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Genome-wide analysis of chromatin profile in astrocytes isolated from EAE mice transduced with astrocyte-specific Mafg-targeting or non-targeting lentiviruses [ATAC-seq]

ABSTRACT: Genome-wide analysis of chromatin profile in astrocytes isolated from EAE mice transduced with astrocyte-specific Mafg-targeting or non-targeting lentiviruses [ATAC-seq]

PROVIDER: PRJNA531925 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8878114_1.fastq.gz	Fastqsanger.gz
	SRR8878114_2.fastq.gz	Fastqsanger.gz
	SRR8878115_1.fastq.gz	Fastqsanger.gz
	SRR8878115_2.fastq.gz	Fastqsanger.gz
	SRR8878116_1.fastq.gz	Fastqsanger.gz

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Genome-wide analysis of chromatin profile in astrocytes isolated from EAE mice transduced with astrocyte-specific Mafg-targeting or non-targeting lentiviruses [ATAC-seq]

Project description:Multiple sclerosis (MS) is an autoimmune neurologic disease leading to demyelination and neurologic dysfunction controlled by both genetic and environmental factors. In addition to CNS-infiltrating immune cells, CNS-resident cells, such as astrocytes, are thought to play an important role in MS pathogenesis. However, a comprehensive understanding of the extent to which gene expression is disrupted in astrocytes is not known. Here, we implement single-cell RNA sequencing, in vivo genetic perturbations, cell-specific RNA profiling by Ribotag, as well as single-cell RNA sequencing of human MS patient samples to identify a transcriptional regulatory network in astrocytes that controls the pathogenesis of EAE and potentially, MS. We defined an astrocyte subpopulation characterized by expression of the small Maf protein, MAFG, which represses NRF2-driven antioxidant mechanisms and promotes EAE pathogenesis. Mechanistically, MAFG suppresses NRF2-dependent antioxidant genetic programs by cooperating with its cofactor, MAT2a, to promote DNA methylation in the context of CNS inflammation, which in turn increases pathogenic signaling processes in astrocytes. MAFG/MAT2a astrocytes are controlled by GM-CSF signaling, which drives EAE pathogenesis and MAFG expression. MAFG is activated in astrocytes derived from MS patients, which are characterized by DNA methylation programs, pro-inflammatory signaling processes including GM-CSF signaling, and repressed NRF2 activation. Together, these data create a transcriptional and epigenetic framework to analyze CNS inflammation in MS and may provide new therapeutic targets. We report MAFG regulation of pathogenic activities in astrocytes during EAE.

2020-02-12 | GSE129608 | GEO

Genome-wide analysis of DNA methylation profile in astrocytes isolated from naïve mice or EAE mice transduced with astrocyte-specific Mafg-targeting or non-targeting lentiviruses [WGBS]

Project description:We report MAFG regulation of DNA methylation in astrocytes during EAE. Multiple sclerosis (MS) is an autoimmune neurologic disease leading to demyelination and neurologic dysfunction controlled by both genetic and environmental factors. In addition to CNS-infiltrating immune cells, CNS-resident cells, such as astrocytes, are thought to play an important role in MS pathogenesis. However, a comprehensive understanding of the extent to which gene expression is disrupted in astrocytes is not known. Here, we implement single-cell RNA sequencing, in vivo genetic perturbations, cell-specific RNA profiling by Ribotag, as well as single-cell RNA sequencing of human MS patient samples to identify a transcriptional regulatory network in astrocytes that controls the pathogenesis of EAE and potentially, MS. We defined an astrocyte subpopulation characterized by expression of the small Maf protein, MAFG, which represses NRF2-driven antioxidant mechanisms and promotes EAE pathogenesis. Mechanistically, MAFG suppresses NRF2-dependent antioxidant genetic programs by cooperating with its cofactor, MAT2a, to promote DNA methylation in the context of CNS inflammation, which in turn increases pathogenic signaling processes in astrocytes. MAFG/MAT2a astrocytes are controlled by GM-CSF signaling, which drives EAE pathogenesis and MAFG expression. MAFG is activated in astrocytes derived from MS patients, which are characterized by DNA methylation programs, pro-inflammatory signaling processes including GM-CSF signaling, and repressed NRF2 activation. Together, these data create a transcriptional and epigenetic framework to analyze CNS inflammation in MS and may provide new therapeutic targets.

2020-02-12 | GSE129606 | GEO

Genome-wide analysis of DNA methylation profile in astrocytes isolated from naïve mice or EAE mice transduced with astrocyte-specific Mafg-targeting or non-targeting lentiviruses [WGBS]

Project description:Genome-wide analysis of DNA methylation profile in astrocytes isolated from naïve mice or EAE mice transduced with astrocyte-specific Mafg-targeting or non-targeting lentiviruses [WGBS]

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Genome-wide analysis of chromatin profile in astrocytes isolated from EAE mice transduced with astrocyte-specific Xbp1-targeting or non-targeting lentiviruses.

Project description:Genome-wide analysis of chromatin profile in astrocytes isolated from EAE mice transduced with astrocyte-specific Xbp1-targeting or non-targeting lentiviruses.

