One in three cancers diagnosed globally is a skin cancer. Yes-associated protein (YAP) is a pivotal regulator of stem cell proliferation that is active in cancer. Mechanical force is a crucial player in the regulation of tissue homeostasis, with YAP rapidly taking the center stage as key mechanoprotein. We have generated a viable, fertile transgenic mouse model that expresses constitutively active YAP2-5SA-ΔC in basal keratinocytes. YAP2-5SA-ΔC mice display a dramatic expansion of epidermal stem cell populations. Wnt/β-catenin signalling also controls epidermal regeneration. Here we describe increased nuclear β-catenin in the hyperplastic YAP2-5SA-ΔC epidermis, and increased β-catenin transcriptional activity in the skin of live YAP2-5SA-ΔC/TOPFLASH mice. Loss of β-catenin in basal keratinocytes of YAP2-5SA-ΔC/K14-creERT/CtnnB1lox/lox mice resulted in reduced epidermal proliferation and rescue of the hyperplastic abnormalities. These data show that YAP requires β-catenin activity to drive keratinocyte proliferation. In addition, YAP2-5SA-ΔC keratinocytes displayed prominent cortical actin and increased ROCK activity. This was accompanied by increased collagen, increased expression of ECM molecules, and increased vimentin, demonstrating ECM remodelling in the YAP2-5SA-ΔC dermis. Moreover, we noticed increased phosphorylation of FAK, AKT and GSK3β in the YAP2-5SA-ΔC epidermis, showing that β-catenin is activated in response to integrin signalling due to ECM remodelling. Altogether, this work shows that YAP activates ROCK-dependent mechanosignalling in mouse skin in vivo, eventually resulting in β-catenin activation and keratinocyte proliferation. Our studies have far-reaching implications for our understanding of human cancer displaying increased YAP, β-catenin and ROCK activity.