction.

Project description:Methionine COFRADIC combined with Arg and Lys SILAC labeling was used to quantify proteins upon induction of miR-17-92 in SHEP neuroblastoma cells. Differently labeled cells treated with tetracycline for 72 h or left untreated, were harvested and mixed lysates were analyzed by methionine COFRADIC to isolate methionyl peptides followed by identification of these peptides by LC-MS/MS and subsequent quantification.

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Complete male-to-female sex reversal in mice lacking the miR-17~92 cluster [RNA-seq]

Project description:The deletion of a single miRNA cluster, miR-17~92, is sufficient to induce primary sex reversal in XY mice. The expression of the testis determining gene, Sry, is delayed in embryonic XY miR-17~92 knockout gonads, which immediately activate the ovarian genetic program. Single cell RNA-seq analysis shows that Sertoli cell differentiation is highly reduced, delayed and unable to trigger testis differentiation. Consistent with the well-known role of miRNAs in gene regulation, the expression of target genes of miR-17~92 is not stabilized in XY mutant gonads at E11.5, affecting, in turn, the fine regulation of large gene networks involved in mammalian sex determination. Our results reveal that the miR-17~92 cluster is a novel sex-determining factor that modulates several gene networks required for accurate timing of Sry expression and Sertoli cell differentiation during testis determination and early differentiation. bulk RNA-seq, single cell RNA-seq as well as IF and other characterizations of a transgenic mice for miR-17~92 cluster

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Complete male-to-female sex reversal in mice lacking the miR-17~92 cluster [scRNA-seq]

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Genome-wide maps of Six2 and b-catenin in mesenchymal nephron progenitors

Project description:Self-renewing undifferentiated nephron progenitors express Six2, a transcription factor that is required for their maintenance as undifferentiated progenitors. Differentiation of nephron progenitors is triggered by Wnt/b-catenin signaling. In order to understand how Six2 and Wnt signaling counteract each other, we performed ChIP-seq of Six2 and b-catenin in mesenchymal nephron progenitor cells. Nephron progenitors were FACS-isolated from BAC transgenic Six2GFPcre-positive embryonic kidneys at E16.5. For Six2 ChIP, freshly FACS isolated Six2+ cells were used. For b-catenin ChIP, FACS isolated Six2+ cells were aggregated by centrifugation at 850g for 5min and incubated in 10%FBS/DMEM containing 4uM BIO for 24hrs.

2012-09-11 | E-GEOD-39837 | biostudies-arrayexpress

Analysis of mir-17~92 targets in motor neurons

Project description:To identify mir-17~92 targets in MNs, a set of target candidate genes from the intersection of upregulated genes found only in the mir-17~92 KO MNs that were predicted to be direct targets of mir-17~92 by TargetScan.

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