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Mus musculus

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

PROVIDER: PRJNA229148 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1032330_1.fastq.gz	Fastqsanger.gz
	SRR1032330_2.fastq.gz	Fastqsanger.gz
	SRR1032340_1.fastq.gz	Fastqsanger.gz
	SRR1032340_2.fastq.gz	Fastqsanger.gz
	SRR1032331_1.fastq.gz	Fastqsanger.gz

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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

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

2014-03-07 | GSE52514 | GEO

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

2019-03-01 | GSE98089 | GEO

The transcription factor TAL1 and the miR-17-92 cluster establish a regulatory loop

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.

2021-09-09 | PXD018052 | Pride

miR-17-92 cluster regulates adult hippocampal neurogenesis, anxiety and depression

Project description:Emerging evidence has shown that noncoding RNAs, particularly microRNAs (miRNAs), contribute to the pathogenesis of mood and anxiety disorders, although the molecular mechanisms are poorly understood. Here we show altered levels of miR-17-92 in adult hippocampal neural progenitors have a significant impact in neurogenesis and anxiety- and depression-related behaviors in mice. miR-17-92 deletion in adult neural progenitors causes a decrease, while its overexpression an increase of neurogenesis in the dentate gyrus, through regulating genes in the glucocorticoid pathway, especially serum- and glucocorticoid-inducible protein kinase-1 (Sgk1). miR-17-92 knockout mice show anxiety- and depression-like behaviors, whereas miR-17-92 overexpressing mice exhibit anxiolytic and antidepression-like behaviors. Furthermore, we show that miR-17-92 expression in the adult mouse hippocampus responds to chronic stress, and miR-17-92 rescues proliferation defects, induced by corticosterone, in hippocampal neural progenitors. Our study uncovers a crucial role for miR-17-92 in adult neural progenitors to regulate neurogenesis and anxiety- and depression-like behaviors.

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Ago2 PAR-CLIP analysis of Abelson kinase transformed murine B cell progenitors

Project description:Knockout of the ubiquitously expressed microRNA-17~92 cluster in mice produces a lethal developmental defect and blocked B lymphopoiesis. We validated the equally widely expressed Bcl2l11 gene as joint target of miR-17~92 cluster members. Bcl2l11 encodes the pro-apoptotic protein BIM, central to life-death decisions in most mammalian cells. To study the contribution of miR-17~92:Bim interaction to miR-17~92 overall function, we set up a system of conditional mutagenesis of the Bim 3’UTR in mice. Ago2 Photoactivatable-Ribonucleoside Cross-linking and Immunoprecipitation (AGO2 PAR-CLIP) allowed us to assess whether the seed match mutations introduced into the Bim 3’UTR in vivo indeed precluded interaction with the miRNAs of the 17~92 cluster. This analysis was done in Abelson Virus transformed B cell progenitors which we generated from wild type and Bim3’UTRmut/mut E14.5 fetal livers, knowing that these cells express both BIM and miR-17~92, can be expanded to large numbers and incorporate 4-thiouridine sufficiently well. Focusing on 21 nt windows around the 9 putative miR-17~92 seed matches in the Bim 3’UTR and excluding reads lacking T-to-C transitions, we we verified that the introduced mutationsare functional, and we discovered differential seed match coverage in the wild type, with one miR-19 seed match co-dominating with two miR-92 seed matches, while in the mutant 3’UTR miR-17~92 binding was completely abolished. These results demonstrate functionality and efficiency of our genetically engineered mouse model for in vivo conditional seed-match inactivation. These results demonstrate functionality and efficiency of our genetically engineered mouse model for in vivo conditional seed-match inactivation.

2019-11-13 | GSE124605 | GEO

The non-coding RNA miR-17∼92 is a central mediator of T cell costimulation [I]

Project description:To unravel the molecular mechanism underlying miR-17∼92 costimulatory function, we performed RNA-seq on CD4+ T cells from mice lacking miR-17∼92 in T cell, wildtype mice and mice overexpressing miR-17∼92 in T cells, in naïve state or activated vitro for 24h and 48h.

2022-09-08 | GSE140525 | GEO

The non-coding RNA miR-17∼92 is a central mediator of T cell costimulation [II]

Project description:To unravel the molecular mechanism underlying miR-17∼92 costimulatory function, we performed RNA-seq on CD4+ T cells from mice lacking miR-17∼92 in T cell, wildtype mice, mice overexpressing miR-17∼92 in T cells , mice with a constitutive knockout of CD28, and rescue mice, in naïve state or activated vitro for 24h.

2022-09-08 | GSE140564 | GEO

Mus musculus

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

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Mus musculus

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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