| First Author | Hasegawa K | Year | 2014 |
| Journal | Biol Reprod | Volume | 91 |
| Issue | 6 | Pages | 145 |
| PubMed ID | 25359900 | Mgi Jnum | J:218400 |
| Mgi Id | MGI:5617424 | Doi | 10.1095/biolreprod.114.121012 |
| Citation | Hasegawa K, et al. (2014) FGF8-FGFR1 signaling acts as a niche factor for maintaining undifferentiated spermatogonia in the mouse. Biol Reprod 91(6):145 |
| abstractText | In mammalian testes, spermatogonial stem cells (SSCs) maintain spermatogenesis over a long period of time by undergoing self-renewal and differentiation. SSCs are among the most primitive of spermatogenic cells (undifferentiated spermatogonia), and their activities are strictly regulated by extrinsic niche factors. However, the factors that constitute a testicular niche remain poorly understood. In this study, we demonstrate that fibroblast growth factor (FGF) signaling maintains undifferentiated spermatogonia through activating ERK1/2 signaling in vivo. Undifferentiated spermatogonia comprise GFRA1(+) and NANOS3(+) subpopulations, which are likely to undergo self-renewal and enter the differentiation pathway, respectively. In the testis, Fgfr1 was expressed in the entire population of undifferentiated spermatogonia, and deleting FGFR1 in spermatogenic cells partially inactivated ERK1/2 and resulted in reduced numbers of both GFRA1(+) and NANOS3(+) cells. In addition, Fgf8 was expressed in spermatogenic cells, and loss- and gain-of-function models of FGF8 demonstrated that FGF8 positively regulated the numbers of undifferentiated spermatogonia through FGFR1, particularly among NANOS3(+) cells. Finally we show a possible involvement of FGF signaling in the reversion from NANOS3(+) into GFRA1(+) undifferentiated spermatogonia. Taken together, our data suggest that FGF signaling is an important component of the testicular niche and has a unique function for maintaining undifferentiated spermatogonia. |
