Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genomic profiling of human spermatogonial stem cells [WGBS]

ABSTRACT: To better understand human spermatogonial stem cells (SSCs), we profiled their transciptome and epigenome, which revealed the mechanism how human SSCs regulates their self-renewal versus differentiation dermination, as well as how latent pluripotency is established in human SSCs. Remarkly, we discovered signaling pathways (e.g. LIF, BMP, WNT) that differentially regulated self-renewal vesus differentiation in SSCs. We also discovered that SSCs repress core pluripotent factors (Sox2, Pou5f1 and Nanog) yet activate ancillary factors (e.g. Klf4, Mbd3, Tcf3, Sall4) transcriptionally and epigenetically.

ORGANISM(S): Homo sapiens

PROVIDER: GSE92278 | GEO | 2017/10/05

SECONDARY ACCESSION(S): PRJNA357085

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genomic profiling of human spermatogonial stem cells [BulkRNA-Seq]

Project description:To better understand human spermatogonial stem cells (SSCs), we profiled their transciptome and epigenome, which revealed the mechanism how human SSCs regulates their self-renewal versus differentiation dermination, as well as how latent pluripotency is established in human SSCs. Remarkly, we discovered signaling pathways (e.g. LIF, BMP, WNT) that differentially regulated self-renewal vesus differentiation in SSCs. We also discovered that SSCs repress core pluripotent factors (Sox2, Pou5f1 and Nanog) yet activate ancillary factors (e.g. Klf4, Mbd3, Tcf3, Sall4) transcriptionally and epigenetically.

2017-10-05 | GSE92277 | GEO

Genomic profiling of human spermatogonial stem cells [ATAC-Seq]

2017-10-05 | GSE92279 | GEO

Genomic profiling of human spermatogonial stem cells [scRNA-Seq]

2017-10-05 | GSE92276 | GEO

FGF2-regulated gene expression in cultured mouse spermatogonial stem cells

Project description:Transcriptional profiling of mouse spermatogonial stem cells (SSCs) comparing control untreated SSCs with SSCs with exogenous FGF2 withdrawn and FGFR inhibitor SU5402 supplemented (-F+S). Results provide insight into the mechanisms of FGF2-supported in vitro self-renewal of SSCs. Two-condition experiment, SSCs-F+S vs. SSCs. Biological replicates: 4 control replicates, 4 -F+S replicates.

2010-08-01 | E-GEOD-21294 | biostudies-arrayexpress

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

FGF2-regulated gene expression in cultured mouse spermatogonial stem cells

2010-08-01 | GSE21294 | GEO

Induced expression of PD-L1 in spermatogonial stem cells by self-renewal division allows allogeneic offspring production [Sequencing]

Project description:Testis immune privilege is thought to be mediated by somatic cells. However, it is not strong enough to protect allogeneic spermatogonial stem cells (SSCs) transplanted into the seminiferous tubules. Here we report successful production of allogeneic offspring by inducing PD-L1 in SSCs. Activation of self-renewal division induced PD-L1 and B7-H3 expression in cultured SSCs, which produced sperm after allogeneic transplantation. While B7-H3 depletion did not influence colonization, PD-L1 depletion prevented donor-derived spermatogenesis. PD-L1 expression was induced by BCL6B via reactive oxygen species (ROS) generation, suggesting that self-renewal stimulation confers immune privilege by ROS. In contrast, reduced ROS or Mapk14 deficiency downregulated PD-L1 expression. Allogeneic offspring were produced by SSC transplantation into congenitally infertile mice and busulfan-treated wild-type mice. Therefore, SSCs can escape rejection when their self-renewal division is stimulated.

2022-04-11 | GSE129658 | GEO

Induced expression of PD-L1 in spermatogonial stem cells by self-renewal division allows allogeneic offspring production [microarray]

2022-04-11 | GSE129546 | GEO

Gene expression profiles of Lhcgr-deficient testes

Project description:Spermatogonial stem cells (SSCs) provide foundation for spermatogenesis by undergoing continuous self-renewal division. Previous studies have reported conflicting results on the role of the pituitary gland activity in SSC self-renewal. In this study, we analyzed the role of hormonal regulation of SSCs using Lhcgr (luteinizing hormone/choriogonadotropin receptor) knockout mice. Analysis of gene expression profiles showed that testes of Lhcgr-deficient mice exhibit significantly enhanced Wnt5a expression in Sertoli cells. Lhcgr KO and control WT mice were treated with busulfan in order to eliminate germ cells. The total RNA samples from their testes were subjected to microarray analysis to compare their gene expression profiles.

2016-07-15 | E-GEOD-77500 | biostudies-arrayexpress

Splicing factor SRSF1 is essential for homing of precursor spermatogonial stem cells in mice

Project description:Spermatogonial stem cells (SSCs) provide a continuous spermatogenesis and male fertility. However, the underlying mechanisms of alternative splicing (AS) in mouse SSCs are still largely unclear. We demonstrated that SRSF1 is essential for gene expression and splicing in mouse SSCs. Specific deletion of Srsf1 in mouse germ cells impairs self-renewal and homing of SSCs leading to male infertility. Whole-mount staining data showed the absence of germ cells in the testes of adult cKO mice, which indicates severe non-obstructive azoospermia (NOA) in cKO mice. Expression of SSC-related genes (Gfra1, Pou5f1, Plzf, Dnd1, Stra8, and Taf4b) was significantly reduced in the testes of conditional knockout (cKO) mice. CLIP-seq data found that SSC-related genes (Plzf, Id4, Setdb1, Stra8, Tial1, Bcas2, Ddx5, Srsf10, Uhrf1, and Bud31) were bound by SRSF1 in the mouse testes. Moreover, multi-omics analysis suggests that SRSF1 directly binds and regulates the expression of Tial1 via AS to implement SSCs self-renewal and differentiation. Collectively, our data reveal the critical role of an SRSF1-mediated AS in SSCs self-renewal and differentiation, which may provide a framework to elucidate the molecular mechanisms of the post-transcriptional network underlying SSCs.

2024-01-08 | GSE227575 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data