New research published this week reveals that our skin is able to “sense” ultraviolet light in the same way as our eyes because skin cells contain rhodopsin, the same photosensitive receptor that the eye uses to detect light. The study also shows that the receptor is part of the skin’s melanin-producing defense against DNA damage, the trigger for which occurs much faster than previously thought.

You can read how biologists at Brown University in Providence, Rhode Island, in the US arrived at these findings in the 3 November online first issue of Current Biology.

Senior author Elena Oancea, assistant professor of biology in the Department of Molecular Pharmacology, Physiology, and Biotechnology at Brown, told the press:

“As soon as you step out into the sun, your skin knows that it is exposed to UV radiation.”

“This is a very fast process, faster than anything that was known before,” she added.

Oancea and colleagues found that melanocytes, specialized skin cells that produce the pigment melanin, detect ultraviolet light using rhodopsin, a light-sensitive receptor previously thought to exist only in the eye. This ability starts the production of melanin within hours, much sooner than previously thought. Melanin not only gives skin its color, but also protects it against DNA damage from the sun by absorbing its UVB rays.

Previous to this study, scientists thought that melanin production only kicked in after a few days, about the same length of time as it takes to develop a “tan”.

Oancea and her team carried out lab experiments with human melanocytes and found not only that the cells contain rhodopsin, but they also discovered how rhodopsin releases the calcium ion signals that trigger melanin production.

In the first experiment, they used ultraviolet light to see if it prompted the calcium signalling, but it didn’t. So acting on a hunch that perhaps the skin behaves like the eyes in sensing light, they added retinal, a “co-factor” that combines with the protein opsin to make photosensitive receptors, including rhodopsin.

Lead author and graduate student Nadine Wicks, said:

“When we did that, we saw an immediate and massive calcium response.”

In further experiments the researchers found that the cells contained rhodopsin RNA and protein, and when they reduced rhodopsin levels in the cells and shone UV light on them, the calcium signalling was reduced.

Then they tried starving the cells of retinal, the co-factor that needs to combine with opsin to make the photosensitive receptors, and found that melanin production went down.

They also found it is the longer wavelength UVA as opposed to shorter wavelength UVB light that triggers rhodopsin in the melanocytes.

Although they learned a lot, the researchers found many questions still remain unanswered. For instance, does rhodopsin act alone, or does it collaborate with other receptors? And do melanocytes start exporting melanin to other skin cells straight away (in order to protect them from DNA damage), or do they stock up first for their own defense and then only export after a certain level is reached?

Although studies like these suggest the skin does more to protect itself from the sun than perhaps we previously thought, we still don’t know enough to be tell people to change what they do to protect themselves against harm from the sun, as Oancea put it:

“This doesn’t say, ‘Don’t use sunscreen’.”

Funds from Brown University, the National Institutes of Health, and the Natural Sciences and Engineering Research Council of Canada helped pay for the study.

Written by Catharine Paddock PhD