Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Purification of GFRα1+ and GFRα1- spermatogonial stem cells reveals a niche-dependent mechanism for fate determination

ABSTRACT: Purification of GFRα1+ and GFRα1- spermatogonial stem cells reveals a niche-dependent mechanism for fate determination

PROVIDER: PRJNA421150 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6347990_1.fastq.gz	Fastqsanger.gz
	SRR6347990_2.fastq.gz	Fastqsanger.gz
	SRR6348000_1.fastq.gz	Fastqsanger.gz
	SRR6348000_2.fastq.gz	Fastqsanger.gz
	SRR6347991_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 34

Similar Datasets

Purification of GFRα1+ and GFRα1- Spermatogonial Stem Cells Reveals a Niche-Dependent Mechanism for Fate Determination.

Project description:Undifferentiated spermatogonia comprise a pool of stem cells and progenitor cells that show heterogeneous expression of markers, including the cell surface receptor GFRα1. Technical challenges in isolation of GFRα1+ versus GFRα1- undifferentiated spermatogonia have precluded the comparative molecular characterization of these subpopulations and their functional evaluation as stem cells. Here, we develop a method to purify these subpopulations by fluorescence-activated cell sorting and show that GFRα1+ and GFRα1- undifferentiated spermatogonia both demonstrate elevated transplantation activity, while differing principally in receptor tyrosine kinase signaling and cell cycle. We identify the cell surface molecule melanocyte cell adhesion molecule (MCAM) as differentially expressed in these populations and show that antibodies to MCAM allow isolation of highly enriched populations of GFRα1+ and GFRα1- spermatogonia from adult, wild-type mice. In germ cell culture, GFRα1- cells upregulate MCAM expression in response to glial cell line-derived neurotrophic factor (GDNF)/fibroblast growth factor (FGF) stimulation. In transplanted hosts, GFRα1- spermatogonia yield GFRα1+ spermatogonia and restore spermatogenesis, albeit at lower rates than their GFRα1+ counterparts. Together, these data provide support for a model of a stem cell pool in which the GFRα1+ and GFRα1- cells are closely related but show key cell-intrinsic differences and can interconvert between the two states based, in part, on access to niche factors.

| S-EPMC5830912 | biostudies-literature

Purification of GFRα1+ and GFRα1- spermatogonial stem cells reveals a niche-dependent mechanism for fate determination

Project description:Undifferentiated spermatogonia comprise a pool of stem cells and progenitor cells that show heterogeneous expression of markers, including the cell surface receptor GFRα1. Technical challenges in isolation of GFRα1+ versus GFRα1- undifferentiated spermatogonia have precluded the comparative molecular characterization of these subpopulations and their functional evaluation as stem cells. Here, we develop a method to purify these subpopulations by FACS and show that GFRα1+ and GFRα1- undifferentiated spermatogonia both demonstrate elevated transplantation activity while differing principally in receptor tyrosine kinase signaling and cell cycle. We identify the cell surface molecule MCAM as differentially expressed in these populations and show that antibodies to MCAM allow isolation of highly enriched populations of GFRα1+ and GFRα1- spermatogonia from adult, wild-type mice. In germ cell culture, GFRα1- cells upregulate MCAM expression in response to GDNF/FGF stimulation. In transplanted hosts, GFRα1- spermatogonia yield GFRα1+ spermatogonia and restore spermatogenesis, albeit at lower rates than their GFRα1+ counterparts. Together, these data provide support for a model of a stem cell pool in which the GFRα1+ and GFRα1- cells are closely related, but show key cell-intrinsic differences and can interconvert between the two states based, in part, on access to niche factors.

