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UXT is required for spermatogenesis in mice

ABSTRACT: Male mammals must simultaneously produce prodigious numbers of sperm and maintain an adequate reserve of stem cells to ensure continuous production of gametes throughout life. Failures in the mechanisms responsible for balancing germ cell differentiation and spermatogonial stem cell (SSC) self-renewal can result in infertility. We discovered a novel requirement for Ubiquitous Expressed Transcript (UXT) in spermatogenesis by developing the first knockout mouse model for this gene. Constitutive deletion of Uxt is embryonic lethal, while conditional knockout in the male germline results in a Sertoli cell-only phenotype during the first wave of spermatogenesis that does not recover in the adult. This phenotype begins to manifest between 6 and 7 days post-partum, just before meiotic entry. Gene expression analysis revealed that Uxt deletion downregulates the transcription of genes governing SSC self-renewal, differentiation, and meiosis, consistent with its previously defined role as a transcriptional co-factor. Our study has revealed the first in vivo function for UXT in the mammalian germline as a regulator of distinct transcriptional programs in SSCs and differentiating spermatogonia.

ORGANISM(S): Mus musculus

PROVIDER: GSE111740 | GEO | 2018/04/18

REPOSITORIES: GEO

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UXT is required for spermatogenesis in mice

Project description:UXT is required for spermatogenesis in mice

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Lovastatin Promotes the Self-renewal of Murine and Primate Spermatogonial Stem Cells

Project description:The spermatogonial stem cells (SSCs) niche is critical for SSC maintenance and the subsequent spermatogenesis. Numerous reproductive hazards impair the SSC niche, thereby result in aberrant SSC self-renewal and male infertility. However, promising agents targeting the impaired SSC niche to promote SSC self-renewal are still limited. Here, we screen out and assess the effects of Lovastatin on the self-renewal of mouse spermatogonial stem cells (mSSCs). Mechanistically, Lovastatin promotes the self-renewal of mSSCs and inhibits its inflammation and apoptosis through the regulation of isoprenoid intermediates. Likewise, other statins exhibit similar effects on SSC self-renewal. Remarkably, the treatment by Lovastatin could promote the self-renewal of mSSCs in the male gonadotoxicity model generated by busulfan injection. Noteworthy, we demonstrate that Lovastatin could significantly enhance the self-renewal of in vitro cultured primate SSCs. Collectively, our findings uncover that lovastatin could promote the self-renewal of both murine and primate SSCs and have implications for the treatment of certain male infertility using small compounds.

2022-06-10 | GSE182897 | GEO

DIS3 ribonuclease is required for the maintenance of spermatogenic lineage in mice

Project description:Spermatogonial stem cells (SSCs) self-renewal and differentiation are the foundation for continious spermatognenesis in mice. Here, we investigate the essential role of DIS3 in maintaining SSC homeostasis and facilitating germ cell differentiation to ensure male fertility. Conditional inactivation of DIS3 in male germ cells have severely impaired SSC self-renewal and differentiation, which results in the failure of spermatogenesis associated with a Sertoli cell-only syndrome and adult sterility. RNA-seq analysis reveales that Dis3 deficiency abolishes its nucleolytic activity and causes significant dysregulation of the expression of transcripts in Dis3 mutant testes. We have also found that the pervasive transcription products described previously, such as Promoter Upstream Transcripts (PROMPTs), accumulate robustly upon DIS3 dysfunction in Dis3 cKO testes. In addition, scRNA-seq analysis indicates that DIS3 mutation significantly impairs germline stem cell development that blocks stem cell proliferation and differentiation. Overall, we show that DIS3 ribonuclease plays a critical role in the maintenance of spermatogenic lineage during spermatogenesis in mice.

