A light-sensitive receptor (rhodopsis) previously thought to exist only in the eye has been found in human skin cells, detecting certain wavelengths of ultraviolet light to protect DNA from damage. Skin cells, called malanocyte, send out calcium ion signals to produce the pigment melanin. Until now, scientists knew only that melanin production occurred days after UVB radiation had already begun damaging DNA. Tanning of the skin is a protective response. Melanin, the pigment responsible for darkening skin, is believed to protect skin cells from damage caused by ultraviolet radiation in sunlight by absorbing the radiation. Elena Oancea, left, and Nadine Wicks discovered that skin cells contain rhodopsin, a photosensitive receptor used by the eye to detect light. It's part of human skin’s self-defense against damage to DNA. (Image: Mike Cohea/Brown University) “As soon as you step out into the sun, your skin knows that it is exposed to UV radiation,” said Elena Oancea, assistant professor of biology in the Department of Molecular Pharmacology, Physiology and Biotechnology at Brown University. “This is a very fast process, faster than anything that was known before.” In lab experiments with melanocytes, researchers discovered that the cells contain rhodopsin, which unleash calcium ion signals that instigate melanin production. The team first looked to see whether UV light instigated a calcium signaling response. They found nothing. But guessing that the skin might sense light in the same way that the eyes do, they added retinal, a co-factor of opsin receptors including rhodopsin. “When we did that, we saw an immediate and massive calcium response,” said graduate student Nadine Wicks. Further investigation found that the cells contained rhodopsin RNA and protein. Under UV light, when the scientists reduced rhodopsin levels in the cells, calcium signaling was reduced. Later, when they starved cells of retinal, they found that melanin production dropped. The authors also determined that long-wavelength UVA light, rather than short-wavelength UVB light, is what stimulates rhodopsin in melanocytes. During several experiments, they traced the following process: When UVA light strikes rhodopsin receptors with retinal, it triggers calcium signals within a few seconds. After an hour, measurable amounts of melanin accumulate, although in relatively small quantities compared with the production that occurs within 24 hours. Human melanocyte skin cells fluoresce as their calcium signaling spikes after exposure to ultraviolet light and retinal, a key step in producing melanin. This led researchers to discover rhodopsin receptors in skin, which detect UVA light. (Image: Brown University) Oancea and Wicks still have questions, however. One is whether rhodopsin is acting alone or in concert with another yet undiscovered receptor. Another is whether melanocytes immediately begin exporting melanin to other kinds of skin cells for protection or whether they keep the early supply for themselves. Although scientists are learning more about how the skin responds to and protects itself against UV radiation, Oancea said, people should not change what they do to protect themselves. “This doesn’t say, ‘Don’t use sunscreen,’” Oancea said. The work was published in Current Biology; Oancea was senior author and Wicks lead author. For more information, visit: www.brown.edu