Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA268642 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1663680.fastq.gz | Fastqsanger.gz | |||
| SRR1663681.fastq.gz | Fastqsanger.gz | |||
| SRR1663673.fastq.gz | Fastqsanger.gz | |||
| SRR1663674.fastq.gz | Fastqsanger.gz | |||
| SRR1663675.fastq.gz | Fastqsanger.gz |
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Project description:RNA sequencing of allelic series of miR-17~92 mutant embryos.
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2015-02-02 | E-GEOD-63813 | biostudies-arrayexpress
Project description:We report the generation of an allelic series of miR-17~92 mutant mice, each carrying the targeted deletion of specific miRNA families encoded by the cluster. We integrate the phenotypic characterization of these strains with RNA-seq analysis showing the consequences of selective miRNA inactivation on gene expression in the developing embryo.
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Project description:BCR repertoire analysis of B cells from wild type, miR-17~92 Tg and miR-17~92 CD19Cre tKO mice
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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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Project description:Ribosome Profiling analysis of Follicular B (FoB) cells purified from WT, miR-17~92 transgenic and miR-17-92 tKO mice
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Project description:Differential gene expression in nephron progenitors lacking miR-17~92
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Project description:A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain the gene expression pattern during hematopoiesis. In this network transcription factors regulate each other and are involved in regulatory loops with microRNAs.The microRNA cluster miR-17-92 is located within the MIR17HG gene and encodes for six mature microRNAs. It is important for hematopoietic differentiation and plays a central role in malignant disease. However, the transcription factors downstream of miR-17-92 are largely elusive and the transcriptional regulation of miR-17-92 is not fully understood. Here we show that miR-17-92 forms a regulatory loop with the transcription factor TAL1. The miR-17-92 cluster inhibits expression of TAL1 and indirectly leads to decreased stability of the TAL1 transcriptional complex. We found that TAL1 and its heterodimerization partner E47 regulate miR-17-92 transcriptionally. Furthermore, miR-17-92 negatively influences erythroid differentiation, a process that depends on gene activation by the TAL1 complex. Our data give example of how transcription factor activity is fine-tuned during normal hematopoiesis. We postulate that disturbance of the regulatory loop between TAL1 and the miR-17-92 cluster could be an important step in cancer development and progression.
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