Cyclobutane pyrimidine dimer lesion in DNA (CPD lesion)

A cyclobutane pyrimidine dimer lesion is a DNA defect caused by UV light, in which two adjacent pyrimidine bases (most commonly thymine-thymine) on the same DNA strand are covalently bonded to form a four-membered cyclobutane ring. This lesion distorts the DNA structure, interrupting normal replication and transcription, and, if unrepaired, promotes mutagenesis leading to cellular dysfunction or cancer. CPDs are recognized and removed by nucleotide excision repair in mammals, or directly reversed by photolyase in most other organisms using light energy. The efficiency of repair and the persistence of these lesions are crucial determinants for UV-associated carcinogenesis, most notably skin cancer. There are no drugs that directly target or remove CPD lesions; therapeutic strategies currently focus on prevention (e.g., sunscreen) or modulation of DNA repair pathways.

Other names

Pyr <> Pyr (Pyrimidine dimer)UV-induced DNA lesionCPD

Not applicable for drugs specifically, but relevant DNA repair mechanisms include: - Photoreactivation (DNA photolyase-mediated direct repair using visible/blue light, found in bacteria, plants, some animals but not placental mammals) - Nucleotide excision repair (NER; dual incisions remove CPD-containing oligonucleotide followed by gap filling/synthesis; primary pathway in humans) - Transcription-coupled repair (accelerates CPD removal from transcribed DNA strands in bacteria; mediated by specialized proteins)