| First Author | Qin Y | Year | 2005 |
| Journal | Hum Mol Genet | Volume | 14 |
| Issue | 9 | Pages | 1221-9 |
| PubMed ID | 15790596 | Mgi Jnum | J:99275 |
| Mgi Id | MGI:3581922 | Doi | 10.1093/hmg/ddi133 |
| Citation | Qin Y, et al. (2005) Sox9 is sufficient for functional testis development producing fertile male mice in the absence of Sry. Hum Mol Genet 14(9):1221-9 |
| abstractText | In the dominant mouse mutant Odd Sex, XXOds/+ mice develop as phenotypic, sterile males due to male-pattern expression of Sox9 in XXOds/+ embryonic gonads. To test whether SOX9 was sufficient to generate a fully fertile male in the absence of Sry, we constructed an XY(Sry(-))Ods/+ male mouse, in which the male phenotype is controlled autosomally by the Ods mutation. Mice were initially fertile, but progressively lost fertility until 5-6 months when they were sterile with very few germ cells in the testis. XY(Sry-)Ods/+ males also failed to establish the correct male-specific pattern of vascularization at the time of sex determination, which could be correlated to an inability of XY(Sry-),Ods/+ males to fully down-regulate Wnt4 expression in the embryonic gonad. Increasing the amount of SOX9 by producing homozygous XY(Sry-)Ods/Ods males was able to completely rescue the phenotype and restore correct vascular patterning and long-term fertility. These data indicate that activation of SOX9 in the gonad is sufficient to trigger all the downstream events needed for the development of a fully fertile male and provide evidence that Sox9 may down-regulate Wnt4 expression in the gonad. |
