Whether an individual develops as male or female is determined by commitment of the developing gonad to testicular or ovarian development. In mammals this decision is made when SRY is expressed in the pre-supporting cells of the bipotential gonad. SRY initiates expression of SOX9 and down-stream targets including FGF9. FGF9 promotes proliferation of the developing Sertoli cells, but is not considered sufficient to drive testis development. In this study we demonstrate that a combination of growth factors, including FGF9, Activin and TGFβ are sufficient to initiate testicular development, including the repression of the ovarian development, expression of key testis development genes, morphological reorganisation of the gonad and formation of laminin delineated testis cords. In addition, we demonstrate that facilitating β-catenin by blocking GSK opposes the testis-promoting activity of FGF9, Activin and TGFβ. Since development of the germline is strongly affected by signaling from the somatic cells including FGF9, we examined the impacts of FGF9 and FGF9, Activin and TGFβ on expression of male germline markers, pluripotency and the cell cycle regulation in germ cells, demonstrating that while FGF9 promotes male germline markers, the combination of FGF9, Activin and TGFb maintain germline pluripotency. This study provides the first evidence that male sex-determination can be induced by a combination of growth factors in the absence of Sry. These findings have implications not only for understanding sex-determination in mammals, but also for non-mammalian species that do not have Sry.