miRNAs, “stemness” and skin.

The epidermis and its appendages provide organisms with protection from the environment, keeping pathogens out and preventing the loss of essential body fluids. To perform both functions, the skin has elaborated a complex differentiation process known as cornification. The skin‟s renewal capacity, responsible for maintaining tissue homeostasis, regenerating hair, and repairing the epidermis after injury, resides in the basal proliferating compartment where epidermal stem cells are located. These cells possess the remarkable capacity to both self-perpetuate and give rise to the differentiating cells that form mature tissues. Recent findings indicate that miRNAs play an essential role in orchestrating the formation of epidermis and skin appendages, in particular at the interface between stemness and differentiation

p63 in epithelial development.

The epidermis, the outer layer of the skin composed of keratinocytes, is a stratified epithelium that functions as a barrier to protect the organism from dehydration and external insults. The epidermis develops following the action of the transcription factor p63, amember of the p53 family of transcription factors. The Trp63 gene contains two promoters driving the production of distinct proteins, one with an N-terminal transactivation domain (TAp63) and one without (ΔNp63), although their relative contribution to epidermal development is not clearly established. Trp63 mutations are involved in the pathogenesis of several human diseases, phenotypically characterized by ectodermal dysplasia. In this review, we summarize the current advances that have been made in understanding the role of p63 in epidermal morphogenesis

TAp73 promotes anti-senescence-anabolism not proliferation

TAp73, a member of the p53 family, has been traditionally considered a tumor suppressor gene, but a recent report has claimed that it can promote cellular proliferation. This assumption is based on biochemical evidence of activation of anabolic metabolism, with enhanced pentose phosphate shunt (PPP) and nucleotide biosynthesis. Here, while we confirm that TAp73 expression enhances anabolism, we also substantiate its role in inhibiting proliferation and promoting cell death. Hence, we would like to propose an alternative interpretation of the accumulating data linking p73 to cellular metabolism: we suggest that TAp73 promotes anabolism to counteract cellular senescence rather than to support proliferation