Researchers at the Institute of Cancer Research have discovered a cellular mechanism that protects DNA during the process of cell division [1].
This finding is significant because it reveals how cells safeguard genetic material during a highly vulnerable phase of their life cycle. If DNA is not properly protected during division, the resulting damage can lead to the development of various diseases [2].
Based in London, the research team identified a process that specifically resolves DNA bridges [3]. These bridges occur when genetic material fails to separate cleanly as a cell splits into two. By resolving these bridges, the mechanism ensures that the daughter cells receive intact genetic information [3].
While the Institute of Cancer Research said it identified a specific protein responsible for resolving these bridges during mitosis [1], other reports highlight the role of the enzyme Pol θ (Pol theta) [4]. This enzyme drives a DNA repair pathway that helps cells survive the damage associated with these genetic bridges [4].
The discovery occurred in July 2026 [2]. The team focused on the specific window of mitosis where the risk of chromosomal instability is highest. By understanding how the cell prevents these bridges from causing permanent mutations, scientists can better understand the origins of genomic instability [3].
This cellular shielding acts as a critical fail-safe. Without this mechanism, the physical tension of dividing cells could snap DNA strands, leading to deletions, or translocations of genetic code [2]. The research provides a new map of the proteins and enzymes that collaborate to maintain the integrity of the human genome during replication [1].
“The mechanism ensures that the daughter cells receive intact genetic information.”
The identification of this DNA-bridge resolution mechanism provides a deeper understanding of how cells avoid mutations during mitosis. By pinpointing the specific proteins and enzymes involved, such as Pol θ, researchers may find new targets for therapeutic intervention in cancers where this repair mechanism is either absent or hyperactive, contributing to tumor growth.
