pyrimidiinidimeerit

Pyrimidiinidimeerit, or pyrimidine dimers, are covalent linkages formed between adjacent pyrimidine bases in DNA when it absorbs ultraviolet (UV) light. The two main photoproducts are cyclobutane pyrimidine dimers (CPD) and (6-4) photoproducts (6-4PP). Formation occurs primarily under UV-B and UV-C irradiation, causing neighboring pyrimidines on the same DNA strand to join and distort the DNA helix.

These lesions block replication and transcription if not repaired, and they are a major source of UV-induced mutations. They occur most frequently at dipyrimidine sequences (for example TT, TC, CT, and CC) and can lead to mutagenesis and genome instability if unrepaired.

Repair mechanisms are crucial for maintaining genome integrity. Nucleotide excision repair (NER) is the primary pathway in humans and many other organisms, recognizing the distortion and removing a short DNA segment containing the dimer followed by resynthesis. Some organisms possess photoreactivation, in which DNA photolyases use light energy to directly reverse CPDs and 6-4PPs, a repair process largely absent in placental mammals. Transcription-coupled repair, a subpathway of NER, preferentially removes lesions on actively transcribed genes.

Detection and prevention strategies include immunoassays that use dimer-specific antibodies and preventive measures such as sunscreen, protective clothing, and limiting UV exposure to reduce dimer formation. See also cyclobutane pyrimidine dimer, 6-4 photoproduct, nucleotide excision repair, and DNA photolyase.