ArticleNucleic acids research2018
DNA lesions proximity modulates damage tolerance pathways in Escherichia coli.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Spatiotemporal characterization of single-stranded DNA Intermediates after UV Irradiation: I: Post-replication gaps formed during slow growth.PLoS genetics · 2026Article
- 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
- Post-replicative lesion processing limits DNA damage-induced mutagenesis.Nucleic acids research · 2025Article
- Single strand gap repair: The presynaptic phase plays a pivotal role in modulating lesion tolerance pathways.PLoS genetics · 2022Article
- Review
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- REV7 confers radioresistance of esophagus squamous cell carcinoma by recruiting PRDX2.Cancer science · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genome of all organisms is constantly threatened by numerous agents that cause DNA damage. When the replication fork encounters an unrepaired DNA lesion, two DNA damage tolerance pathways are possible: error-prone translesion synthesis (TLS) that requires specialized DNA polymerases, and error-free damage avoidance that relies on homologous recombination (HR). The balance between these two mechanisms is essential since it defines the level of mutagenesis during lesion bypass, allowing genetic variability and adaptation to the environment, but also introduces the risk of generating genome instability. Here we report that the mere proximity of replication-blocking lesions that arise in Escherichia coli's genome during a genotoxic stress leads to a strong increase in the use of the error-prone TLS. We show that this increase is caused by the local inhibition of HR due to the overlapping of single-stranded DNA regions generated downstream of the lesions. This increase in TLS is independent of SOS activation, but its mutagenic effect is additive with the one of SOS. Hence, the combination of SOS induction and lesions proximity leads to a strong increase in TLS that becomes the main lesion tolerance pathway used by the cell during a genotoxic stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.