Essential Role of Polarity Protein Par3 for Epidermal Homeostasis Through Regulation of Barrier Function, Keratinocyte Differentiation, and Stem Cell Maintenance

The document from December 2016 presents evidence that the loss of the polarity protein Par3 in the epidermis disrupts the skin's barrier function, alters the expression and localization of tight junction components, and leads to increased epidermal differentiation and thickness. Additionally, the absence of Par3 initially causes an expansion followed by a decline in hair follicle bulge stem cells, an increase in committed progenitors, hypertrophic sebaceous glands, and suggests improper cell fate decisions. Unlike the deletion of aPKCλ, Par3 loss does not promote perpendicular cell divisions; instead, it causes spindle orientations to shift toward a planar alignment. This indicates that the abnormal differentiation seen with Par3 inactivation is not due to changes in spindle orientation. Overall, Par3 is essential for maintaining the epidermal barrier, keratinocyte differentiation, and stem cell populations within the pilosebaceous unit, which are crucial for the homeostasis of this barrier-forming epithelium.