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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

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

Project description:We have previously demonstrated that loss of miR-17~92 in nephron progenitors in a mouse model results in renal hypodysplasia and chronic kidney disease. Clinically, decreased congenital nephron endowment because of renal hypodysplasia is associated with an increased risk of hypertension and chronic kidney disease, and this is at least partly dependent on the self-renewal of nephron progenitors. Here, we present evidence for a novel molecular mechanism regulating the self-renewal of nephron progenitors and congenital nephron endowment by the highly conserved miR-17~92 cluster. Whole transcriptome sequencing revealed that nephron progenitors lacking this cluster demonstrated increased Cftr expression. We showed that one member of the cluster, miR-19b, is sufficient to repress Cftr expression in vitro and that perturbation of Cftr activity in nephron progenitors results in impaired proliferation. Together, these data suggest that miR-19b regulates Cftr expression in nephron progenitors, with this interaction playing a role in appropriate nephron progenitor self-renewal during kidney development to generate normal nephron endowment.

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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.

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