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A non-canonical bivalent gene Wfdc15a controls spermatogenic protease and immune homeostasis

ABSTRACT: A non-canonical bivalent gene Wfdc15a controls spermatogenic protease and immune homeostasis

PROVIDER: PRJNA923583 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23073124_1.fastq.gz	Fastqsanger.gz
	SRR23073124_2.fastq.gz	Fastqsanger.gz
	SRR23073125_1.fastq.gz	Fastqsanger.gz
	SRR23073125_2.fastq.gz	Fastqsanger.gz
	SRR23073126_1.fastq.gz	Fastqsanger.gz

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A non-canonical bivalent gene Wfdc15a controls spermatogenic protease and immune homeostasis

Project description:A non-canonical bivalent gene Wfdc15a controls spermatogenic protease and immune homeostasis

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A non-canonical bivalent gene Wfdc15a controls spermatogenic protease and immune homeostasis [P25]

Project description:A non-canonical bivalent gene Wfdc15a controls spermatogenic protease and immune homeostasis [P25]

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A non-canonical bivalent gene Wfdc15a controls spermatogenic protease and immune homeostasis

Project description:Male infertility can be caused by chromosomal abnormalities, mutations, and epigenetic defects. Epigenetic modifiers pre-program hundreds of spermatogenic genes in spermatogonial stem cells (SSCs) for expression later in spermatids, but it remains mostly unclear whether and how those genes are involved in fertility. Here, we report that Wfdc15a, a WFDC family protease inhibitor pre-programmed by KMT2B, is essential for spermatogenesis. We found that Wfdc15a is a non-canonical bivalent gene carrying both H3K4me3 and facultative H3K9me3 in SSCs but is later activated along with the loss of H3K9me3 and acquisition of H3K27ac during meiosis. We show that WFDC15A deficiency causes defective spermiogenesis at the beginning of spermatid elongation. Notably, depletion of WFDC15A causes substantial disturbance of the testicular protease-antiprotease network and leads to an orchitis-like inflammatory response associated with TNFa expression in round spermatids. Together, our results reveal a unique epigenetic program regulating innate immunity crucial for fertility.

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A non-canonical bivalent gene Wfdc15a controls spermatogenic protease and immune homeostasis

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Competition for mitogens regulates spermatogenic stem cell homeostasis in an open niche

Project description:In many tissues, homeostasis is maintained by physical contact between stem cells and an anatomically-defined niche. However, how stem cell homeostasis is achieved in environments where cells are motile and dispersed among their progeny remains unknown. Using murine spermatogenesis as a model, we find that spermatogenic stem cell density is tightly regulated by the supply of fibroblast growth factors (FGFs) from lymphatic endothelial cells. We propose that stem cell homeostasis is achieved through competition for a limited supply of FGFs. We show that the quantitative dependence of stem cell density on FGF dosage, the biased localization of stem cells toward FGF sources, and stem cell dynamics during regeneration following injury can all be predicted and explained within the framework of a minimal theoretical model based on “mitogen competition”. We propose that this model provides a generic and robust mechanism to support stem cell homeostasis in open, or facultative, niche environments.

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Competition for mitogens regulates spermatogenic stem cell homeostasis in an open niche

Project description:Competition for mitogens regulates spermatogenic stem cell homeostasis in an open niche

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Changes in Expressions of Spermatogenic Marker Genes and Spermatogenic Cell Population Caused by Stress

Project description:Purpose: Many young adults are in a state of stress due to social and psychological pressures, which may result in male reproductive dysfunction. To provide new insight into this phenomenon, we investigated the relationship between pathological changes in rat spermatogenic cells and the expression of genes specific to spermatogenic cell types under different stress conditions. Methods: After establishing rat stress models of different time durations, we observed pathological changes in testicular tissues through haematoxylin and eosin staining, and analysed gene expression in spermatogenic cells by RNA-seq, bioinformatic analysis, and reverse transcription qPCR (RT-qPCR).Three testicular samples were taken from each group to construct 12 cDNA libraries. For each sample, 3 μg RNA was used as the starting material. Ribosomal RNA was removed using the Epicentre Ribo-Zero™ Gold kit (Rat) (Epicentre, an Illumina company, Madison, WI, USA). Results:Compared with the control group, there were 1,194 DEGs in the 3-day RS+IS group , including 455 upregulated genes and 739 downregulated genes , 1,774 DEGs in the 14-day RS+IS group including 1,124 upregulated genes and 650 downregulated genes, and 2,267 DEGs in the 21-day RS+IS group including 1,366 upregulated genes and 901 downregulated genes. Mean-while, some same expression patterns were observed in three phenotypes.After comparison with single-cell sequencing data, 349 DEGs of spermatogenic cells at different developmental stages were found. Conclusions: Our study suggest that chronic psychosomatic stress can affect the spermatogenic transcriptome of the testes, leading to a significant change in the expression of the spermatogenic genes. At the same time, histopathological and immunohistochemical results showed that chronic stress may lead to pathological changes in spermatogenic cells and to a significant decrease in key regulatory proteins

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