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UC Davis researchers discover complexities of DNA repair
Date:10/23/2011

57) that favors recombination repair and another (Srs2) that inhibits recombination repair. By controlling the balance between the two enzymes, Rad51 can initiate genetic repair - or the u-turn - as needed.

"It is a tug-of-war that has important implications for the cell because, if recombination occurs at the wrong time in the wrong place, the cell may die as a consequence." The ability of the repair system to abort ill-fated repair attempts, gives the cell a second shot, improving cellular survival after its DNA is damaged. This is exactly what is dreaded in cancer treatment.

"There are a lot of hints in the scientific literature suggesting that DNA repair contributes to resistance to treatments that are based on inducing DNA damage such as radiation or certain types of chemotherapy," Heyer said. "The ability of cancer cells to withstand DNA damage directly affects treatment outcome, and understanding the fundamental mechanisms of the DNA repair systems will enable new approaches to overcome treatment resistance."

Heyer said the team's next step is to look at the enzyme system in humans and see whether they find the same principles at work. This work has received funding and has already begun. One application of this work will be to target the self-correcting mechanism in cancer cells as a way of sensitizing them to radiation and/or chemotherapy treatments.

"If we can confirm that these types of mechanisms exist in human cells, then we will have an approach for making cancer cells more sensitive to DNA damage-inducing treatments."


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Contact: Dorsey Griffith
dorsey.griffith@ucdmc.ucdavis.edu
916-734-9118
University of California - Davis Health System
Source:Eurekalert

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