FULL NAME: (6-4) photoproduct

Pyrimidine dimers are molecular lesions formed from thymine or cytosine bases in DNA 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 dimers (CPDs, including thymine dimers) and 6,4 photoproducts. These premutagenic lesions alter the structure of DNA and consequently inhibit polymerases and arrest replication. Dimers may be repaired by photoreactivation or nucleotide excision repair, but unrepaired dimers are mutagenic. In humans they are the primary cause of melanomas. Nucleotide excision repair is a more general mechanism for repair of CPD lesions. This process excises the CPD and synthesizes new DNA to replace the surrounding region in the molecule. Xeroderma pigmentosum is a genetic disease in humans in which the nucleotide excision repair process is lacking, resulting in skin discolouration and multiple tumours on exposure to UV light. Unrepaired pyrimidine dimers in humans may lead to melanoma. Cytotoxicity of the (6-4) photoproduct may be important in the etiology of sunlight-induced carcinogenesis, affecting mutagenesis as well as tumorigenesis. The intricate photochemistry of the (6-4) photoproduct, its formation and photoisomerization, is in itself extremely interesting and may also be relevant to sunlight carcinogenesis. (6-4) photoproducts: T[6-4]T T[6-4]C Dewar isomer of (6-4) photoproduct

DAMAGE TYPE: photoproduct

UV radiation

point mutation
stalled replication fork

nucleotide excision repair (NER)
prokaryotic (SOS) response

DNA repair protein(s) related to damage:

Last modification date: Dec. 20, 2011