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Resident macrophages in adult testis and epididymis originate from different waves of embryonic hematopoiesis

ABSTRACT: Resident macrophages in adult testis and epididymis originate from different waves of embryonic hematopoiesis

PROVIDER: PRJNA548161 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9228610.fastq.gz	Fastqsanger.gz
	SRR9228611.fastq.gz	Fastqsanger.gz
	SRR9228612.fastq.gz	Fastqsanger.gz
	SRR9228613.fastq.gz	Fastqsanger.gz
	SRR9228614.fastq.gz	Fastqsanger.gz

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Resident macrophages in adult testis and epididymis originate from different waves of embryonic hematopoiesis

Project description:Macrophages are principal immune cells of the epididymis and testis. Here we described that epididymal and testicular macrophages share core markers with tissue macrophages of other organs while concomitantly expressing a unique set of genes to perform organ specific functions.

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Transcriptomic analysis of testis and epididymis tissues from Banna mini-pig inbred line (BMI) boars with single-molecule long-read sequencing

Project description:The testis and epididymis tissues collected from 12-month-old adult BMI boars were carried out PacBio Iso-Seq sequencing and Illumina RNA-seq sequencing. The full-length isoforms, extensive alternative splicing events, lncRNAs, some genes and novel isoforms related to spermatogenesis were evaluated.

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Project description:Microglia arise exclusively from yolk sac (YS) progenitors during primitive hematopoiesis, while other tissue resident macrophages (TRMs)originate during transient-definitive and definitive hematopoiesis. Macrophages require the transcriptional repressor Zeb2 for development, and macrophages developing during definitive hematopoiesis require the ‒165 kb Zeb2 enhancer. However, microglia develop normally in Zeb2 ‒165kb mice lacking this enhancer, indicating that a distinct genetic program supports macrophage development in primitive hematopoiesis. Here, we identify the molecular basis that distinguishes macrophage development in primitive vs. definitive hematopoiesis. We show that all tissue resident macrophages (TRMs) that develop in Zeb2 ‒165kb mice arise exclusively during primitive hematopoiesis, showing that even erythro-myeloid progenitors (EMPs) from the transient-definitive stage rely on the ‒165 Zeb2 enhancer. Next, we identified the transcription factors Maf and Jun as being expressed by yolk sac (YS) progenitors during primitive hematopoiesis, but not by progenitors during definitive hematopoiesis. Further, we find that Maf and Jun together induce Zeb2 expression independently of the ‒165 kb Zeb2 enhancer and restore macrophage development from adult bone marrow progenitors in Zeb2 ‒165kb mice. Finally, Maf-deficient embryos show severe ablation of microglia development, confirming the in vivo requirement for Maf in supporting Zeb2 during primitive hematopoiesis. These results illustrate distinct transcriptional pathways controlling macrophage development during primitive and subsequent waves of hematopoiesis.

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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.

2019-01-16 | PXD010125 | Pride

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