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Deletion of nucleoporin Seh1 impaired neurogenesis through transcriptional regulation

ABSTRACT: Deletion of nucleoporin Seh1 impaired neurogenesis through transcriptional regulation

PROVIDER: PRJNA846167 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19543966_1.fastq.gz	Fastqsanger.gz
	SRR19543966_2.fastq.gz	Fastqsanger.gz
	SRR19543967_1.fastq.gz	Fastqsanger.gz
	SRR19543967_2.fastq.gz	Fastqsanger.gz
	SRR19543968_1.fastq.gz	Fastqsanger.gz

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Deletion of nucleoporin Seh1 impaired neurogenesis through transcriptional regulation

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Deletion of nucleoporin Seh1 impaired neurogenesis through transcriptional regulation

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Deletion of nucleoporin Seh1 impaired neurogenesis through transcriptional regulation (ChIP-Seq)

Project description:Nucleoporin Seh1 and chromodomain helicase DNA binding protein 4 have been involved in gene regulation. To dissect direct regulated genes, we performed chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for nucleoporin Seh1 or chromodomain helicase DNA binding protein 4 in neural stem cells.

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Effect of depletion of Nucleoporin Seh1 on gene expression during proliferation and differentiation of neural stem cell

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Nucleoporin Seh1 Maintain Schwann Cell Homeostasis by Regulating Genome Stability and Necroptosis

Project description:Schwann cells play critical roles in peripheral neuropathies, however, the regulatory mechanisms of their homeostasis remain largely unknown. Here we show that nucleoporin Seh1, a component of nuclear pore complex, is important for Schwann cell homeostasis and loss of Seh1 led to necroptosis of non-myelinating Schwann cell and degeneration of sensory neurons. While myelinogenesis, myelinating Schwann cell, and wrapped large fibers were not affected, mice with depletion of Seh1 in Schwann cell lineage developed progressive reduction of non-myelinating Schwann cells in sciatic nerves, followed by the degeneration of unmyelinated small sensory fibers and malfunction of the sensory system. Mechanistically, Seh1 safeguards genome stability by mediating the interaction between SETDB1 and KAP1. The disrupted interaction after ablation of Seh1 derepresses endogenous retroviruses, which triggers ZBP1-dependent necroptosis in non-myelinating Schwann cells. Collectively, our results reveal that Seh1 is required for homeostasis of Schwann cells and suggest that decrease of nucleoporins as aging may participate in the pathogenesis of periphery neuropathies.

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Deletion of nucleoporin Seh1 impaired neurogenesis through transcriptional regulation

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Seh1 Interacts with Olig2 and Brd7 to Promote Oligodendrocyte Differentiation and Myelination (ATAC_Seq)

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