Pyrimidine dimers

Pyrimidine dimers

Pyrimidine dimers (cyclobutane dimer) are pairs of thymine and cytosine bases in DNA that arise via photochemical reactions. Ultraviolet light induces the formation of covalent linkages by reactions localized on the C=C double bonds. Two common UV products are cyclobutane pyrimidine dimer (CPD) and 6,4 photoproduct. These premutagenic lesions alter the structure of DNA and consequently inhibit polymerases and arrest replication. Translesion polymerases introduce coding mutations at these points frequently, both in prokaryotes (SOS mutagenesis) and in eukaryotes. The mutational "hotspots," however, do not correspond to the more vulnerable sites to UV irradiation. Although the TT CPD are the most frequent lesions caused by UV light, the mutational spectrum derived from this source of DNA damage is biased towards the increase in T and A. The reason for this bias is that TT CPDs still can pair with AA and are replicated error free by translesion polymerases. Any C involved in CPDs is prone to be deaminated, inducing a C to T transition.

Cyclobutane photodimers

Cyclobutane pyrimidine dimer (CPD) features a four membered ring arising from the coupling of the C=C double bonds of pyrimidines. T-T dimers thymine dimers formed in between two thymines are most abundant of CPDs. CPD's are readily repaired by nucleotide excision repair machinery. In most organisms they can also be repaired by photolyases, a light-dependent family of enzymes. Xeroderma pigmentosum is a genetic disease where this damage can't be repaired resulting in skin discolouration and multiple tumours on exposure to UV light.


The "6,4-photoproduct," or 6,4 pyrimidine-pyrimidone, occur at one third the frequency of CPD but are more mutagenic.[7] Spore photoproduct lyase provides another enzymatic pathway for repair of thymine photodimers.

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