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Genome-wide analysis of MAFG binding in astrocytes during EAE [ChIP-seq]

Project description:We report MAFG recruitment to ARE elements in astrocytes during EAE compared to naïve mice Multiple sclerosis (MS) is an autoimmune neurologic disease leading to demyelination and neurologic dysfunction controlled by both genetic and environmental factors. In addition to CNS-infiltrating immune cells, CNS-resident cells, such as astrocytes, are thought to play an important role in MS pathogenesis. However, a comprehensive understanding of the extent to which gene expression is disrupted in astrocytes is not known. Here, we implement single-cell RNA sequencing, in vivo genetic perturbations, cell-specific RNA profiling by Ribotag, as well as single-cell RNA sequencing of human MS patient samples to identify a transcriptional regulatory network in astrocytes that controls the pathogenesis of EAE and potentially, MS. We defined an astrocyte subpopulation characterized by expression of the small Maf protein, MAFG, which represses NRF2-driven antioxidant mechanisms and promotes EAE pathogenesis. Mechanistically, MAFG suppresses NRF2-dependent antioxidant genetic programs by cooperating with its cofactor, MAT2a, to promote DNA methylation in the context of CNS inflammation, which in turn increases pathogenic signaling processes in astrocytes. MAFG/MAT2a astrocytes are controlled by GM-CSF signaling, which drives EAE pathogenesis and MAFG expression. MAFG is activated in astrocytes derived from MS patients, which are characterized by DNA methylation programs, pro-inflammatory signaling processes including GM-CSF signaling, and repressed NRF2 activation. Together, these data create a transcriptional and epigenetic framework to analyze CNS inflammation in MS and may provide new therapeutic targets.

2020-02-12 | GSE129607 | GEO

Genome-wide analysis of chromatin profile in astrocytes isolated from EAE mice transduced with astrocyte-specific Xbp1-targeting or non-targeting lentiviruses.

Project description:We report XBP1 activation and regulation of pro-inflammatory gene expression in astrocytes during EAE.

2019-01-18 | GSE121923 | GEO

Genome-wide analysis of the transcriptional profile of WT and Mafg KD astrocytes during EAE in B6 mice.

Project description:We identify pathways regulated by Mafg in astrocytes during EAE

2020-02-12 | GSE135571 | GEO

Genome-wide analysis of the transcriptional profile of WT and CSF2RB astrocyte conditional KO during EAE in B6 mice [Csf2rb RNA-seq]

Project description:We identify pathways regulated by Csf2rb in astrocytes during EAE Multiple sclerosis (MS) is an autoimmune neurologic disease leading to demyelination and neurologic dysfunction controlled by both genetic and environmental factors. In addition to CNS-infiltrating immune cells, CNS-resident cells, such as astrocytes, are thought to play an important role in MS pathogenesis. However, a comprehensive understanding of the extent to which gene expression is disrupted in astrocytes is not known. Here, we implement single-cell RNA sequencing, in vivo genetic perturbations, cell-specific RNA profiling by Ribotag, as well as single-cell RNA sequencing of human MS patient samples to identify a transcriptional regulatory network in astrocytes that controls the pathogenesis of EAE and potentially, MS. We defined an astrocyte subpopulation characterized by expression of the small Maf protein, MAFG, which represses NRF2-driven antioxidant mechanisms and promotes EAE pathogenesis. Mechanistically, MAFG suppresses NRF2-dependent antioxidant genetic programs by cooperating with its cofactor, MAT2a, to promote DNA methylation in the context of CNS inflammation, which in turn increases pathogenic signaling processes in astrocytes. MAFG/MAT2a astrocytes are controlled by GM-CSF signaling, which drives EAE pathogenesis and MAFG expression. MAFG is activated in astrocytes derived from MS patients, which are characterized by DNA methylation programs, pro-inflammatory signaling processes including GM-CSF signaling, and repressed NRF2 activation. Together, these data create a transcriptional and epigenetic framework to analyze CNS inflammation in MS and may provide new therapeutic targets.

2020-02-12 | GSE129773 | GEO

Comparison of gene expression profiles of MafF-/-: MafG-/-: MafK-/- embryos and MafF-/-: MafG+/+: MafK-/- embyos

Project description:MafF-/-: MafG+/+: MafK-/- mice are viable, while MafF-/-: MafG-/-: MafK-/- mice are embryonic lethal. To get an insight into the cause of the lethality of small Maf triple knockout mice, transcriptome analysis was performed using whole embyos of MafF-/-: MafG-/-: MafK-/- at E10.5 and those of MafF-/-: MafG+/+: MafK-/- at E9.5 or E10.5. Because MafF-/-: MafG-/-: MafK-/- embryos exhibit growth retardation, the gene expression profile of MafF-/-: MafG-/-: MafK-/- embryos at E10.5 was compared with that of MafF-/-: MafG+/+: MafK-/- embyos at E9.5. The gene expression profile of MafF-/-: MafG+/+: MafK-/- embryos at E10.5 was also examined as an alternative control. Total RNA was prepared from pooled three embryos for each sample.

2012-01-09 | E-GEOD-29558 | biostudies-arrayexpress

Genome-wide analysis of MAFG binding in astrocytes during EAE [ChIP-seq]

Project description:Genome-wide analysis of MAFG binding in astrocytes during EAE [ChIP-seq]

| PRJNA531923 | ENA