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Alteration of gene expression in E11.5 XY Cdyl deficient gonadal somatic cells

ABSTRACT: Alteration of gene expression in E11.5 XY Cdyl deficient gonadal somatic cells

PROVIDER: PRJNA938426 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23611924_1.fastq.gz	Fastqsanger.gz
	SRR23611924_2.fastq.gz	Fastqsanger.gz
	SRR23611925_1.fastq.gz	Fastqsanger.gz
	SRR23611925_2.fastq.gz	Fastqsanger.gz
	SRR23611926_1.fastq.gz	Fastqsanger.gz

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Alteration of gene expression in E11.5 XY Cdyl deficient gonadal somatic cells

Project description:Cdyl deficient mice exhibited partial sex reversal. To determine this cause, RNA-seq was used to identify genes with altered expression in Cdyl deficient gonads.

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Transcription profiling of mouse strain differences in e11.5 XY gonad transcriptome suggest a mechanism for the sensitivity of C57BL/6J to sex reversal

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Project description:Here we report that the epigenetic factor Chromodomain Y-like (CDYL) protein is a critical regulator for the initiation and maintenance of activity-dependent intrinsic neuroplasticity. Genome-wide ChIP-sequencing analysis revealed that CDYL regulates multiple neuronal functional pathways including voltage-gated ion channels in mouse brains. We showed that CDYL binds to a regulatory element in the intron region of SCN8A and mainly recruits H3K27me3 activity for transcriptional repression of the gene. Injection of lentivirally-delivered CDYL shRNA to rat hippocampal neurons resulted in augmented Nav1.6-mediated sodium currents, lower neuronal threshold and increased seizure susceptibility, whereas transgenic mice over-expressing CDYL had higher neuronal threshold and were less prone to epileptogenesis. Finally, examination of human brain tissues revealed decreased expression of CDYL and increased expression of SCN8A in the temporal lobe epilepsy group. Together, our findings indicate CDYL is a critical player for experience-dependent gene regulation in controlling intrinsic excitability, which potentially contributes to learning and memory and CNS disorders involving change in activity such as epilepsy.

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