2018-12-01 | GSE107694 | GEO

Fate determination of msc by inflammatory niche in HO

Project description:Fate determination of msc by inflammatory niche in HO

| PRJNA1032942 | ENA

Multiomics Approach to Profiling Development of the Spermatogonial Stem Cell Niche Focused on Sertoli cell Maturation

Project description:Spermatogonial stem cells are the foundation of spermatogenesis and as such can serve as a tool for the treatment of infertility in prepubertal cancer survivors. Spermatogonial stem cells are unique as they develop from primordial germ cells (PGCs), which colonize the developing tubules as immature SSC precursors. It has been controversial, when SSCs are maturing to an adult-like stem cell and recent research has found that prepubertal SSCs are actually metabolically distinct from adult SSCs until puberty. Sertoli cells picture a major part of the SSC niche and undergo drastic changes with puberty and polarize to compartmentalize the seminiferous epithelium with formation of tight junctions to a tight basal part where SSCs reside and an apical part with more differentiated stages of spermatogenesis. In the study were mapping the progression of Sertoli cells maturation events to the metabolic changes SSCs undergo during prepubertal development.

2023-02-24 | PXD037764 | Pride

Fate determination of msc by inflammatory niche in HO [scRNA-Seq]

Project description:Fate determination of msc by inflammatory niche in HO [scRNA-Seq]

| PRJNA1032940 | ENA

Fate determination of msc by inflammatory niche in HO [spatial transcriptomics]

Project description:Fate determination of msc by inflammatory niche in HO [spatial transcriptomics]

| PRJNA1032946 | ENA

Decoding the spermatogonial stem cell niche under physiological and recovery conditions in adult mice and humans

Project description:The intricate interaction between spermatogonial stem cell (SSC) and testicular niche is essential for maintaining SSC homeostasis; however, this interaction remains largely uncharacterized. In this study, to characterize the underlying signaling pathways and related paracrine factors, we delineated the intercellular interactions between SSC and niche cell in both adult mice and humans under physiological conditions and dissected the niche-derived regulation of SSC maintenance under recovery conditions.

2023-08-06 | GSE164787 | GEO

Transcriptional profiling of testicular biopsies with Sertoli-cell-only and spermatogonial presence

Project description:The aim of the study was to identify in vivo spermatogonial gene expression within the context of their biological niche. Identification of spermatogonial genes was done by t-testing on the replicates of Score 3 (Spermatogonia) and Score 2 (SCO) testicular biopsies. 3 biological replicates with spermatogonial presence in the tubuli seminiferi, 5 biological replicates with Sertoli-cell-only syndrome.

2009-11-12 | E-GEOD-18997 | biostudies-arrayexpress

Fate determination of msc by inflammatory niche in HO [spatial transcriptomics]

Project description:Heterotopic ossification (HO), usually following traumatic challenges, is initiated by the aberrant osteochondral differentiation of mesenchymal stem cell (MSC). However, the role of trauma-induced inflammatory exposure in MSC fate determination remains unclear. Here, we found that quiescent MSC transited into cycling MSC and later gave rise to chondrogenic (cMSC) and/or osteogenic (oMSC) commitment following either muscle or tendon injury via single-cell RNA sequencing and lineage tracing analysis. Further spatial transcriptome analysis revealed that cycling MSC, cMSC and oMSC resided in the inflammatory niche comprised of monocytes/macrophages, neutrophils, dendritic cells (DCs), NK cells, T and B lymphocytes. We uncovered the diversity of each type of immune cells during MSC development and demonstrated that macrophages, including M1 and M2 subtypes, dynamically promotes proliferation and osteochondral differentiation of MSCs. Additionally, neutrophils and NK cells are essential for cycling MSC transition from quiescent MSC. CD4+ and CD8+ T lymphocytes promotes chondrogenesis. CellchatDB analysis and regulon analysis identify several gene networks, which could be essential for aberrant MSC proliferation and osteochondral differentiation respectively. Collectively, our findings indicate that inflammation is necessary to regulate MSC fate and uncovered the molecular landscape of osteoimmunological interactions that occur during aberrant osteochondral differentiation that could be useful for HO treatment.

2025-03-06 | GSE246448 | GEO

Fate determination of msc by inflammatory niche in HO [scRNA-Seq]

2025-03-06 | GSE246445 | GEO