If you leave your skin unprotected in the sun for a longer duration, you will get a sunburn. In other words, UV radiation from the sun causes an inflammatory response in exposed skin cells.
If you are burned too many times, you’ll have premature skin ageing, wrinkles, and a higher chance of skin cancer. But what occurs inside your skin cells when they are attacked by UV rays?
Gabriele Alessandro Fontana, a James Mitchell Award awardee and ETH scientist, is interested in how cells repair damaged DNA. The mechanisms he has discovered will contribute to a better understanding of diseases and the development of new treatments.
These mechanisms are critical because more extreme damage can result in malignant mutations, which can lead to cancer.
“In the course of my work with colleagues at the Friedrich Miescher Institute, we discovered the key role of a protein called Rif1,” the researcher says. This protein acts as a kind of molecular “sticking plaster” for damaged DNA.
In this study, the biologist found that this process takes place at very specific locations within the cell.
“When a DNA strand is broken,” he says, “the damaged DNA is shunted to the edge of the nucleus, where the protein Rif1 is located, waiting to receive the broken DNA extremities and start the repair process.”
When the ETH researcher first saw this procedure under the microscope, he couldn’t believe his eyes. It demonstrated that there is, in fact, a distinct location within the cell — a sort of workshop with its own delivery service – where certain sorts of DNA damage are repaired. No one has ever proved this so plainly before.
Fontana exposed human skin cells that had been grown in the lab to UV radiation in a methodical manner. He then examined what happens inside the cells as a result of this exposure using a microscope and other biochemical and genetic procedures. In the process, he discovered a mechanism that scientists have long failed to fully understand.
“Increased UV radiation causes damage and mutations in specific locations in the nuclear and mitochondrial DNA – and we can use these changes in skin cells as a new indicator of skin disease and ageing,” says the author, summarising the findings of a study he and his supervisor, Hailey Gahloncall made, will publish.
In the future, those precise mutations could be used as biomarkers to improve and accelerate the detection of diseased skin cells.
However, the biologist reveals more than just a chemical link between UV light and DNA mutations in skin cells. Fontana is also researching the molecular basis of how UV-induced DNA damage might be prevented by unique active ingredients that can be easily added to cosmetic products in the future.
“These findings could form the basis for a new generation of sunscreens with more efficient UV filters,” he says, with understandable pride.
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