Translesion DNA synthesis polymerases in DNA interstrand crosslink repair

Environmental and Molecular Mutagenesis
The Vinh Ho, Orlando D Schärer

Abstract

DNA interstrand crosslinks (ICLs) are induced by a number of bifunctional antitumor drugs such as cisplatin, mitomycin C, or the nitrogen mustards as well as endogenous agents formed by lipid peroxidation. The repair of ICLs requires the coordinated interplay of a number of genome maintenance pathways, leading to the removal of ICLs through at least two distinct mechanisms. The major pathway of ICL repair is dependent on replication, homologous recombination, and the Fanconi anemia (FA) pathway, whereas a minor, G0/G1-specific and recombination-independent pathway depends on nucleotide excision repair. A central step in both pathways in vertebrates is translesion synthesis (TLS) and mutants in the TLS polymerases Rev1 and Pol zeta are exquisitely sensitive to crosslinking agents. Here, we review the involvement of Rev1 and Pol zeta as well as additional TLS polymerases, in particular, Pol eta, Pol kappa, Pol iota, and Pol nu, in ICL repair. Biochemical studies suggest that multiple TLS polymerases have the ability to bypass ICLs and that the extent ofbypass depends upon the structure as well as the extent of endo- or exonucleolytic processing of the ICL. As has been observed for lesions that affect only one strand of DNA, TLS p...Continue Reading

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Citations

Jun 28, 2011·Nature Reviews. Cancer·Andrew J Deans, Stephen C West
Jun 15, 2012·The Journal of Biological Chemistry·Danielle L DaeeKyungjae Myung
Jun 15, 2011·Nucleic Acids Research·The Vinh HoOrlando D Schärer
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Jan 8, 2021·Frontiers in Cell and Developmental Biology·Manideep C PachvaRegina Groisman

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