Suffering in silence: the tolerance of DNA damage - PubMed (original) (raw)
Review
doi: 10.1038/nrm1781.
Affiliations
- PMID: 16341080
- DOI: 10.1038/nrm1781
Review
Suffering in silence: the tolerance of DNA damage
Errol C Friedberg. Nat Rev Mol Cell Biol. 2005 Dec.
Abstract
When cells that are actively replicating DNA encounter sites of base damage or strand breaks, replication might stall or arrest. In this situation, cells rely on DNA-damage-tolerance mechanisms to bypass the damage effectively. One of these mechanisms, known as translesion DNA synthesis, is supported by specialized DNA polymerases that are able to catalyse nucleotide incorporation opposite lesions that cannot be negotiated by high-fidelity replicative polymerases. A second category of tolerance mechanism involves alternative replication strategies that obviate the need to replicate directly across sites of template-strand damage.
Similar articles
- How are specialized (low-fidelity) eukaryotic polymerases selected and switched with high-fidelity polymerases during translesion DNA synthesis?
Fischhaber PL, Friedberg EC. Fischhaber PL, et al. DNA Repair (Amst). 2005 Feb 3;4(2):279-83. doi: 10.1016/j.dnarep.2004.08.011. DNA Repair (Amst). 2005. PMID: 15590336 Review. - [Advances of study on human translesion synthesis DNA polymerase eta].
Hu GH, Zhuang ZX. Hu GH, et al. Wei Sheng Yan Jiu. 2006 Nov;35(6):808-11. Wei Sheng Yan Jiu. 2006. PMID: 17290774 Review. Chinese. - Mechanisms of dealing with DNA damage-induced replication problems.
Budzowska M, Kanaar R. Budzowska M, et al. Cell Biochem Biophys. 2009;53(1):17-31. doi: 10.1007/s12013-008-9039-y. Epub 2008 Nov 26. Cell Biochem Biophys. 2009. PMID: 19034694 Review. - Replication of damaged DNA by translesion synthesis in human cells.
Lehmann AR. Lehmann AR. FEBS Lett. 2005 Feb 7;579(4):873-6. doi: 10.1016/j.febslet.2004.11.029. FEBS Lett. 2005. PMID: 15680966 Review. - [Eukaryotic error prone DNA polymerases: suggested roles in replication, repair and mutagenesis].
Krutiakov VM. Krutiakov VM. Mol Biol (Mosk). 2006 Jan-Feb;40(1):3-11. Mol Biol (Mosk). 2006. PMID: 16523685 Review. Russian.
Cited by
- A defect in homologous recombination leads to increased translesion synthesis in E. coli.
Naiman K, Pagès V, Fuchs RP. Naiman K, et al. Nucleic Acids Res. 2016 Sep 19;44(16):7691-9. doi: 10.1093/nar/gkw488. Epub 2016 Jun 1. Nucleic Acids Res. 2016. PMID: 27257075 Free PMC article. - RIP140 regulates POLK gene expression and the response to alkylating drugs in colon cancer cells.
Palassin P, Lapierre M, Bonnet S, Pillaire MJ, Győrffy B, Teyssier C, Jalaguier S, Hoffmann JS, Cavaillès V, Castet-Nicolas A. Palassin P, et al. Cancer Drug Resist. 2022 May 7;5(2):401-414. doi: 10.20517/cdr.2021.133. eCollection 2022. Cancer Drug Resist. 2022. PMID: 35800380 Free PMC article. - Replication and recombination factors contributing to recombination-dependent bypass of DNA lesions by template switch.
Vanoli F, Fumasoni M, Szakal B, Maloisel L, Branzei D. Vanoli F, et al. PLoS Genet. 2010 Nov 11;6(11):e1001205. doi: 10.1371/journal.pgen.1001205. PLoS Genet. 2010. PMID: 21085632 Free PMC article. - Working on Genomic Stability: From the S-Phase to Mitosis.
Ovejero S, Bueno A, Sacristán MP. Ovejero S, et al. Genes (Basel). 2020 Feb 20;11(2):225. doi: 10.3390/genes11020225. Genes (Basel). 2020. PMID: 32093406 Free PMC article. Review. - Spatial separation between replisome- and template-induced replication stress signaling.
García-Rodríguez N, Morawska M, Wong RP, Daigaku Y, Ulrich HD. García-Rodríguez N, et al. EMBO J. 2018 May 2;37(9):e98369. doi: 10.15252/embj.201798369. Epub 2018 Mar 26. EMBO J. 2018. PMID: 29581097 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources