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Screening of miR-379 target RNAs by comparison of WT and miR-379 KO mouse primary kidney mesangial cells by using CLASH technique

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE142598 | GEO | 2020/12/01

REPOSITORIES: GEO

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Screening of miR-379 target RNAs by comparison of WT and miR-379 KO mouse primary kidney mesangial cells by using CLASH technique [CLASH-Seq]

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Screening of miR-379 target RNAs by comparison of WT and miR-379 KO mouse primary kidney mesangial cells by using CLASH technique [RNA-Seq]

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Screening of miR-379 target RNAs by comparison of WT and miR-379 KO mouse primary kidney mesangial cells by using CLASH technique [CLASH-Seq]

Project description:Screening of miR-379 target RNAs by comparison of WT and miR-379 KO mouse primary kidney mesangial cells by using CLASH technique [CLASH-Seq]

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Screening of miR-379 target RNAs by comparison of WT and miR-379 KO mouse primary kidney mesangial cells by using CLASH technique

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Screening of miR-379 target RNAs by comparison of WT and miR-379 KO mouse primary kidney mesangial cells by using CLASH technique [RNA-Seq]

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miR-379 deletion ameliorates features of diabetic kidney disease by enhancing adaptive mitophagy via FIS1.

Project description:Diabetic kidney disease (DKD) is a major complication of diabetes. Expression of members of the microRNA (miRNA) miR-379 cluster is increased in DKD. miR-379, the most upstream 5'-miRNA in the cluster, functions in endoplasmic reticulum (ER) stress by targeting EDEM3. However, the in vivo functions of miR-379 remain unclear. We created miR-379 knockout (KO) mice using CRISPR-Cas9 nickase and dual guide RNA technique and characterized their phenotype in diabetes. We screened for miR-379 targets in renal mesangial cells from WT vs. miR-379KO mice using AGO2-immunopreciptation and CLASH (cross-linking, ligation, sequencing hybrids) and identified the redox protein thioredoxin and mitochondrial fission-1 protein. miR-379KO mice were protected from features of DKD as well as body weight loss associated with mitochondrial dysfunction, ER- and oxidative stress. These results reveal a role for miR-379 in DKD and metabolic processes via reducing adaptive mitophagy. Strategies targeting miR-379 could offer therapeutic options for DKD.

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CLASH RNAseq of RNP bound RNAs

Project description:We are investigating the possible role of ribonucleoprotein-bound RNAs on the pathogenesis of AML. This study uses antibody-pulldown of specific ribonucleoproteins followed by RANSeq. We hope to describe this interaction in wild type cells befire studying the effects of specific mutations This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

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Project description:BACKGROUND: MicroRNAs (miRNAs) are non-uniformly distributed in genomes and ~30% of the miRNAs in the human genome are clustered. In this study we have focused on the imprinted miRNA cluster miR-379/miR-656 on 14q32.31 (hereafter C14) to test their coordinated function. We have analyzed expression profile of >1000 human miRNAs in >1400 samples representing seven different human tissue types obtained from cancer patients along with matched and unmatched controls. RESULTS: We found 68% of the miRNAs in this cluster to be significantly downregulated in glioblastoma multiforme (GBM), 61% downregulated in kidney renal clear cell carcinoma (KIRC), 46% in breast invasive carcinoma (BRCA) and 14% in ovarian serous cystadenocarcinoma (OV). On a genome-wide scale C14 miRNAs accounted for 12-30% of the total downregulated miRNAs in different cancers. Pathway enrichment for the predicted targets of C14 miRNA was significant for cancer pathways, especially Glioma (p< 3.77x10??, FDR<0.005). The observed downregulation was confirmed in GBM patients by real-time PCR, where 79% of C14 miRNAs (34/43) showed downregulation. In GBM samples, hypermethylation at C14 locus (p<0.003) and downregulation of MEF2, a crucial transcription factor for the cluster was observed which likely contribute to the observed downregulation of the entire miRNA cluster. CONCLUSION: We provide compelling evidence that the entire C14 miRNA cluster is a tumor suppressor locus involved in multiple cancers, especially in GBM, and points toward a general mechanism of coordinated function for clustered miRNAs.

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