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Pri-miRNA identification by generating a Drosha null/conditional-null mouse model.

ABSTRACT: We report the ability of the Drosha null/conditional-null mouse model to enable the identification of pri-miRNA transcripts. The conditional-null allele of Drosha phenocopies the null allele both in mESC and in mice, upon conversion to the null state with Cre. Examination of the effects of Drosha deficiency in mouse embryonic stem cells.

ORGANISM(S): Mus musculus

SUBMITTER: Artemis Hatzigeorgiou

PROVIDER: E-GEOD-55735 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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microTSS: accurate microRNA transcription start site identification reveals a significant number of divergent pri-miRNAs.

Georgakilas Georgios G Vlachos Ioannis S IS Paraskevopoulou Maria D MD Yang Peter P Zhang Yuhong Y Economides Aris N AN Hatzigeorgiou Artemis G AG

Nature communications 20141210

A large fraction of microRNAs (miRNAs) are derived from intergenic non-coding loci and the identification of their promoters remains 'elusive'. Here, we present microTSS, a machine-learning algorithm that provides highly accurate, single-nucleotide resolution predictions for intergenic miRNA transcription start sites (TSSs). MicroTSS integrates high-resolution RNA-sequencing data with active transcription marks derived from chromatin immunoprecipitation and DNase-sequencing to enable the charact ...[more]

PMID: 25492647

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Pri-miRNA identification by generating a Drosha null/conditional-null mouse model.

Project description:We report the ability of the Drosha null/conditional-null mouse model to enable the identification of pri-miRNA transcripts. The conditional-null allele of Drosha phenocopies the null allele both in mESC and in mice, upon conversion to the null state with Cre.

2015-02-09 | GSE55735 | GEO

Transcriptome wide identification of Dicer binding in human and C. elegans reveals a variety of substrates (HEK RNA-Seq)

Project description:Dicer is a deeply conserved endoribonuclease with key functions in small RNA biogenesis. Here we employed PAR-CLIP/iPAR-CLIP to identify direct Dicer binding sites in the transcriptomes of human cells and human. We found hundreds of novel miRNAs and non-canonical Dicer substrates with high sensitivity. Small RNA production depended on structure of the binding site and is globally biased towards the 5' arm of hairpins. Unexpectedly, in both species Dicer bound numerous hairpins inside mRNAs without observable small RNA production. Our data revealed ~100 mRNAs of protein coding genes to be targeted in both human and worm. These mRNAs significantly overlapped with the RNAi pathway. We also, unexpectedly, found that mitochondrial transcripts are Dicer targets in both species. We demonstrate functional consequences of Dicer binding by perturbation analysis. Taken together,we provide the first genome-wide catalog of direct Dicer targets. Our results suggest widespread function outside of miRNA biogenesis. Regulatory impact of Dicer binding was assessed by knock down experiments in human HEK293 cells. Drosha knockdown and mock transfections were used as controls. In total 3 samples.

2014-11-20 | E-GEOD-55326 | biostudies-arrayexpress

Transciptome profiling of RNaseIII null cells reconstituted with Drosha

Project description:To assess the impact of Drosha reconstitution on the overall transcriptome of RNaseIII null cells.

2017-06-28 | GSE89790 | GEO

Gene expression microarray of: 1) Cbx1 null versus revertant (single allele expression), and 2) Jarid2 null versus revertant, mutant mouse ES cells.

