A gene that prevents cancer also controls the skin's suntanning machinery, researchers report in the March 9, 2007 issue of the journal Cell.
"The p53 tumor suppressor is commonly mutated in human cancer," explained David Fisher, director of the Melanoma Program in Medical Oncology at Dana-Farber Cancer Institute. "Now, we've found that it plays a role in the skin's tanning response."
The researchers also linked the p53-driven process to other instances of skin darkening not associated with the sun.
It is the most superficial cells in skin that react to sun exposure, Fisher said. When those "keratinocytes" are exposed to the sun, they produce melanocyte-stimulating hormone (MSH), triggering other cells to manufacture the skin-bronzing pigment.
Variation in tanning ability stems from differences in the MSH receptor, Fisher said. For example, the receptor variant found in redheads doesn't respond to MSH, leaving them unable to tan.
However, researchers hadn't identified the factors ultimately responsible for the tanning hormone's production.
MSH is one product of a larger gene sequence that also encodes the natural morphine-like substance, called beta-endorphin, Fisher added. While MSH drives the suntan response, beta-endorphin is believed to drive sun-seeking behavior.
Fisher's team showed that mice require p53 in order to switch on genes that produce MSH and tan. Similarly, the induction of beta-endorphin by the sun also depends on p53.