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Somatic Cell Fate Maintenance in Mouse Fetal Testes via Autocrine/Paracrine Regulation of anti-Müllerian hormone and Activin B

ABSTRACT: Somatic Cell Fate Maintenance in Mouse Fetal Testes via Autocrine/Paracrine Regulation of anti-Müllerian hormone and Activin B

PROVIDER: PRJNA808096 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18062064.fastq.gz	Fastqsanger.gz
	SRR18062065.fastq.gz	Fastqsanger.gz
	SRR18062066.fastq.gz	Fastqsanger.gz
	SRR18062067.fastq.gz	Fastqsanger.gz
	SRR18062068.fastq.gz	Fastqsanger.gz

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Somatic Cell Fate Maintenance in Mouse Fetal Testes via Autocrine/Paracrine Regulation of anti-Müllerian hormone and Activin B

Project description:Fate determination and maintenance of fetal testes in most mammals occur cell autonomously as a result of the action of key transcription factors in Sertoli cell. In the mouse testis AMH and Activin B are required for the maintenance of Sertoli cell fate. In the absence of both AMH and Activin B (in the global dKO) Sertoli cells at the testis poles transdifferentiate into granulosa cells by embryonic day 15.5.

2022-05-12 | GSE196973 | GEO

Somatic cell fate maintenance in mouse fetal testes via autocrine/paracrine action of AMH and activin B.

Project description:Fate determination and maintenance of fetal testes in most mammals occur cell autonomously as a result of the action of key transcription factors in Sertoli cells. However, the cases of freemartin, where an XX twin develops testis structures under the influence of an XY twin, imply that hormonal factor(s) from the XY embryo contribute to sex reversal of the XX twin. Here we show that in mouse XY embryos, Sertoli cell-derived anti-Mullerian hormone (AMH) and activin B together maintain Sertoli cell identity. Sertoli cells in the gonadal poles of XY embryos lacking both AMH and activin B transdifferentiate into their female counterpart granulosa cells, leading to ovotestis formation. The ovotestes remain to adulthood and produce both sperm and oocytes, although there are few of the former and the latter fail to mature. Finally, the ability of XY mice to masculinize ovaries is lost in the absence of these two factors. These results provide insight into fate maintenance of fetal testes through the action of putative freemartin factors.

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PyMINEr Finds Gene and Autocrine/Paracrine Networks from Human Islet scRNAseq

Project description:Toolsets available for in-depth analysis of scRNAseq datasets by biologists with little informatics experience is limited. Here we describe an informatics tool (PyMINEr) that fully automates cell type identification, cell type-specific pathway analyses, graph theory-based analysis of gene regulation, and detection of autocrine/paracrine signaling networks in silico. We applied PyMINEr to interrogate human pancreatic islet scRNAseq datasets and discovered several features of co-expression graphs including: concordance of scRNAseq-graph structure with both protein-protein interactions and 3D-genomic architecture; association of high connectivity and low expression genes with cell type-enrichment; and potential for graph-structure to clarify potential etiologies of enigmatic disease-associated variants. We further created a consensus co-expression network and autocrine/paracrine signaling networks within and across islet cell types from 7-datasets. PyMINEr correctly identified changes in BMP/WNT signaling associated with cystic fibrosis pancreatic acinar-cell loss. This proof-of-principle study demonstrates that the PyMINEr framework will be a valuable resource for scRNAseq analyses.

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Arginine utilization following mycobacteria infection in macrophages is dependent on autocrine-paracrine signaling

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The gene expression analysis of paracrine/autocrine factors in patients with spermatogenetic failure compared to normal spermatogenesis

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