La Jolla, CAIn order to preserve our DNA, cells have developed an intricate system for monitoring and repairing DNA damage. Yet precisely how the initial damage signal is converted into a repair response remains unclear. Researchers at the Salk Institute for Biological Studies have now solved a crucial piece of the complex puzzle.
In a forthcoming article in the Dec. 24 issue of Molecular Cell, they show that a protein named CtIP plays an essential role in the DNA damage "signal-to-repair" conversion process. "Being able to repair damaged DNA is extremely important; the cell has to know when it has received this type of damage and respond appropriately," explains Tony Hunter, Ph.D., American Cancer Society Professor in the Molecular and Cell Biology Laboratory and director of the Salk Institute Cancer Center, who led the study. "Failure to do so can have disastrous consequences."
The DNA in our cells is under constant attack from reactive chemicals generated as byproducts of cellular metabolism. In addition, it is assaulted by x-rays, ultraviolet radiation from the sun, and environmental carcinogens such as tobacco smoke. As a result of this continuous bombardment, some studies have estimated that the DNA in a single human cell gets damaged over 10,000 times every day.
If not repaired properly, the damage leads to mutations, which over time can cause cancer. "As a result, individuals with an inherited impairment in DNA repair capability are often at increased risk of cancer," notes first author Zhongsheng You, Ph.D., a former postdoctoral researcher at the Salk Institute and now an assistant professor at Washington University School of Medicine in St. Louis.
DNA consists of two intertwined strands so that when the DNA is broken, two ends are revealed, one from each strand. In order to repair the DNA break, one strand is trimmed awayor resectedlike a loose thread, leaving only the second strand. This exposed strand th
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