Scientists have confirmed the secondary repair mechanism of DNA damage, demonstrating that cells can sequester damaged DNA through the 53BP1 nuclear bodies and delay replication time to complete the repair.The related research results were published in Nature Cell Biology on 25 February,2019, entitled“53BP1 nuclear bodies enforce replication timing at under-replicated DNA to limit heritable DNA damage”. The research team used fluorescent dyes to label 53BP1-NBs in living cells and tracked them under a microscopes for multiple generations.
    The formation of the 53BP1-NBs interrupts the replication of the DNA chain with the wrong gene, inhibiting DNA replication until the late S phase, leaving valuable time for specific repair.The key molecule of this repair mechanism is a RAD52 enzyme. The enzyme is a tumor suppressor protein that protects DNA from cancer mutations. In addition, this study demonstrates that absence or malfunction of 53BP1-NBs causes premature replication of the affected gene loci.
    The 53BP1-NBs completes the repair of damage in DNA replication, preventing the conversion of stochastic under-replications into genome instability,and slowing the spread of DNA damage in cells. In addition, the study showed that 53BP1-NBs completed gene repair after mitosis, revealing for the first time the possibility that whole genome replication may need to exceed one cell division cycle.
    This finding may play an important role in improving cancer treatment. Many anticancer drugs destroy the DNA of rapidly dividing cancer cells, so understanding the timing and mechanisms of DNA repair is critical to the development of new drugs and minimizing the side effects of current treatments.
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