Comedonal acne is a common skin disease characterized by cystic dilation of the hair follicle junctional zone. While the molecular mechanisms of acne pathogenesis are not well understood, an emerging hypothesis holds that imbalances in key signalling pathways may lead to abnormal fate determination of sebaceous progenitor cells. The subsequent accumulation of cells could then cause cyst formation in the hair follicle junctional zone and lower infundibulum, forming blackheads. This notion is supported by the observation that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes severe comedonic acne and seboatrophy by inducing fate changes in Lrig1-expressing stem cells, as well as recent human GWAS studies implicating the Wnt signalling pathway in acne. To test the possible involvement of Wnt signals in blackhead formation, we used an Lrig1-CreERT2 mouse line to modulate Wnt signalling in stem cells of the junctional zone, which are known to contribute to the junctional zone, infundibulum, and sebaceous glands. We find that persistent activation of Wnt signalling in the junctional zone leads to formation of comedone-like cysts with associated atrophic sebaceous glands. The cysts strongly express stem cell markers and can be partially reduced by treatment with all-trans retinoic acid, a well-established acne treatment, as well as by inhibition of Hedgehog signalling. In contrast, loss of Wnt signalling leads to enlargement of the junctional zone, infundibulum and sebaceous glands. These data lead us to suggest that abnormal Wnt signalling could be involved in acne pathogenesis by inhibiting differentiation and retaining junctional zone cells in a proliferative progenitor state, leading to their accumulation into comedones.