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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE140525 | GEO | 2022/09/08

REPOSITORIES: GEO

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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

Ribosome Profiling analysis of Follicular B (FoB) cells purified from WT, miR-17~92 transgenic and miR-17-92 tKO mice

Project description:We have generated a miR-17~92 transgene and fl/fl allele whose expression can be turned on and off conditionally by Cre recombinase. The mice were crossed to CD19-Cre mice to turn on and off the expression of miR-17~92 specifically in B cells and stimulated LPS/IL-4 for 25.5hr. tKO mice were generated in the miR-106a-363-/-;miR-106b-25-/- background, so that all three homologous cluster of miR-17~92 family miRNAs are deleted in B cells.

2017-03-08 | GSE83684 | GEO

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.

2019-05-20 | GSE130282 | GEO

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.

2016-12-09 | GSE83636 | 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-17-92/106b regulate beta cell mitotic checkpoint and insulin secretion

Project description:Adult beta cells in the pancreas are the sole source of insulin in our body. Beta cell loss or increased demand for insulin, impose metabolic challenges because adult beta cells are generally quiescent and infrequently re-enter the cell division cycle. miR-17-92/106b is a family of proto-oncogene microRNAs, that regulate proliferation in normal tissues and in cancer. Here, we employ mouse genetics to demonstrate a critical role for miR-17-92/106b in glucose homeostasis and in controlling insulin secretion. Mass spectrometry analysis was performed on miR-17-92LoxP/LoxP;106-25-/- MEF lysate, without or with CRE-Adenovirus. miR-17-92LoxP/LoxP;106-25+/+ MEFs with GFP-Adenovirus served as controls. We demonstrate that miR-17-92/106b regulate the adult beta cell mitotic checkpoint and that miR-17-92/106b deficiency results in reduction in beta cell mass in-vivo. Furthermore, protein kinase A (PKA) is a new relevant molecular pathway downstream of miR-17-92/106b in control of adult beta cell division and glucose homeostasis. Therefore, contributes to the understanding of proto-oncogene miRNAs in the normal, untransformed endocrine pancreas, and illustrates new genetic means for regulation of beta cell mitosis and function by non-coding RNAs.

2019-06-17 | PXD012610 | Pride

Follicular B (FoB) cells purified from miR-17-92 tKO mice

Project description:We have generated a miR-17~92 fl/fl allele whose expression can be turned off conditionally by Cre recombinase in the miR-106a-363-/-;miR-106b-25-/- background. The mice were crossed to CD19-Cre mice to turn off the expression of miR-17~92 specifically in B cells.

2014-04-01 | GSE56376 | GEO

Analysis of mir-17~92 targets in motor neurons

Project description:To identify mir-17~92 targets in MNs, a set of target candidate genes from the intersection of upregulated genes found only in the mir-17~92 KO MNs that were predicted to be direct targets of mir-17~92 by TargetScan.

2015-04-14 | GSE67795 | GEO

Follicular B (FoB) cells purified from miR-17-92 transgenic mice

Project description:We have generated a miR-17-92 transgenic allele (termed miR-17-92 Tg) whose expression can be turned on conditionally by Cre recombinase (Xiao et al, Nature Immunology, 9:405-14, 2008). The mice were crossed to CD19-Cre mice to turn on the transgene expression specifically in B cells.

2011-07-22 | GSE30877 | GEO

The role of microRNA miR-17-92 in MYC oncogene addiction

Project description:miR-17-92 mediates the MYC oncogene addiction in a conditional mouse lymphoma model. To identify targets of miR-17-92 in this model, miR-17-92 was expressed in the conditional lymphoma cell lines using MSCV-puro.

2014-05-29 | GSE57507 | GEO

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