Candidatus Caldatribacterium californiense OP9-cSCG
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA178520 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR609896.fastq.gz | Fastqsanger.gz |
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Project description:In the bone marrow B cell development occurs in initimate and essential association with stromal cells. Known effects of stromal cells on B cell development have been shown to be mediated through direct contact and by soluble factors produced by stromal cells. Our findings suggest that cell-nonautonomous Hh signaling may play an important role in B cell lymphopoiesis. We therefore interrogated OP9 stromal cells for Hh-dependent transcripts that may confer B lymphopoietic identity. We generated OP9 stromal cells deficient in Hh signaling through targeting the non-redundant, pathway-obligate GPCR Smoothened. OP9 cells were transduced with RNAi pLKO.1-Puro lentiviral particles expressing a scrambled control shRNA (NT) or shRNA targeting Smoothened (Smo-kd). RNA from stable NT and Smo-kd OP9 cells were isolated in triplicate and global changes in transcripts were analyzed using the Affymetrix Mouse Exon 1.0 ST gene chip.
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Project description:Mesenchymal stem cells (MSCs), being multipotent progenitors, have received the most widespread regulatory approval for commercialization as off-the-shelf cell therapies. Understanding the key molecular mechanisms regulating MSC differentiation is crucial for advancing their clinical utilization. Drosha is a critical enzyme in miRNA biogenesis. Despite its established role in diverse physiological processes, the involvement of Drosha in the adipogenic differentiation of MSCs has not been previously characterized. Here the role of Drosha/microRNA pathway in regulating the adipogenesis of OP9, a MSC derived from mouse bone marrow stroma, is characterized. Knocking down Drosha in OP9 significantly reduced its adipogenic capacity. Small RNA-seq analysis revealed that miR-204 and miR-15b were significantly downregulated in the adipogenic process of OP9 cells upon Drosha removal. Further exploration showed that the activity of ERK1/2 was significantly increased in Drosha KO OP9 cells, which was proved can suppress the transcriptional activity of PPARγ. Introducing miR-204 or miR-15b into OP9 cells significantly enhanced their adipogenic capacity and partially rescued the adipogenic defects caused by Drosha knockout. Mechanistically, miR-15b regulates ERK mediated adpogenic differentiation via repressing NRP2. Our data demonstrate that the Drosha/miR-15/NRP2 axis regulates adipogenesis of MSCs by modulating the ERK/PPARγ pathway. This discovery unveils a previously unappreciated molecular mechanism governing MSC adipogenic differentiation and suggests new avenues for exploring the therapeutic potential of MSCs.
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Project description:Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. In this study, we aimed to establish a comprehensive compendium of the long non-coding RNA transcriptome under control of Notch signaling. For this purpose, we measured the transcriptional response of all protein coding genes and long non-coding RNAs upon pharmacological Notch inhibition in the human T-cell acute lymphoblastic leukemia cell line CUTLL1 using RNA-sequencing. Similar Notch dependent profiles were established for normal human CD34+ thymic T-cell progenitors exposed to Notch signaling activity in vivo. In addition, we generated long non-coding RNA expression profiles (array data) from GSI treated T-ALL cell lines, ex vivo isolated Notch active CD34+ and Notch inactive CD4+CD8+ thymocytes and from a primary cohort of 15 T-cell acute lymphoblastic leukemia patients with known NOTCH1 mutation status. Integration of these expression datasets with publically available Notch1 ChIP-sequencing data resulted in the identification of long non-coding RNAs directly regulated by Notch activity in normal and malignant T-cell context. Given the central role of Notch in T-cell acute lymphoblastic leukemia oncogenesis, these data pave the way towards development of novel therapeutic strategies that target hyperactive Notch1 signaling in human T-cell acute lymphoblastic leukemia. CD34+ cells of 2 healthy donors are cultured on a OP9-GFP or OP9-DLL1 feeder layer.
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