Mice lacking p53 (top) don't tan.


The guardian of the genome, p53, can induce DNA repair, hold the cell cycle while repair work is done, and induce apoptosis if the damage is too great. Now, Rutao Cui, David Fisher (Harvard Medical School, Boston, MA), and colleagues have discovered a new way in which p53 protects our genomes—it gives us a suntan.

The DNA damage caused by UV exposure has long been known to up-regulate p53. Mice that lack p53 have a propensity to develop tumors upon UV exposure. The team now finds that these mice also fail to tan.

Tanning occurs when keratinocytes make more melanocyte-stimulating hormone (MSH) and thus induce melanocytes to produce large amounts of the pigment melanin. MSH is a cleavage product of the POMC pro-hormone. The team found that p53 directly binds to, and increases transcription from, the POMC gene promoter in response to UV treatment.

p53 also promoted POMC and melanin production when induced by factors other than UV, such as the cancer drug etoposide. Melanin provides protection to the skin by mopping up free radicals and by acting as a direct shield from UV radiation. Inducing melanin via the p53 pathway might potentially provide a sunless golden tan. This strategy might be good for reducing cancer risk, although vitamin D levels may need supplementing if the sun were continuously avoided.


Cui, R., et al.