Characterization of a newly-identified myelinating oligodendroglial population expressing NDRG1 in the adult mouse central nervous system
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ABSTRACT:
PROVIDER: PRJNA453399 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7061210.fastq.gz | Fastqsanger.gz | |||
| SRR7061211.fastq.gz | Fastqsanger.gz | |||
| SRR7061212.fastq.gz | Fastqsanger.gz | |||
| SRR7061204_1.fastq.gz | Fastqsanger.gz | |||
| SRR7061204_2.fastq.gz | Fastqsanger.gz |
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Project description:Oligodendrocytes are the main myelinating and remyelinating cells of the central nervous system. We identified N-myc downstream regulated gene family member 1 (NDRG1) as a specific mature marker of the oligodendroglial lineage, regulated by mTORC2 kinase activity. By generating a transgenic reporter murine line, we managed to precisely characterize the effect of cuprizone-induced treatment on myelinating cells. We also created a new and adult-specific whole genome transcriptomic profile of the oligodendroglial lineage, from proliferative OPC (using P60 PDGFRa::GFP sorted cells), to pre-myelinating OL (using P60 PLP::GFP sorted cells) and then mature OL (using P60 NDRG1-eGFP sorted cells). This new reporter murine line and its associated RNA-Sequencing dataset could help us better understand the specific biology of adult myelinating oligodendrocytes, compared to previously published developmental tools and databases.
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2020-09-04 | PXD016043 | Pride
Project description:N-myc downstream regulated gene 1 (NDRG1) is a member of the NDRG family of intracellular proteins, and plays a central role in a wide range of biological processes including stress response, differentiation, and maintenance of the myelin sheath. The overexpression of NDRG1 is an indicator of poor prognosis in various pathological conditions. Here, we found that NDRG1 is an independent prognostic marker of poor outcome in breast cancer (BC). NDRG1 expression is regulated by a variety of molecular mechanisms, including transcriptional and post-translational control. In the present study, CRISPR-based inactivation of NDRG1 allowed us to demonstrate that this protein is required for breast cancer cell invasion, without affecting viability. We observed that different acute stress conditions converge on protein kinase C (PKC) activation driving enhanced NDRG1 expression through a signaling pathway that involves ROCK/AMPK/Akt kinases. This newly discovered mechanism was specific for NDRG1 as the expression of other NDRG members was not affected. Together, our results suggest that pathophysiological PKC-mediated activation of NDRG1 may be a response mechanism to metabolic stress and anticancer agents.
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Project description:N-myc downstream-regulated gene 1 (*NDRG1*) is induced by cellular stress such as hypoxia and DNA damage, and in humans, germ line mutations cause Charcot-Marie-Tooth disease. However, the roles of NDRG1 in the cell are not fully understood. Previously, NDRG1 was shown to mediate doxorubicin resistance under hypoxia, suggesting a role for NDRG1 in cell survival under these conditions. We found decreased apoptosis in doxorubicin-treated cells expressing NDRG1 shRNAs under normoxia, demonstrating a requirement for NDRG1 in apoptosis in breast epithelial cells under normal oxygen pressure. We further compared expression profiles in human breast epithelial cells ectopically over-expressing NDRG1 with cells expressing NDRG1 shRNAs in order to identify biological pathways where NDRG1 is involved. The results suggest that NDRG1 may have roles connected to vesicle transport. The previously reported roles of NDRG1 in apoptosis, myelin sheet maintenance, enhanced exocytosis in mast cells and in cellular responses to hypoxia, heavy metals, and androgen may all converge by NDRG1 having a role linked to vesicle transport.
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Project description:N-myc downstream-regulated gene 1 (*NDRG1*) is induced by cellular stress such as hypoxia and DNA damage, and in humans, germ line mutations cause Charcot-Marie-Tooth disease. However, the roles of NDRG1 in the cell are not fully understood. Previously, NDRG1 was shown to mediate doxorubicin resistance under hypoxia, suggesting a role for NDRG1 in cell survival under these conditions. We found decreased apoptosis in doxorubicin-treated cells expressing NDRG1 shRNAs under normoxia, demonstrating a requirement for NDRG1 in apoptosis in breast epithelial cells under normal oxygen pressure. We further compared expression profiles in human breast epithelial cells ectopically over-expressing NDRG1 with cells expressing NDRG1 shRNAs in order to identify biological pathways where NDRG1 is involved. The results suggest that NDRG1 may have roles connected to vesicle transport. The previously reported roles of NDRG1 in apoptosis, myelin sheet maintenance, enhanced exocytosis in mast cells and in cellular responses to hypoxia, heavy metals, and androgen may all converge by NDRG1 having a role linked to vesicle transport. SUM102 and ME16C2 stably transduced with siRNA against NDRG1 compared with empty vector control ZR-75-1 stably transduced with NDRG1 overexpression construct compared with empty vector control Two condition design
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Project description:We showed that the composition of the nuclear lamina changes with the differentiation state of oligodendrocyte lineage cells, with Lamin B highly expressed in progenitor cells and Lamin A highly expressed in mature oligodendrocytes. The genetic deletion of LMNA in mice results in the onset of a progressive motor phenotype in adult mice. We performed ATAC-Seq in myelinating Oligodendrocytes expressing the myelin marker NDRG1-EGFP ( Marechal et al., 2021) in the presence or absence of LMNA. The goal is to identify regions of chromatin accessibility that distinguish the LMNA KO mutant cells from the WT.
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Project description:The generation of myelinating cells in the central nervous system (CNS) requires the initiation of specific gene-expression programs in oligodendrocytes. We reasoned that miRNAs could play an important role in this process by regulating critical developmental genes. Microarray profiling of cultured oligodendrocytes identifies the miR-17~92 family of miRNA cluster as highly enriched miRNAs in oligodendrocytes.We specifically deleted the miR-17~92 cluster in oligodendrocytes using the 2´3´-cyclic nucleotide 3´-phosphodiesterase (CNP)-Cre mice. Absence of miR-17~92 leads to a reduction of oligodendrocyte number in vivo and we find that the expression of these miRNAs in primary cultures of oligodendrocytes promotes cell proliferation by influencing Akt signalling. Together, these results suggest that the miRNA pathway is essential in determining oligodendroglial cell number and that the miR-17~92 cluster is crucial in this process.
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