Journal
CELL STEM CELL
Volume 24, Issue 1, Pages 79-+Publisher
CELL PRESS
DOI: 10.1016/j.stem.2018.11.013
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Funding
- KAKENHI from MEXT
- JSPS [JP25122719, JP24112526, JP22770226, JP20116004, JP25114004, JP16H02507, JP18H05551]
- AMED-CREST [JP18gm1110005]
- Royal Society EP Abraham Research Professorship
- Wellcome Trust Senior Investigator Award [098357/Z/12/Z]
- AMED
- Wellcome Trust [092096]
- CRUK [C6946/A14492]
- Wellcome Trust [098357/Z/12/Z] Funding Source: Wellcome Trust
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In many tissues, homeostasis is maintained by physical contact between stem cells and an anatomically defined niche. However, how stem cell homeostasis is achieved in environments where cells are motile and dispersed among their progeny remains unknown. Using murine spermatogenesis as a model, we find that spermatogenic stem cell density is tightly regulated by the supply of fibroblast growth factors (FGFs) from lymphatic endothelial cells. We propose that stem cell homeostasis is achieved through competition for a limited supply of FGFs. We show that the quantitative dependence of stem cell density on FGF dosage, the biased localization of stem cells toward FGF sources, and stem cell dynamics during regeneration following injury can all be predicted and explained within the framework of a minimal theoretical model based on mitogen competition.'' We propose that this model provides a generic and robustmechanism to support stem cell homeostasis in open, or facultative, niche environments.
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