Researchers from Yale University have identified how the molecule DNA2 helps begin the complex process of repairing breaks in DNA that can cause chromosome rearrangements – abnormalities linked to cancer.
Biochemical analysis by James Daley, Adam Miller, and colleagues in the lab of Patrick Sung, professor of molecular biophysics and biochemistry and of therapeutic radiology, identifies a novel role for this enzyme. It shows that DNA2 travels down a single-stranded DNA tail, and then cuts the damaged DNA when it reaches a double-stranded region, an important early step in repair. Daley notes that DNA2 is a potential target for cancer therapeutics because it is overexpressed in many tumors and promotes their proliferation.
The research was published March 23 in the journal Genes and Development.
Reference: “A novel role of the Dna2 translocase function in DNA break resection” by Adam S. Miller, James M. Daley, Nhung Tuyet Pham, Hengyao Niu, Xiaoyu Xue, Grzegorz Ira and Patrick Sung, 23 March 2017, Genes & Development.