Project description:Gene expression as measured by microarray, in order to determine the cohort of differentially expressed genes, in each of two different mutant ES cell lines (Cbx1 and Jarid2), each comparing the respective null mutant ES cells to revertant (single allele expression) mutant ES cells. Hybridization was performed concurrently. Experiments are: 1) Cbx1 null mutant (Cbx1^tm1a(EUCOMM)Wtsi/Cbx1^tm1Wcs) compared to revertant mutant (Cbx1^tm1c(EUCOMM)Wtsi/Cbx1^tm1Wcs) ES cell lines (n=6 per genotype). 2) Jarid2 null mutant (Jarid2^tm1a(KOMP)Wtsi/Jarid2tm1Wcs) compared to revertant mutant (Jarid2^tm1c(KOMP)Wtsi/Jarid2tm1Wcs) ES cell lines (n=3 per genotype). Biological replicates (individual ES clones) were used. Parental ES cell lines are from the International Knockout Mouse Consortium (IKMC - EUCOMM and KOMP-CSD programmes) and were modified to generate null ES cells using bi-allelic gene targeting with a targeted trapping vector generated by re-purposing Intermediate Vectors from the IKMC resource. Revertant ES cell lines were generated by using Flp recombinase to revert the IKMC tm1a null allele to the conditional tm1c allele, in order to reinstate gene expression from one allele. The tm1Wcs allele is constitutive null.

2017-09-12 | E-MTAB-5930 | biostudies-arrayexpress

Mus musculus

Project description:Pri-miRNA identification by generating a Drosha null/conditional-null mouse model.

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Timecourse gene expression microarray analysis of bi-allelic targeted Setdb1 mutant mouse ES cells, comparing cells with one inducible conditional (floxed) null allele and a second constitutive null allele, to control mouse ES cell lines.

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2017-09-12 | E-MTAB-5931 | biostudies-arrayexpress

Expression profiling of secondary wild type (WT) and Ezh2-null murine MLL-AF9 AML

Project description:We evaluated gene expression changes in secondary recipient murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of a homozygous conditional allele for Ezh2, a component of the Polycomb Repressive Complex2. For WT cells, 4 biological replicates were hybridized. For Ezh2-null cells, 5 biological replicates were hybridized.

2012-02-22 | E-GEOD-34961 | biostudies-arrayexpress

Functional evidence that Drosha over-expression in cervical squamous cell carcinoma affects cell phenotype and microRNA profiles [miRNA]

Project description:Comparison of miRNA expression profiles in cervical carcinoma cell lines to study the effects of Drosha expression levels Analyzed global miRNA expression profiles from 18 samples (7 samples in duplicate, 4 single sample) representing cervical carcinoma cell lines with either relative Drosha over-expression (Cluster 2) or Drosha under-expression (Cluster 1), due to wild-type expression in those cell lines or manipulation with RNAi.

2011-05-25 | E-GEOD-26175 | biostudies-arrayexpress

An efficient method for generation of bi-allelic null mutant mouse embryonic stem cell lines and its application for investigating epigenetic modifiers

Project description:Mouse embryonic stem (ES) cells are a popular model system to study biological processes, though uncovering recessive phenotypes requires inactivating both alleles. Building upon resources from the International Knockout Mouse Consortium (IKMC), we developed a targeting vector for second allele inactivation in conditional-ready IKMC ‘knockout-first’ ES cell lines. We applied our technology to several epigenetic regulators, recovering bi-allelic targeted clones with a high efficiency of 60%, and used Flp recombinase to restore expression in two null cell lines to demonstrate how our system confirms causality through mutant phenotype reversion. We designed our strategy to select against re targeting the ‘knockout-first’ allele, and identify essential genes in ES cells, including the histone methyltransferase Setdb1. For confirmation, we exploited the flexibility of our system, enabling tamoxifen inducible conditional gene ablation while controlling for genetic background and tamoxifen effects. Setdb1 ablated ES cells exhibit severe growth inhibition, which is not rescued by exogenous Nanog expression or culturing in naive pluripotency ‘2i’ media, suggesting that the self-renewal defect is mediated through pluripotency network independent pathways. Our strategy to generate null mutant mouse ES cells is applicable to thousands of genes and repurposes existing IKMC Intermediate Vectors.

2017-09-02 | GSE31777 | GEO

scRNA-seq of E14 Bax null, Atoh7 null, and Bax null/Atoh7 null retinas

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