An atlas of cell types in the mammalian epididymis and vas deferens
Abstract
Following testicular spermatogenesis, mammalian sperm continue to mature in a long epithelial tube known as the epididymis, which plays key roles in remodeling sperm protein, lipid, and RNA composition. To understand the roles for the epididymis in reproductive biology, we generated a single cell atlas of the murine epididymis and vas deferens. We recovered key epithelial cell types including principal cells, clear cells, and basal cells, along with associated support cells that include fibroblasts, smooth muscle, macrophages and other immune cells. Moreover, our data illuminate extensive regional specialization of principal cell populations across the length of the epididymis. In addition to region-specific specialization of principal cells, we find evidence for functionally specialized subpopulations of stromal cells, and, most notably, two distinct populations of clear cells. Our dataset extends on existing knowledge of epididymal biology, and provides a wealth of information on potential regulatory and signaling factors that bear future investigation.
Data availability
Data are available at GEO, Accession #GSE145443.
-
An atlas of cell types in the mammalian epididymis and vas deferens [single-cell RNA-Seq]NCBI Gene Expression Omnibus, GSE145443.
Article and author information
Author details
Funding
Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD080224)
- Vera D Rinaldi
- Elisa Donnard
- Kyle Gellatly
- Morten Rasmussen
- Alper Kucukural
- Onur Yukselen
- Manuel Garber
- Oliver J Rando
NIH Office of the Director (1DP2AG066622)
- Upasna Sharma
John Templeton Foundation (61350)
- Vera D Rinaldi
- Oliver J Rando
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Animal experimentation: All animal care and use procedures were in accordance with guidelines of the University of Massachusetts Medical School Institutional Animal Care and Use Committee (Protocol # A-1833-18).
Copyright
© 2020, Rinaldi et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Metrics
-
- 6,029
- views
-
- 784
- downloads
-
- 61
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
Further reading
-
- Developmental Biology
- Genetics and Genomics
The establishment and growth of the arterial endothelium require the coordinated expression of numerous genes. However, regulation of this process is not yet fully understood. Here, we combined in silico analysis with transgenic mice and zebrafish models to characterize arterial-specific enhancers associated with eight key arterial identity genes (Acvrl1/Alk1, Cxcr4, Cxcl12, Efnb2, Gja4/Cx37, Gja5/Cx40, Nrp1, and Unc5b). Next, to elucidate the regulatory pathways upstream of arterial gene transcription, we investigated the transcription factors binding each arterial enhancer compared to a similar assessment of non-arterial endothelial enhancers. These results found that binding of SOXF and ETS factors was a common occurrence at both arterial and pan-endothelial enhancers, suggesting neither are sufficient to direct arterial specificity. Conversely, FOX motifs independent of ETS motifs were over-represented at arterial enhancers. Further, MEF2 and RBPJ binding was enriched but not ubiquitous at arterial enhancers, potentially linked to specific patterns of behaviour within the arterial endothelium. Lastly, there was no shared or arterial-specific signature for WNT-associated TCF/LEF, TGFβ/BMP-associated SMAD1/5 and SMAD2/3, shear stress-associated KLF4, or venous-enriched NR2F2. This cohort of well-characterized and in vivo-verified enhancers can now provide a platform for future studies into the interaction of different transcriptional and signaling pathways with arterial gene expression.
-
- Developmental Biology
- Genetics and Genomics
What determines whether an endothelial cell becomes part of an artery, a vein or a capillary?