The highly conserved Wnt signalling pathway is required in diverse processes during development such as sex determination and ovary growth as well as for adult tissue homeostasis. The importance of Wnt signalling in postnatal testis function has been studied in several mouse models with chronic pathway disruption, addressing its function in Sertoli cells and in post-meiotic germ cells. We initially used two mouse models with acute disruption of Wnt signalling to explore the importance of regulated Wnt pathway activity for normal germ cell development in adult male mice. Short term induction of mutations, in Apc and β-catenin, that increase and decrease Wnt signalling levels, respectively, were generated in AhCre Apcflox/flox and AhCre β-catflox/flox mice. Each exhibited distinct phenotypes of disrupted spermatogenesis involving germ cell loss and apoptosis predominantly in post-mitotic germ cells, with perturbations in Sertoli cell morphology including altered distribution of the blood testis barrier protein, connexin 43. Our detection of nuclear β-catenin protein in spermatocytes and round spermatids, the key indicator of canonical Wnt signalling, highlights these cells as an important target for Wnt actions, and the need to understand the nature of Wnt signalling in these specific cell types. Transcriptional profiling of wild type and mutant testes identified transcripts encoding Wnt receptors (e.g. Fzd4), ligands (e.g. Wnt3, Wnt3a, Wnt5b, Wnt7a and Wnt8b) and other signalling components that are developmentally regulated, including those deduced as present in post-mitotic cells; we are now establishing their cellular expression profiles. To delineate the specific impact of nuclear β-catenin and Wnt signaling in germ cells, we are developing several new mouse strains, including VasaCre β-catflox/flox mice. This demonstration that Wnt signalling control is essential for adult spermatogenesis highlights that its transient disruption may underpin some cases of male infertility.