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Genome-wide maps of Qki-5 and PPARb in mouse oligodendrocytes

ABSTRACT: Genome-wide maps of Qki-5 and PPARb in mouse oligodendrocytes

PROVIDER: PRJNA522428 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8578610_1.fastq.gz	Fastqsanger.gz
	SRR8578610_2.fastq.gz	Fastqsanger.gz
	SRR8578611_1.fastq.gz	Fastqsanger.gz
	SRR8578611_2.fastq.gz	Fastqsanger.gz
	SRR8578612_1.fastq.gz	Fastqsanger.gz

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Genome-wide maps of Qki-5 and PPARb in mouse oligodendrocytes

Project description:We found that there is a big overlap between the Qki5- and PPARb-binding events by ChIP-seq. Interestingly, the genomic distribution analyses of Qki-5- and PPARβ-binding events showed significant enrichment at the regions of the promoter/transcription start site (TSS) which were indicated by Pol II-binding events. The strong preference of the promoter/TSS co-occupancy suggested that Qki-5 might play an important role in PPARβ-mediated transcriptional regulation of its downstream genes.

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Genome-wide maps of Qki-5, Srebp2, and Pol II in oligodendrocytes

Project description:We found the genome-wide co-localization of Qki-5 and Srebp2. Notably, the genomic distribution analysis revealed that Qki-5 and Srebp2 highly co-occupied the regions of the promoter/transcription start site (TSS), where active transcription was taken place in a oligodendrocyte-specific manner, which was indicated by Pol II binding events. GO analysis of the genes whose promoters were co-bound by Qki-5, Srebp2, and Pol II showed a significant enrichment of the Srebp2-mediated cholesterol biosynthesis pathway, and Qki depletion led to reduced recruitment of Srebp2 and Pol II on the promoters of the genes involved in cholesterol biosynthesis. These data suggest Qki-5 as a potential transcription co-activator of Srebp2-mediated cholesterol biosynthesis in oligodendrocytes.

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Genome-wide maps of Qki-5, Srebp2, and Pol II in oligodendrocytes

Project description:Genome-wide maps of Qki-5, Srebp2, and Pol II in oligodendrocytes

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RNA-seq profiles of WT and Qk-KO freshly isolated oligodendrocytes

Project description:Lipid-rich myelin forms insulating axon-wrapping multilayers essential for neural function, but how mature myelin maintains its structural lipid components remains obscure. Here we identify Quaking (Qki) as a major regulator of myelin lipid homeostasis. Qki depletion in adult myelinating oligodendrocytes disrupted myelin lipid metabolism and caused demyelination, resulting in progressive neurological deficits that could be partially rescued by high-fat diet. Mechanistically, Qki serves as a coactivator of the PPARb-RXRa complex, which controls transcription of lipid-metabolism genes, particularly those for fatty acid desaturation and elongation. Treatment of Qki-depleted mice with PPARb or RXR agonists alleviated neurological disability and significantly extended mouse survival. Furthermore, a subset of lesions from patients with primary progressive multiple sclerosis were characterized by preferential reduction of myelin lipids and activities of lipid-metabolism pathways. Together, our findings demonstrate that continuous lipid synthesis is indispensable for mature myelin maintenance and highlight an underappreciated role of lipid metabolism in demyelinating diseases.

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Project description:We found the genome-wide co-binding of QKI-5 and SREBP2. Notably, the genomic distribution analysis revealed that the co-binding events between QKI-5 and SREBP2 highly occurred at the regions of the promoter/transcription start site (TSS), where active transcription was taken place in a lens cell-specific manner, which was indicated by POL II binding events. Cellular pathway analysis of the genes whose promoters were co-bound by QKI-5, SREBP2, and POL II showed a significant enrichment of the SREBP2-medaited cholesterol biosynthesis pathway, and QKI depletion led to reduced co-occupancies of SREBP2 and POL II on the promoters of the genes involved in cholesterol biosynthesis. These data suggest QKI-5 as a potential transcription co-activator mediating SREBP2-dependent cholesterol biosynthesis in eye lens cells.

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Project description:Genome-wide maps of QKI-5, SREBP2, and POL II in eye lens cells

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Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: QKI data

Project description:To assess whether the transcripts identified by PAR-CLIP are regulated by the RNA-binding protein (RBP) Quaking (QKI), we analyzed the mRNA levels of mock-transfected and QKI-specific siRNA-transfected cells with microarrays. Transcripts crosslinked to QKI were significantly upregulated upon siRNA transfection, indicating that QKI negatively regulates bound mRNAs (Figure 3H of PMID 20371350), consistent with previous reports of QKI being a repressor. The RBP QKI was depleted by siRNAs and the expression level was compared to mock-transfected HEK 293 cells.

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