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

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

PROVIDER: PRJNA976911 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24752564_1.fastq.gz	Fastqsanger.gz
	SRR24752564_2.fastq.gz	Fastqsanger.gz
	SRR24752565_1.fastq.gz	Fastqsanger.gz
	SRR24752565_2.fastq.gz	Fastqsanger.gz
	SRR24752566_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

Project description:Nucleoporin Seh1 has been involved in gene regulation. To dissect nucleoporin's direct regulated genes, we performed chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for nucleoporin Seh1 in neural stem cells.

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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

Project description:To investigate the function of chromodomain helicase DNA binding protein 4 in the regulation of neural stem cell proliferation, we find out different expression of genes in neural stem cell of Chd4 knockdown

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

Project description:Nuclear pore complex components (Nups) are involved in neural development and alterations in Nup genes are linked to human neurological diseases. However, the physiological functions of specific Nups and the underlying mechanisms involved in these processes remain elusive. Here we show that tissue-specific depletion of nucleoporin Seh1 causes dramatic myelination defects in the Central Nervous System (CNS). Seh1-deficient Oligodendrocyte Progenitor Cells (OPCs) proliferate properly, but fail to differentiate into mature oligodendrocytes, which impairs myelin production and remyelination after demyelinating injury. Genome-wide analyses show that Seh1 regulates a core myelinogenic regulatory network and depletion of Seh1 alters open chromatin configurations at its target genes. Mechanistically, Seh1 regulates OPCs differentiation by assembling Olig2 and Brd7 into a transcription complex at nuclear pores. Together, our results reveal that Seh1 is required for oligodendrocyte differentiation and myelination by promoting assembly of an Olig2-dependent transcription complex and expose nucleoporins as key players in the CNS.

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