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RNA-seq analysis from epididymis and testis of ArKI mice

ABSTRACT: RNA-seq analysis from epididymis and testis of ArKI mice

PROVIDER: PRJNA448753 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6939290.fastq.gz	Fastqsanger.gz
	SRR6939300.fastq.gz	Fastqsanger.gz
	SRR6939310.fastq.gz	Fastqsanger.gz
	SRR6939320.fastq.gz	Fastqsanger.gz
	SRR6939291.fastq.gz	Fastqsanger.gz

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Project description:The wild-type p53-induced phosphatase 1 (WIP1) frustrated mice exhibited defects in reproductive organs. This study aimed to understand how Wip1 deficiency affects the spermatogenesis or maturation. We employed the Wip1-/- mouse model and conducted a gel-free iTRAQ LC-MS/MS based quantitative proteomics analysis of whole epididymis including the sperms and somatic tissue. A total of 8763 proteins were identified, of which 91 were significantly differentially expressed proteins (DEPs) in the Wip1 depleted mice. Four DEPs (PRM2, ODF1, PIWIL1 and KLHL10) were confirmed with western blotting. The DEPs enriched in biological process of reproduction were identified by GO analysis and further confirmed in the mouse phenotype database. Pathway analysis suggested that Smac/Diablo-mediated apoptosis pathway and SERPINA3-mediated inflammatory process might contribute to the atrophy and the marked sperm decrease in epididymis. Network analysis of productivity related DEPs revealed possible interactions that WIP1 might affect the sperm maturation by decreasing the outer dense fiber protein 1 (ODF1) and protamine-2 (PRM2), and increasing the PIWIL1/MIWI through p53. PRM2 was down-regulated and PIWIL1 was up-regulated by immunohistochemistry staining. It was further confirmed that the spermatid deficiency began from the testis observed by HE staining. Therefore, WIP1 disruption caused the deficiency of spermatogenesis potentially through regulating the expression of the above DEPs and pathways.

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