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Genome-wide analysis of XBP1 binding in astrocytes during EAE

ABSTRACT: Genome-wide analysis of XBP1 binding in astrocytes during EAE

PROVIDER: PRJNA499097 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8130960_1.fastq.gz	Fastqsanger.gz
	SRR8130960_2.fastq.gz	Fastqsanger.gz
	SRR8130961_1.fastq.gz	Fastqsanger.gz
	SRR8130961_2.fastq.gz	Fastqsanger.gz
	SRR8130962_1.fastq.gz	Fastqsanger.gz

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Genome-wide analysis of XBP1 binding in astrocytes during EAE

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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.

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Genome-wide maps of XBP1 binding sites in different breast cancer cell lines [ChIP-Seq]

Project description:We report the application of ChIP-seq, which combines chromatin immunoprecipitation (ChIP) with massively parallel DNA sequencing, to map genome-wide XBP1 binding sites in different breast cancer cell lines. We showed that HIF1M-NM-1 motif was enriched in XBP1 binding sites in triple negative breast cancer (TNBC) cell lines, but not enriched in ER positive breast cancer cell line. We also demonstrated that different breast cancer cell lines of the same sub-type had similar XBP1 binding sites, whereas different breast cancer sub-types had majorly different XBP1 binding sites. Finally, a model was applied to integrate XBP1 ChIP-seq data with expression data to predict XBP1's direct targets in TNBC cell line; the predicted direct targets were shown to be predictive of patient survival, and the prediction power was specific to TNBC patients. The above evidence indicates that XBP1 performs important functions in TNBC by interacting with HIF1M-NM-1, and such regulation mechanism is specific to TNBC, which is later proved by follow-up experiments.This study represents the first detailed anaysis of XBP1 binding sites in different breast cancer cell lines. Examination of XBP1 binding sites in 2 cell types (3 cell lines).

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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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Project description:We report the application of ChIP-seq, which combines chromatin immunoprecipitation (ChIP) with massively parallel DNA sequencing, to map genome-wide XBP1 binding sites in different breast cancer cell lines. We showed that HIF1α motif was enriched in XBP1 binding sites in triple negative breast cancer (TNBC) cell lines, but not enriched in ER positive breast cancer cell line. We also demonstrated that different breast cancer cell lines of the same sub-type had similar XBP1 binding sites, whereas different breast cancer sub-types had majorly different XBP1 binding sites. Finally, a model was applied to integrate XBP1 ChIP-seq data with expression data to predict XBP1's direct targets in TNBC cell line; the predicted direct targets were shown to be predictive of patient survival, and the prediction power was specific to TNBC patients. The above evidence indicates that XBP1 performs important functions in TNBC by interacting with HIF1α, and such regulation mechanism is specific to TNBC, which is later proved by follow-up experiments.This study represents the first detailed anaysis of XBP1 binding sites in different breast cancer cell lines.

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RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vivo during EAE

Project description:To determine the role of RIPK1 kinase signaling in microglia and astrocytes during EAE (mouse model of MS), we extracted spinal cords of naive, EAE-vehicle and EAE mice treated with RIPK1 kinase inhibitor (GSK’547) for transcript profiling using RNAseq. We identify various genes that are differentially expressed in EAE disease compared to naive mice, and a subset of these are modulated in a RIPK1 kinase-dependent manner in both astrocytes and microglia. The top RIPK1 kinase-dependent gene pathways include oxidative phosphorylation and mitochondrial dysfunction in microglia and EIF2 signaling and cholesterol biosynthesis in astrocytes. This study demonstractes critical and distinct roles for RIPK1 kinase signaling in both microglia and astrocytes during EAE

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