Researchers from Tokyo Metropolitan University have made a groundbreaking discovery in the field of DNA repair, shedding light on the role of the RecA protein in homologous recombination. This process is crucial for repairing breaks in double-stranded DNA, and the findings promise new directions in cancer research.

Homologous recombination (HR) is a fundamental process found in all living organisms, playing a vital role in repairing DNA damage caused by various internal and environmental stressors. When double-strand breaks occur, HR facilitates the accurate repair of DNA, as well as the exchange of genetic information, contributing to biodiversity.

During HR, the RecA protein binds to the exposed single strand and an intact double strand nearby, initiating a process known as strand invasion. However, the exact mechanism of this process, particularly the role of RecA in unwinding the double strand, has remained unclear.

Professor Kouji Hirota and his team at Tokyo Metropolitan University conducted a study to investigate the competing models for HR. They aimed to determine whether RecA unwinds the double strand during the ‘homology search’ or if unwinding only occurs during strand invasion.

Their research involved testing a mutant of RecA that cannot separate the double strands, and the results revealed minimal impact on DNA repair. Additionally, their collaboration with the Tokyo Metropolitan Institute of Medical Science provided further insights into the intricate biochemical processes involved in DNA repair.

These findings have significant implications for cancer research and the understanding of DNA repair mechanisms. By elucidating the role of RecA in homologous recombination, this research paves the way for potential advancements in cancer treatment and the development of targeted therapies.