The mechanism that repairs our DNA takes precedence over all other systems in the cell, temporarily inhibiting the pigmentation mechanism.

New research uncovers the science behind why the body's tanning process does not occur immediately after sun exposure, but only after a few hours or even days. 

The mechanism that repairs our DNA takes precedence over all other systems in the cell, temporarily inhibiting the pigmentation mechanism. Only after the cells repair the genetic information to the best of their ability do they begin to produce the increased melanin, according to the study in the Journal of Investigative Dermatology.

“We have two mechanisms designed to protect the skin from exposure to dangerous UV radiation,” says researcher doctoral student Nadav Elkoshiof the Department of Human Molecular Genetics and Biochemistry at Tel Aviv University’s Faculty of Medicine in a news release. “The first mechanism repairs the DNA in the skin cells damaged by the radiation, while the second mechanism involves increased production of melanin, which darkens the skin in order to protect it from future exposure to radiation.”

To test their hypothesis, the researchers activated the DNA repair mechanism in both animal models and human skin tissues. In both, a tan developed even without any exposure to UV radiation, substantiating their findings.

“The genetic information must be protected from mutations, so this repair mechanism takes precedence inside the cell during exposure to ultraviolet radiation from the sun,” Prof. Carmit Levy of the Department of Human Molecular Genetics and Biochemistry at Tel Aviv University’s Faculty of Medicine. “The DNA repair mechanism essentially tells all the other mechanisms in the cell, ‘Stop everything, and let me work in peace.’ One system effectively paralyzes the other, until the DNA correction reaches its peak, which occurs a few hours after the UV exposure. Only then does the pigment production mechanism get to work.”

In previous research, the team showed that a protein called MITF, which is activated during exposure, is responsible for regulating these two mechanisms. In the current study,  they show that another protein, called ATM, which plays a key role in DNA repair, activates one mechanism while disabling the other. “This process likely harnesses the pigmentation mechanism’s components to maximize the chances of the cell surviving without mutations following radiation exposure,” Levy said.

“This scientific discovery has revealed a molecular mechanism that could serve as a foundation for further research that may lead to innovative treatments that will provide maximum protection of the skin against radiation damage; in the long run, it may even contribute to the prevention of skin cancer.”

PHOTO CAPTION: Prof. Carmit Levy

PHOTO CREDIT: Tel Aviv University