The recent finding of a role for the recA gene in DNA replication restart does not negate previous data showing the existence of recA‐dependent recombinational DNA repair, which occurs when there are two DNA duplexes present, as in the case for recA‐dependent excision repair, for postreplication repair (i.e., the repair of DNA daughter‐strand gaps), and for the repair of DNA double‐strand breaks. Recombinational DNA repair is critical for the survival of damaged cells. BioEssays 26:1322–1326, 2004. © 2004 Wiley Periodicals, Inc.

In the genomics era, bioinformatic analysis, especially in non‐model species, facilitates the identification and naming of numerous new proteins, the function of which is then inferred through homology searches. Here, we question certain aspects of these approaches. What are the criteria that permit such a determination? What are their limits? Naming is classifying. We review the different criteria that are used to name a protein and discuss their constraints. We observe that the name given to a protein often introduces a (...) bias for further functional analyses, a bias that is not often taken into account when analysing results. Last but not least, the heterogeneity of criteria used for naming proteins leads to self‐inconsistent or contradictory protein classification that is potentially misleading. Finally, we recommend a wider use of phylogenetic criteria in protein naming. BioEssays 30:349–357, 2008. © 2008 Wiley Periodicals, Inc. (shrink)

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. (shrink)