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Mus musculus

ABSTRACT: Transcriptome analyses of fetal and adult Leydig cells

PROVIDER: PRJDB4234 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR046452.fastq.gz	Fastqsanger.gz
	DRR046453.fastq.gz	Fastqsanger.gz
	DRR046454.fastq.gz	Fastqsanger.gz
	DRR046455.fastq.gz	Fastqsanger.gz
	DRR046456.fastq.gz	Fastqsanger.gz

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Bulk RNA-seq of fetal and adult murine Leydig cells

Project description:To compare expression profiles of fetal and adult mouse Leydig cells, we performed bulk RNA sequencing.

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NR2F2 regulation of interstitial cell fate in the embryonic mouse testis and its impact on differences of sex development [ChIP-Seq]

Project description:Testicular fetal Leydig cells are specialized for androgen production during embryogenesis. Testosterone is essential for regulating sex differentiation, spermatogenesis, and fertility. Deficiencies in Leydig cell differentiation can lead to various disorders of sex development and male reproductive conditions, such as ambiguous genitalia, hypospadias, cryptorchidism, and infertility. Understanding the differentiation of fetal Leydig cells is essential for comprehending male sexual differentiation, reproductive health, and fertility. Fetal Leydig cells originate from proliferating progenitor cells in the gonadal interstitium, marked by genes like Arx, Pdgfra, Tcf21, Wnt5a, and Nr2f2 (COUP-TFII). However, the precise mechanisms governing the transition from interstitial cells to Leydig cells remain elusive. Through integrated approaches involving animal models and multiomics, we have demonstrated that fetal Leydig cells originate from a COUP-TFII positive non-steroidogenic interstitial cell population. COUP-TFII promotes progenitor cell fate while suppressing Leydig cell differentiation. Moreover, embryonic deletion of COUP-TFII in mouse testes resulted in disorders of sex development, including reduced testicular size, Leydig cell hypoplasia, cryptorchidism, and hypospadias. Collectively, our findings highlight the critical role of COUP-TFII in orchestrating the transition from interstitial cells to Leydig cells during testicular development.

2025-03-24 | GSE275900 | GEO

CUT&RUN analyses of fetal Leydig cells and testicular interstitial cells

Project description:CUT&RUN analyses of fetal Leydig cells and testicular interstitial cells

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Bulk RNA-seq of fetal and adult murine Leydig cells

Project description:Bulk RNA-seq of fetal and adult murine Leydig cells

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Purification and transcriptomic analysis of mouse fetal Leydig cells reveals candidate genes for disorders of sex development

Project description:To examine the transcriptome of early testicular somatic cells during gonadogenesis at 12.5dpc RNA sequencing (RNA-Seq) was performed on murine primary testicular cell lineages isolated from the Sf1-eGFP line by FACS. The three main somatic cell lineages of the testis were isolated: the Sertoli cells which direct male development; the fetal Leydig cells (FLCs) that produce steroid hormones and virilise the XY individual and a heterogenous population of interstitial cells, some of which give rise to the adult Leydig cells (ALCs). This dataset provides a platform for exploring the biology of FLCs and understanding the role of these cells in testicular development and masculinization of the embryo, and a basis for targeted studies designed to identify causes of idiopathic XY DSD. RNA-Seq of 3 enriched cell populations from 12.5dpc mouse gonad (Sertoli cells, Leydig cells and Interstitial cells isolated by FACS-sorting) on an Illumina HiSeq 1500, in triplicate.

2015-05-21 | E-GEOD-65498 | biostudies-arrayexpress

NR2F2 Regulation of Fetal Leydig Cell Differentiation: Insights into Differences of Sex Development [multiome]

Project description:Testicular fetal Leydig cells are specialized for androgen production during embryogenesis. Testosterone is essential for regulating sex differentiation, spermatogenesis, and fertility. Deficiencies in Leydig cell differentiation can lead to various disorders of sex development and male reproductive conditions, such as ambiguous genitalia, hypospadias, cryptorchidism, and infertility. Understanding the differentiation of fetal Leydig cells is essential for comprehending male sexual differentiation, reproductive health, and fertility. Fetal Leydig cells originate from proliferating progenitor cells in the gonadal interstitium, marked by genes like Arx, Pdgfra, Tcf21, Wnt5a, and Nr2f2. However, the precise mechanisms governing the transition from interstitial cells to Leydig cells remain elusive. Through integrated approaches involving animal models and multiomics, we have demonstrated that fetal Leydig cells originate from a Nr2f2 positive non-steroidogenic interstitial cell population. NR2F2 promotes progenitor cell fate while suppressing Leydig cell differentiation. Moreover, embryonic deletion of Nr2f2 in mouse testes resulted in disorders of sex development, including reduced testicular size, Leydig cell hypoplasia, cryptorchidism, and hypospadias. Collectively, our findings highlight the critical role of Nr2f2 in orchestrating the transition from interstitial cells to Leydig cells during testicular development.

2025-03-24 | GSE275901 | GEO

Transcriptomic analyses of the testicular interstitial cells in murine neonates

Project description:Previous studies have established that fetal Leydig cells (FLCs) and adult Leydig cells (ALCs) show distinct functional characteristics. However, the lineage relationship between FLCs and ALCs has not been clarified yet. Here we reveal that a subset of FLCs dedifferentiate at fetal stages to give rise to ALCs at the pubertal stage. Moreover, the dedifferentiated cells contribute to the peritubular myoid cells and vascular pericyte populations in the neonatal testis, and these non-steroidogenic cells serve as potential ALC stem cells. We generated FLC lineage-specific Nr5a1 (Ad4BP/SF-1) gene disrupted mice and mice lacking the fetal Leydig enhancer (FLE) of the Nr5a1 gene. Phenotypes of these mice support the conclusion that most of the ALCs arise from dedifferentiated FLCs, and that the FLE of Nr5a1 gene is essential for both initial FLC differentiation and pubertal ALC redifferentiation.

2018-11-26 | GSE122886 | GEO

Transcriptome analyses of fetal testicular interstitial cells (W-EGFP) treated with Smoothened Agonist (SAG)

Project description:Fetal Leydig cells are essential for masculinization through androgen production during fetal development. Previous studies have indicated that Desert Hedgehog regulates differentiation from progenitor cells. Our previous research showed a significant upregulation of energy metabolism-related genes during fetal Leydig cell differentiation. However, the underlying regulatory mechanisms remain unresolved. Here, we reveal that Desert Hedgehog rapidly activates energy metabolisms in testicular interstitial cells (W-EGFP cells) containing fetal Leydig progenitor cells without activating gene expression.

2025-03-24 | GSE292010 | GEO

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