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MiRNA expression in E18.5 murine total lung tissue

ABSTRACT: miRNA expression in E18.5 murine total lung tissue

PROVIDER: PRJNA509483 | ENA |

REPOSITORIES: ENA

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miRNA expression in E18.5 murine total lung tissue

Project description:Knockout of the ubiquitously expressed microRNA-17~92 cluster in mice produces a lethal developmental lung defect. We validated the equally widely expressed pro-apoptotic Bim gene as joint target of miR-17~92 cluster members. 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. Blocking miR-17~92:Bim interaction early in development phenocopied the lethal lung phenotype of miR-17~92 ablation. Thus, despite hundreds of overall predicted targets vital miRNA functions can be mediated by a single target gene.

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MiRNA expression in embryonic murine hepatocytes versus murine cholangiocytes at E18.5

Project description:Differentially expressed miRNAs between hepatocytes (GFP-neg in SOX9-GFP mice) and cholangiocytes (GFP-pos in SOX9-GFP mice) in mice at E18.5. We want to compare miRNA population in biliary cells and parenchymal cells (depleted from hematopoietic cells) during liver development. Cholangiocytes specifically express the transcription factor Sox9. This enables to separate cholangiocytes from the rest of the liver parenchyma by FACS from Sox9-GFP transgenic mice. In conclusion, we want to compare miRNA population in our GFP+ cells (cholangiocytes) and our GFP- cells (liver parenchyma depleted from hematopoietic cells).

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Single-cell ATAC sequencing of murine dermal cells at E14.5 and E18.5

Project description:Single Cell open chromatin fragments genome-wide using Chromium Single Cell ATAC kit from murine dermal cells at E14.5 and E18.5

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Total RNA-seq of barrelette neurons at E14.5, E18.5 and P4

Project description:Bulk total RNA-seq using the ovation soloSeq protocol in mouse barrelette neurons at E14.5, E18.5 and P4 in different genotypes.

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Quantitative proteomics analysis of lung tissue from E18.5 embryos with mesenchymal deletion of VLK

Project description:Vertebrate lonesome kinase (VLK) is the only known secreted tyrosine kinase and responsible for the phosphorylation of a broad range of secretory pathway-resident and extracellular matrix proteins. However, its cell-type specific functions in vivo are still largely unknown. Therefore, we generated mice with a mesenchyme-specific knockout of the VLK gene (protein kinase domain containing, cytoplasmic (Pkdcc)). Most of the homozygous mice die shortly after birth, most likely as a consequence of their lung abnormalities and consequent respiratory failure. E18.5 embryonic lungs showed a reduction of alveolar type II cells, smaller bronchi, and an increased lung tissue density. Global mass spectrometry-based quantitative proteomics identified 112 proteins with significantly and at least 1.5fold differential abundance between genotypes. Twenty-five of these had been assigned to the extracellular region and 15 to the mouse matrisome. Specifically, fibromodulin and matrilin 4, which are involved in extracellular matrix organization, were significantly more abundant in lungs from Pkdcc knockout embryos. These results support a role for mesenchyme-derived VLK in lung development through regulation of matrix dynamics and the resulting non-cell-autonomous modulation of alveolar epithelial cell differentiation.

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Gene expression analysis of control and Dnmt1 CKO E18.5 murine lungs.

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Expression data from Tnrc6a (GW182) mutant E18.5 lungs

Project description:GW182 (Tnrc6a) is a key component of RISC (miRNA-Induced Silencing Complex) that plays a critical role in miRNA-mediated gene silencing. Here, we show that GW182 is expressed in airway multiciliated cells (MCCs), and that gene-trap disruption of GW182 leads to defective multicilia formation and downregulation of broad miRNA targets To investigate roles of GW182 in airway multiciliated cells (MCCc), we assessed changes in mRNA expression in E18.5 Tnrc6a mutant lungs using microarrays (Affymetrix).

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