In a new study, researchers at the University at Buffalo have discovered how an enzyme called UvrB detects damage to DNA caused by ultraviolet (UV) light. The findings, published in the journal Nature Communications, could lead to the development of new treatments for skin cancer and other diseases caused by UV radiation.

UV radiation from the sun can damage DNA, leading to mutations that can cause skin cancer and other diseases. To protect themselves from this damage, cells have a number of mechanisms to repair damaged DNA. One of these mechanisms is the nucleotide excision repair (NER) pathway, which is initiated by the UvrB enzyme.

UvrB detects damaged DNA by binding to a specific type of DNA damage called a cyclobutane pyrimidine dimer (CPD). CPDs are formed when two adjacent pyrimidine bases on the same strand of DNA are cross-linked by UV light.

The new study reveals how UvrB is able to detect CPDs. The researchers found that UvrB has a special "pocket" that binds to the CPD. This pocket is lined with amino acids that interact with the CPD and help to stabilize the enzyme-DNA complex.

The researchers also found that UvrB undergoes a conformational change when it binds to a CPD. This conformational change exposes a previously hidden region of the enzyme that is essential for the NER pathway.

"This study provides a detailed understanding of how UvrB detects damaged DNA," said study senior author Dr. Valerie Weaver, PhD, SUNY Distinguished Professor in the Department of Biochemistry at UB. "This information could lead to the development of new treatments for skin cancer and other diseases caused by UV radiation."

In addition to skin cancer, UV radiation can also cause cataracts, macular degeneration, and immune suppression. The findings from this study could help to develop new treatments for these diseases as well.