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ATAC-seq in myelinating oligodendrocytes from wt and Lmna knockout mice

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE190404 | GEO | 2023/06/01

REPOSITORIES: GEO

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RNA-seq of myelinating oligodendrocytes in Lmna wt and knockout mice

Project description:We showed that the composition of the nucler 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 oligodendrocytes results in the onset of a progressive motor phenotype in adult mice. We performed RNA-Seq in myelinating oligodendrocytes expressing the reporter myelin marker NDRG1-EGFP ( Marechal et al., 2021) in the presence or absence of LMNA. The goal is to identify the transcriptome profile in mice LMNA ablated cells compared to the controls.

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Induction of Myelinating Oligodendrocytes in Human Cortical Spheroids

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Induction of Myelinating Oligodendrocytes in Human Cortical Spheroids

Project description:Organoid technologies provide an accessible system in which to examine the generation, self-organization,and 3-dimensional cellular interactions during development of the human cerebral cortex. However, oligodendrocytes, the myelinating glia of the central nervous system and third major neural cell type, are conspicuously absent from current protocols. Here we reproducibly generate human oligodendrocytes and myelin in pluripotent stem cell-derived cortical spheroids. Transcriptional and immunohistochemical analysis of the spheroids demonstrates molecular features consistent with maturing human oligodendrocytes within 14 weeks of culture, including expression of MyRF, PLP1, and MBP proteins. Histological analysis by electron microscopy shows initial wrapping of human neuronal axons with myelin by 20 weeks and maturation to compact myelin by 30 weeks in culture. Treatment of spheroids with previously identified promyelinating drugs enhances the rate and extent of human oligodendrocyte generation and myelination. Furthermore, generation of spheroids from patients with a severe genetic myelin disorder, Pelizaeus-Merzbacher disease, demonstrates the ability to recapitulate human disease phenotypes, which were in turn improved with both pharmacologic and CRISPR-based approaches. Collectively, these 3-dimensional, multi-lineage cortical spheroids provide a versatile platform to observe and perturb the complex cellular interactions that occur during developmental myelination of the brain and offer new opportunities for disease modeling and therapeutic development in human tissue.

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Gene expression profiles of livers from male LMNA+/+, LMNA flx/+, and LMNA flx/flx; Alb-Cre+ C57BL/6 mice fed normal chow or high fat diet

Project description:To investigate the molecular basis for male-specific steatohepatitis in Lamin A/C-deficient livers, microarray gene expression analysis was performed on total liver RNA isolated from 26- to 39-week-old, male LMNA+/+, LMNA flx/+, and LMNA flx/flx; Alb-Cre+ C57BL/6 mice fed either normal chow (NC) or high fat diet plus carbohydrate-supplemented water (HFD). Lamins are nuclear intermediate filament proteins that comprise the major components of the nuclear lamina in metazoan cells. Mutations in LMNA, which encodes lamins A/C, cause diseases termed laminopathies, including lipodystrophy, cardiomyopathy, and premature aging. The lamin A/C mutation-associated Dunnigan familial partial lipodystrophy is typically accompanied by fatty liver disease. The role of lamins in the liver is unknown, and it is unclear whether laminopathy-associated liver disease is due to primary hepatocyte defects or systemic alterations. To address these questions, mice carrying a hepatocyte-specific deletion of Lmna (KO mice) were generated. KO hepatocytes manifested abnormal nuclear morphology, and KO mice developed spontaneous male-selective hepatosteatosis, with increased susceptibility to high fat diet-induced steatohepatitis and fibrosis. The molecular mechanism by which liver-specific Lamin A/C deficiency induces male-specific steatohepatitis is unknown. The microarray data presented here demonstrates that hepatic Lmna deficiency is associated with upregulated expression of fatty acid transporters, lipid biosynthetic enzymes, lipid-droplet associated proteins, and interferon-regulated genes and other pro-inflammatory mediators.

2017-01-16 | GSE93643 | GEO

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