Vinculin, a mechanotransducing protein is found both cell-cell and cell-substratum junctions where it links the actin cytoskeleton to these cell junctions in a force dependent manner. Constitutive knock out of vinculin in mouse results in embryonic lethality due to defects in cell adhesion and migration suggesting its importance in embryonic development. Vinculin is expressed in bulge stem cells of the hair follicle, which is the main pool of quiescent stem cells in the skin. In order to study the role of vinculin in mouse skin, a conditional K14 driven knock out was generated in skin epidermis. We observed that the vinculin knockout mice displayed loss of hair and acceleration of the hair follicle cycle, which interestingly did not lead to complete hair loss. Label retaining experiments revealed that the bulge stem cells fail to maintain their quiescence in the KO, which may explain the continuous cycling of the hair follicles. The bulge cells in the KO show defects in maintaining normal cell-cell junctions, which results in the nuclear translocation of YAP. Our results suggest that the loss of cell junctional stablilty can override the intrinsic quiescence of bulge stem cells.