2020-08-20 | GSE156505 | GEO

DIS3 mediated RNA decay is required for maintenance of spermatogenic lineage in mice

Project description:Spermatogonial stem cells (SSCs) self-renewal and differentiation are the foundation for continious spermatognenesis in mice. Here, we investigate the essential role of DIS3 in maintaining SSC homeostasis and facilitating germ cell differentiation to ensure male fertility. Conditional inactivation of DIS3 in male germ cells have severely impaired SSC self-renewal and differentiation, which results in the failure of spermatogenesis associated with a Sertoli cell-only syndrome and adult sterility. RNA-seq analysis reveals that Dis3 deficiency abolishes its nucleolytic activity and causes significant dysregulation of the expression of transcripts in Dis3 mutant testes. We have also found that the pervasive transcription products described previously, such as Promoter Upstream Transcripts (PROMPTs), accumulate robustly upon DIS3 dysfunction in Dis3 cKO testes. In addition, scRNA-seq analysis indicates that DIS3 mutation significantly impairs germline stem cell development that blocks stem cell proliferation and differentiation. Overall, we show that DIS3 ribonuclease plays a critical role in the maintenance of spermatogenic lineage during spermatogenesis in mice.

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Transcriptome changes after overexpression, knockdown and condItional knockout of UXT in mice

Project description:Ubiquitously expressed transcript (UXT) has been shown to play a role in regulating the process of autophagy. Here, we investigated roles of UXT in the innnate immune responses after overexpression, knockdown and condItional knockout of UXT in mice

2024-05-18 | GSE175928 | GEO

Transcriptome changes in mouse retina after conditional knockout of UXT

Project description:Ubiquitously expressed transcript (UXT), a small chaperone-like protein, is widely expressed in diverse human and mouse tissues and is more abundant in retina and kidney. Here, we investigated changes after conditional knockout of UXT in mouse retina at molecular, morphological and functional aspects.

2020-08-07 | GSE143281 | GEO

Epigenetic profiling of young and aged spermatogonial stem cells (ChIP-Seq)

Project description:Spermatogonial stem cells (SSC), the foundation of spermatogenesis and male fertility, possess lifelong self-renewal activity. Aging leads to the decline in stem cell function and increased risk of paternal age-related genetic diseases. Epigenetic profiling revealed reduced H3K27me3 deposition at numerous pro-differentiation genes during SSC differentiation as well as aberrant H3K27me3 distribution at genes in Wnt and TGF-β signaling upon aging.

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Epigenetic profiling of young and aged spermatogonial stem cells (RRBS)

Project description:Spermatogonial stem cells (SSC), the foundation of spermatogenesis and male fertility, possess lifelong self-renewal activity. Aging leads to the decline in stem cell function and increased risk of paternal age-related genetic diseases. Aged SSCs exhibited gene body hypomethylation, which is accompanied by an elevated 5hmC level.

2021-06-14 | GSE164606 | GEO

EZH1/SUZ12 complex positively regulates the transcription of NF-κB target genes via interaction with UXT

Project description:EZH1 is one of polycomb group genes which positively regulates transcription in the genome-wide scale. However, the underlying mechanisms still remain elusive. Here we report that EZH1 physically interacts with UXT, one small chaperon-like transcription co-activator of NF-κB. UXT specifically interacts with EZH1 and SUZ12, but not EED or EZH2. Similar to UXT, RNA interference of EZH1 and SUZ12 in the cell impairs the transcriptional activation of NF-κB target genes after TNFα treatment, and increases the induced cell death. Then RNA-Sequencing analysis was used to analysis the transcriptome in HCT116 cells after EZH1 or UXT knockdown. EZH1 or UXT deficiency nearly impaired the induced expression of all the genes by TNFα. ChIP-Sequencing was used to analysis the H3K27me1, H3K27me2 and H3K27me3 levels in HCT116 cells after EZH1 or UXT knockdown. However, the results show that H3K27 mono-, di- and trimethylation on NF-κB target genes are not affected with EZH1 or UXT deficiency. EZH1 does not affect the translocation of RELA/p65 from cytosol to nuclear either. Instead, EZH1 regulates the recruitment of RELA/p65 and RNA POLII to target genes. Taken together, our study demonstrates EZH1 as a positive regulator for NF-κB signaling and reveals the underlying mechanism how EZH1 and UXT work together in transcription regulation.

2016-05-11 | GSE75217 | GEO

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