ArticleProceedings of the National Academy of Sciences of the United States of America2014
Chronology in lesion tolerance gives priority to genetic variability.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- The RecBC complex protects single-stranded DNA gaps during lesion bypass.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The LexA-RecA* structure reveals a cryptic lock-and-key mechanism for SOS activation.Nature structural & molecular biology · 2024Article
- Review
- Changes in the architecture and abundance of replication intermediates delineate the chronology of DNA damage tolerance pathways at UV-stalled replication forks in human cells.Nucleic acids research · 2022Article
- Single strand gap repair: The presynaptic phase plays a pivotal role in modulating lesion tolerance pathways.PLoS genetics · 2022Article
- Eukaryotic stress-induced mutagenesis is limited by a local control of translesion synthesis.Nucleic acids research · 2022Article
- Review
- Sending out an SOS - the bacterial DNA damage response.Genetics and molecular biology · 2022Article
- Visualizing mutagenic repair: novel insights into bacterial translesion synthesis.FEMS microbiology reviews · 2020Review
- A gatekeeping function of the replicative polymerase controls pathway choice in the resolution of lesion-stalled replisomes.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Chronological Switch from Translesion Synthesis to Homology-Dependent Gap RepairToxicological research · 2018Review
- DNA lesions proximity modulates damage tolerance pathways in Escherichia coli.Nucleic acids research · 2018Article
- Processing closely spaced lesions during Nucleotide Excision Repair triggers mutagenesis in E. coli.PLoS genetics · 2017Article
- A non-catalytic role of RecBCD in homology directed gap repair and translesion synthesis.Nucleic acids research · 2017Article
- A defect in homologous recombination leads to increased translesion synthesis in E. coli.Nucleic acids research · 2016Article
- Single-strand gap repair involves both RecF and RecBCD pathways.Current genetics · 2016Review
- Bacterial Proliferation: Keep Dividing and Don't Mind the Gap.PLoS genetics · 2015Article
- Homologous recombination maintenance of genome integrity during DNA damage tolerance.Molecular & cellular oncologyReview
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The encounter of a replication fork with a blocking DNA lesion is a common event that cells need to address properly to preserve genome integrity. Cells possess two main strategies to tolerate unrepaired lesions: potentially mutagenic translesion synthesis (TLS) and nonmutagenic damage avoidance (DA). Little is known about the partitioning between these two strategies. Because genes involved in DA mechanisms (i.e., recA) are expressed early and genes involved in TLS (i.e., Pol V) are expressed late during the bacterial SOS response, it has long been thought that TLS was the last recourse to bypass DNA lesions when repair and nonmutagenic DA mechanisms have failed. By using a recently described methodology, we followed the fate of a single replication-blocking lesion introduced in the Escherichia coli genome during acute genotoxic stress. We show that lesion tolerance events (i) only occur when the SOS response is fully induced and (ii) are executed in chronological order, with TLS coming first, followed by DA. Therefore, in response to genotoxic stress, bacterial cells give priority to TLS, a minor pathway able to generate genetic diversity before implementing the major nonmutagenic pathway that ensures survival.
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