Beachgoers are aware of the experience of spending hours within the sun, going home, and noticing only hours later that their skin has modified color.

A latest Tel Aviv University study uncovers the science behind the mystery of why the body’s tanning process doesn’t occur immediately after sun exposure, but only after just a few hours and even days.

The research findings reveal the mechanism behind this phenomenon, in line with which the body’s initial response is to prioritize repairing DNA damage within the skin cells, which inhibits the mechanism answerable for skin pigmentation, commonly generally known as tanning.

The study, published within the Nature Group’s Journal of Investigative Dermatology, was led by doctoral student Nadav Elkoshi and Prof. Carmit Levy of the Department of Human Molecular Genetics and Biochemistry at Tel Aviv University’s Faculty of Medicine, and in collaboration with a lot of other researchers from Tel Aviv University, Wolfson Medical Center, the Weizmann Institute of Science, the University of California, and Paris-Saclay University.

We’ve two mechanisms designed to guard the skin from exposure to dangerous UV radiation. The primary mechanism repairs the DNA within the skin cells damaged by the radiation, while the second mechanism involves increased production of melanin, which darkens the skin as a way to protect it from future exposure to radiation. In our study, we discovered why the tanning phenomenon doesn’t occur immediately when the body is exposed to the sun, but only following a delay. It seems that the mechanism that repairs our DNA takes precedence over all other systems within the cell, temporarily inhibiting the pigmentation mechanism. Only after the cells repair the genetic information to the perfect of their ability do they start to supply the increased melanin.”

Nadav Elkoshi, Doctoral Student, Tel Aviv University

To check their hypothesis, the Tel Aviv University researchers activated the DNA repair mechanism in each animal models and human skin tissues. In each, a tan developed even with none exposure to UV radiation, substantiating their findings.

Prof. Carmit Levy: “The genetic information should be shielded from mutations, so this repair mechanism takes precedence contained in the cell during exposure to ultraviolet radiation from the sun. The DNA repair mechanism essentially tells all the opposite mechanisms within the cell, ‘Stop every thing, and let me work in peace.’ One system effectively paralyzes the opposite, until the DNA correction reaches its peak, which occurs just a few hours after the UV exposure. Only then does the pigment production mechanism get to work. In our previous research, we showed that a protein called MITF, which is activated during exposure, is answerable for regulating these two mechanisms. In the present study we show that one other protein, called ATM, which plays a key role in DNA repair, prompts one mechanism while disabling the opposite. This process likely harnesses the pigmentation mechanism’s components to maximise the possibilities of the cell surviving without mutations following radiation exposure.”

Prof. Levy concludes: “This scientific discovery has revealed a molecular mechanism that would function a foundation for further research which will result in progressive treatments that can provide maximum protection of the skin against radiation damage; in the long term, it might even contribute to the prevention of skin cancer.”

Source:

Journal reference:

Elkoshi, N., et al. (2023) ATM signaling delays skin pigmentation upon UV exposure by mediating MITF function towards DNA repair mode. Journal of Investigative Dermatology. doi.org/10.1016/j.jid.2023.03.1686.