New Discoveries in DNA Repair Point to Exciting Paths in Cancer Research
In Tokyo, on January 21st, researchers at Tokyo Metropolitan University made significant progress in understanding how DNA repair works, especially in relation to cancer.
by TAUHID SHAH: January 21: Sunday: 23:12 PM| 2024 Updated.
At the heart of their work is a protein called RecA, which acts like a molecular conductor, guiding the repair of breaks in the double-stranded DNA. Think of it as putting together puzzle pieces. This protein smoothly integrates a dangling single strand into intact double strands, fixing the broken parts based on the correct sequence.
The researchers discovered how RecA knows where to place the single strand without unwinding the DNA. This process, known as homologous recombination (HR), is essential for all living things, from animals and plants to fungi and bacteria.
In the intricate dance of HR, one of the exposed ends of the broken DNA gracefully disappears, revealing a single-stranded outcome. This is called resection. Then, a protein called RecA steps in, searching for the right sequence. Once found, it merges the single strand into the double helix—a process known as strand invasion.
This whole dance repairs the damaged DNA, using the existing DNA as a guide.
Professor Kouji Hirota and his team at Tokyo Metropolitan University investigated two different ideas about how RecA works. One suggests that RecA unfolds a part of the double strand during the “homology search.” The other says that RecA binds without unwinding until strand invasion happens.
Working with colleagues from the Tokyo Metropolitan Institute of Medical Science, they used two methods to unravel this mystery and determine which idea was correct.
Insights into homologous recombination are crucial for understanding what happens when things go wrong. For example, in breast cancer, genes BRCA1 and BRCA2 influence how single-stranded DNA gets loaded onto RAD51—the human version of RecA. This connection suggests that problems with homologous recombination might contribute to a higher risk of breast cancer in people with genetic issues in BRCA1 or BRCA2.
The researchers hope their findings will open new paths in cancer research and lead to a better understanding of how things work in this complex field.
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