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Post‐replication repair in DT40 cells: translesion polymerases versus recombinases
Author(s) -
Hochegger Helfrid,
Sonoda Eichiro,
Takeda Shunichi
Publication year - 2004
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.10403
Subject(s) - biology , homologous recombination , genetics , control of chromosome duplication , dna repair , dna replication , postreplication repair , recombinase , eukaryotic dna replication , dna re replication , genetic recombination , replication protein a , dna polymerase , microbiology and biotechnology , nucleotide excision repair , dna , gene , recombination , dna binding protein , transcription factor
Abstract Replication forks inevitably stall at damaged DNA in every cell cycle. The ability to overcome DNA lesions is an essential feature of the replication machinery. A variety of specialized polymerases have recently been discovered, which enable cells to replicate past various forms of damage by a process termed translesion synthesis. Alternatively, homologous recombination can be used to restart DNA replication across the lesion. Genetic and biochemical studies have shed light on the impact of these two post‐replication repair pathways in bacteria and yeast. In vertebrates, however, a genetic approach to study post‐replication repair has been compromised because many of the genes involved appear to be essential for embryonic development. We have taken advantage of the chicken cell line DT40 to perform a genetic analysis of translesion synthesis and homologous recombination and to characterize genetic interactions between these two pathways in vertebrates. In this article, we aim to summarize our current understanding of post‐replication repair in DT40 in the perspective of bacterial, yeast and mammalian genetics. BioEssays 26:151–158, 2004. © 2004 Wiley Periodicals, Inc.