A group of researchers, led by molecular biologist Anna Constance Vind from University of Copenhagen, has found that the RNA, not the DNA, plays a major role in triggering acute sunburn reactions. The work is published in the journal Molecular Cell.

Spending enough time in the sun without proper protection can lead to sunburn. Unlike low-intensity thermal burns, which occur because heat damages body proteins, sunburn is caused by prolonged exposure to short-wave ultraviolet (UV) radiation. However, regardless of how the damage is caused, the result is the same: Various cellular stresses alert the immune system to a threat, triggering a signaling effect that dilates some blood vessels, constricts others, and increases sensitivity to pain.

“Sunburn damages the DNA, leading to cell death and inflammation. So the textbooks say,” Vind noted.

New work by researchers, however, has cast doubt on this theory. The researchers were able to prove that the RNA, not DNA, is the main cause of sunburn.

Vind and her colleagues showed this by using genetically modified mice. These mice lacked a protein responsible for the stress response, called ZAK-alpha. This protein interacts with the cellular machinery that converts messenger RNAs into proteins. When the process does not go according to plan, it sends certain signals to the body.

When ZAK-alpha mice were exposed to ultraviolet light, the researchers found that the stress response triggered by the RNA played a key role in the development of sunburn symptoms. Mice without ZAK-alpha, however, did not get sunburns. This further confirmed that RNA damage is the cause of our body's sensitivity to the sun.

"The fact that the DNA does not control the skin’s initial response to UV radiation, but that something else does and that it does so more effectively and more quickly, is quite the paradigm shift," Vind concluded.