Researchers from Tokyo Metropolitan University have identified key factors in the mechanism behind DNA repair in our bodies.
Nov 12 2023Tokyo Metropolitan University For the first time, they showed that the "proofreading" portion of the DNA replicating enzyme polymerase epsilon ensured safe termination of replication at damaged portions of the DNA strand, ultimately saving DNA from severe damage. This new knowledge arms scientists with ways to make anti-cancer drugs more effective, and new diagnostic methods.
The exact mechanism behind fork reversal remains unknown. Understanding how DNA damage is prevented is paramount not only to prevent cancers, but also ensure the effectiveness of cancer drugs which rely on DNA damage. Take camptothecin , an anti-cancer drug that introduces lots of single-strand breaks; since cancer cells tend to replicate quicker, they create lots of seDSBs and die out, leaving normal cells less harmed.
Firstly, they found that cells which are deficient in the exonuclease part showed strong susceptibility to exposure to CPT. Suppression of a factor known as PARP, the only other player known to affect fork reversal, also led to increased cell death. However, when both were suppressed, there was no further increase in cell death beyond what was seen with PARP. This suggests that PARP and the polymerase epsilon exonuclease work together to trigger fork reversal.
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