DNA damage-induced mutation: tolerance via translesion synthesis
Translesion synthesis (TLS) appears to be required for most damage-induced mutagenesis in the yeast Saccharomyces cerevisiae, whether the damage arises from endogenous or exogenous sources. Thus, the production of such mutations seems to occur primarily as a consequence of the tolerance of DNA lesio...
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Published in | Mutation research Vol. 451; no. 1-2; p. 169 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
30.06.2000
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Abstract | Translesion synthesis (TLS) appears to be required for most damage-induced mutagenesis in the yeast Saccharomyces cerevisiae, whether the damage arises from endogenous or exogenous sources. Thus, the production of such mutations seems to occur primarily as a consequence of the tolerance of DNA lesions rather than an error-prone repair mechanism. Tolerance via TLS in yeast involves proteins encoded by members of the RAD6 epistasis group for the repair of ultraviolet (UV) photoproducts, in particular two non-essential DNA polymerases that catalyse error-free or error-prone TLS. Homologues of these RAD6 group proteins have recently been discovered in rodent and/or human cells. Furthermore, the operation of error-free TLS in humans has been linked to a reduced risk of UV-induced skin cancer, whereas mutations generated by error-prone TLS may increase the risk of cancer. In this article, we review and link the evidence for translesion synthesis in yeast, and the involvement of nonreplicative DNA polymerases, to recent findings in mammalian cells. |
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AbstractList | Translesion synthesis (TLS) appears to be required for most damage-induced mutagenesis in the yeast Saccharomyces cerevisiae, whether the damage arises from endogenous or exogenous sources. Thus, the production of such mutations seems to occur primarily as a consequence of the tolerance of DNA lesions rather than an error-prone repair mechanism. Tolerance via TLS in yeast involves proteins encoded by members of the RAD6 epistasis group for the repair of ultraviolet (UV) photoproducts, in particular two non-essential DNA polymerases that catalyse error-free or error-prone TLS. Homologues of these RAD6 group proteins have recently been discovered in rodent and/or human cells. Furthermore, the operation of error-free TLS in humans has been linked to a reduced risk of UV-induced skin cancer, whereas mutations generated by error-prone TLS may increase the risk of cancer. In this article, we review and link the evidence for translesion synthesis in yeast, and the involvement of nonreplicative DNA polymerases, to recent findings in mammalian cells. |
Author | Vonarx, E J Straffon, A F Kunz, B A |
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Snippet | Translesion synthesis (TLS) appears to be required for most damage-induced mutagenesis in the yeast Saccharomyces cerevisiae, whether the damage arises from... |
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SubjectTerms | DNA Damage - genetics DNA Polymerase theta DNA Repair - physiology DNA-Directed DNA Polymerase - genetics DNA-Directed DNA Polymerase - metabolism Fungal Proteins - genetics Fungal Proteins - metabolism Humans Mutagenesis Mutation Saccharomyces cerevisiae - genetics Saccharomyces cerevisiae Proteins |
Title | DNA damage-induced mutation: tolerance via translesion synthesis |
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