Journal article
Role of homologous recombination in DNA interstrand crosslink repair
Environmental and molecular mutagenesis, Vol.51(6), pp.582-603
07/2010
Handle:
https://hdl.handle.net/2376/106036
PMID: 20658649
Abstract
Homologous recombination repair (HRR) encompasses mechanisms that employ homologous DNA sequences as templates for repair or tolerance of a wide range of DNA lesions that inhibit DNA replication in S phase. Arguably the most imposing of these DNA lesions is that of the interstrand crosslink (ICL), consisting of a covalently attached chemical bridge between opposing DNA strands. ICL repair requires the coordinated activities of HRR and a number of proteins from other DNA repair and damage response systems, including nucleotide excision repair, base excision repair, mismatch repair, and translesion DNA synthesis (TLS). Interestingly, different organisms favor alternative methods of HRR in the ICL repair process. E. coli perform ICL repair using a homology-driven damage bypass mechanism analogous to daughter strand gap repair. Eukaryotes from yeast to humans initiate ICL repair primarily during DNA replication, relying on HRR activity to restart broken replication forks associated with double-strand break intermediates induced by nucleolytic activities of other excision repair factors. Higher eukaryotes also employ several additional factors, including members of the Fanconi anemia damage-response network, which further promote replication-associated ICL repair through the activation and coordination of various DNA excision repair, TLS, and HRR proteins. This review focuses on the proteins and general mechanisms of HRR associated with ICL repair in different model organisms.
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Details
- Title
- Role of homologous recombination in DNA interstrand crosslink repair
- Creators
- John M Hinz - School of Molecular Biosciences, Washington State University, Pullman, Washington, USA. jmhinz@wsu.edu
- Publication Details
- Environmental and molecular mutagenesis, Vol.51(6), pp.582-603
- Academic Unit
- Molecular Biosciences, School of
- Publisher
- United States
- Grant note
- ES004106 / NIEHS NIH HHS ES002614 / NIEHS NIH HHS
- Identifiers
- 99900546897801842
- Language
- English
- Resource Type
- Journal article