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The Fanconi anemia (FA) protein FANCC is essential for chromosome stability in vertebrate cells, a feature underscored by the extreme sensitivity of FANCC-deficient cells to agents that crosslink DNA. However, it is not known how this FA protein facilitates the repair of both endogenously acquired and mutagen-induced DNA damage. Here, we use the model vertebrate cell line DT40 to address this question. We discover that apart from functioning in homologous recombination, FANCC also promotes the mutational repair of endogenously generated abasic sites. Moreover in these vertebrate cells, the efficient repair of crosslinks requires the combined functions of FANCC, translesion synthesis, and homologous recombination. These studies reveal that the FA proteins cooperate with key mutagenesis and repair processes that enable replication of damaged DNA.

Original publication

DOI

10.1016/j.molcel.2004.08.009

Type

Journal article

Journal

Mol Cell

Publication Date

27/08/2004

Volume

15

Pages

607 - 620

Keywords

Animals, Cell Cycle Proteins, Cell Line, Chickens, Chromosomal Instability, Cross-Linking Reagents, DNA, DNA Damage, DNA Repair, DNA Replication, DNA-Binding Proteins, DNA-Directed DNA Polymerase, Epistasis, Genetic, Fanconi Anemia, Fanconi Anemia Complementation Group C Protein, Fanconi Anemia Complementation Group D2 Protein, Fanconi Anemia Complementation Group Proteins, Humans, Nuclear Proteins, Nucleotidyltransferases, Proteins, Recombinant Fusion Proteins, Recombination, Genetic, X-Rays