A researcher has made a discovery that alters our understanding of how the body’s DNA repair process works and may lead to new chemotherapy treatments for cancer and other disorders. Researchers discovered that base excision repair has a built-in mechanism to increase its effectiveness — it just needs to be captured at a very precise point in the cell life cycle.

The fact that DNA can be repaired after it has been damaged is one of the great mysteries of medical science, but pathways involved in the repair process vary during different stages of the cell life cycle. In one of the repair pathways known as base excision repair (BER), the damaged material is removed, and a combination of proteins and enzymes work together to create DNA to fill in and then seal the gaps.

Led by Eminent Professor Zucai Suo, FSU researchers discovered that BER has a built-in mechanism to increase its effectiveness — it just needs to be captured at a very precise point in the cell life cycle.

The study appears in the current issue of Proceedings of the National Academy of Sciences.

In BER, an enzyme called polymerase beta (PolyB) fulfills two functions: It creates DNA, and it initiates a reaction to clean up the leftover «chemical junk.» Through five years of study, Suo’s team learned that by capturing PolyB when it is naturally cross-linked with DNA, the enzyme will create new genetic material at a speed 17 times faster than when the two are not cross-linked. This suggests that the two functions of PolyB are interlocked, not independent, during BER.

The research improves the understanding of cellular genomic stability, drug efficacy and resistance associated with chemotherapy.

Story Source:
Materials provided by Florida State University. Original written by Audrey Post. Note: Content may be edited for style and length.