DNA Repair, DNA Replication, and UV Mutagenesis
Autor: | W. Glenn McGregor |
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Rok vydání: | 1999 |
Předmět: |
DNA Replication
Hypoxanthine Phosphoribosyltransferase DNA Repair DNA repair DNA polymerase Ultraviolet Rays DNA polymerase II cyclobutane pyrimidine dimer Dermatology DNA polymerase delta 030207 dermatology & venereal diseases 03 medical and health sciences 0302 clinical medicine DNA polymers Animals Humans Replication protein A Molecular Biology Polymerase 030304 developmental biology Skin 0303 health sciences REV3 DNA clamp biology General Medicine DNA xeroderma pigmentosum Cell Biology 6-4 photoproduct Molecular biology Mutagenesis biology.protein Nucleotide excision repair Biotechnology |
Zdroj: | Journal of Investigative Dermatology Symposium Proceedings. 4(1):1-5 |
ISSN: | 1087-0024 |
DOI: | 10.1038/sj.jidsp.5640172 |
Popis: | Cells that have been irradiated with ultraviolet light (UV) suffer damage to their DNA, primarily in the form of covalent linkage between adjacent pyrimidines. Such photoproducts represent blocks to RNA and DNA polymerases and are potentially mutagenic. Blockage of RNA polymerase II by a photoproduct in the transcribed strand of an active gene leads to induction of the p53 protein, which induces pleiotropic responses that may include apoptotic cell death. If a cell survives, the blocked polymerase targets the nucleotide excision repair machinery to the site of the lesion, which is repaired in an error-free manner. Repair coupled to transcription in this manner strongly influences the mutation spectrum induced by UV, reducing the proportion of base substitutions that arise from photoproducts on the transcribed strand. If the damage persists when the DNA is replicated in S-phase, either because the cell is unable to repair the damage or because there is insufficient time between the induction of damage and the onset of S-phase. To do so, the replicative DNA polymerase complex may be blocked. In this situation, lesion bypass can be accomplished using an error-free mechanism, or using an error-prone mechanism that involves the newly described, non-processive DNA polymerase zeta encoded by the human homolog of the yeast REV3 gene. |
Databáze: | OpenAIRE |
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