A team led by a Baylor University researcher has revealed a breakthrough article that gives a better understanding of the dynamic process by which the molecular repair machinery recognizes sunlight-induced DNA damage in cells as needing repair.
Ultraviolet light from the sun is a universal carcinogen that may inflict structural harm to the cellular DNA. As DNA carries essential blueprints for cellular functions, failure in eradicating and restoring damaged components of DNA in a timely fashion can have detrimental outcomes and result in skin cancers in people, stated lead author Jung-Hyun Min, Ph.D., associate professor of chemistry and biochemistry in Baylor’s College of Arts & Sciences.
Min and her staff showed how the restore protein Rad4/XPC would bind to one such UV-induced DNA damage—6-4 photoproduct—to mark the damaged site along the DNA in preparation for the remainder of the nucleotide excision repair (NER) process in cells.
The research—”Structure and mechanism of pyrimidine-pyrimidone (6-4) photoproduct recognition by the Rad4/XPC nucleotide excision repair complex”—is revealed in the journal Nucleic Acids Research (NAR) as a “breakthrough article.”
Breakthrough articles current high-impact studies answering long-standing questions within the field of nucleic acids research and opening new areas and mechanistic hypotheses for investigation. They’re the very best papers revealed at NAR, constituting 1 to 2 % of those received by the journal.
UV light threatens the integrity of the genome by generating cellular DNA harm referred to as intra-strand crosslink injury, Min stated. Two major varieties of these lesions are cyclobutane pyrimidine dimer (CPD), which makes up about 70 % of such damage; and 6-4 photoproduct (6-4PP), which constitutes about 30 %.