ArticleGenetics2007
Involvement of Escherichia coli DNA polymerase IV in tolerance of cytotoxic alkylating DNA lesions in vivo.
Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed, 90 citations in OpenAlex.
- Sequential gene loss promotes expansion of monophasic Salmonella Typhimurium ST34.Nature microbiology · 2026Article
- The B. subtilis translesion polymerase Pol Y1 is not strongly recruited to sites of replication upon different types of DNA damage.PLoS genetics · 2026Article
- "ThebioRxiv : the preprint server for biology · 2026Article
- Transcription-replication collisions trigger high-fidelity replication reset.Nucleic acids research · 2025Article
- Protein Engineering of Biosynthetic Enzymes Unlocks Libraries of Bioactive Tilimycin Analogs.ACS catalysis · 2025Article
- A bipartite interaction with the processivity clamp potentiates Pol IV-mediated TLS.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Hallmarks of DNA replication stress responses in Escherichia coli and Bacillus subtilis.FEMS microbiology reviews · 2025Review
- A bipartite interaction with the processivity clamp potentiates Pol IV-mediated TLS.bioRxiv : the preprint server for biology · 2024Article
- Replication stalling activates SSB for recruitment of DNA damage tolerance factors.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Compartmentalization of the replication fork by single-stranded DNA-binding protein regulates translesion synthesis.Nature structural & molecular biology · 2022Article
- Distinctive roles of translesion polymerases DinB1 and DnaE2 in diversification of the mycobacterial genome through substitution and frameshift mutagenesis.Nature communications · 2022Article
- During Translesion Synthesis, Escherichia coli DinB89 (T120P) Alters Interactions of DinB (Pol IV) with Pol III Subunit Assemblies and SSB, but Not with the β Clamp.Journal of bacteriology · 2022Article
- Sending out an SOS - the bacterial DNA damage response.Genetics and molecular biology · 2022Article
- The Mutant βJournal of bacteriology · 2021Article
- Single-molecule live-cell imaging reveals RecB-dependent function of DNA polymerase IV in double strand break repair.Nucleic acids research · 2020Article
- Visualizing mutagenic repair: novel insights into bacterial translesion synthesis.FEMS microbiology reviews · 2020Review
- Degeneration of industrial bacteria caused by genetic instability.World journal of microbiology & biotechnology · 2020Review
- Genetic dominance governs the evolution and spread of mobile genetic elements in bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Role of error-prone DNA polymerases in spontaneous mutagenesis in Caulobacter crescentus.Genetics and molecular biology · 2020Article
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Escherichia coli PolIV, a DNA polymerase capable of catalyzing synthesis past replication-blocking DNA lesions, belongs to the most ubiquitous branch of Y-family DNA polymerases. The goal of this study is to identify spontaneous DNA damage that is bypassed specifically and accurately by PolIV in vivo. We increased the amount of spontaneous DNA lesions using mutants deficient for different DNA repair pathways and measured mutation frequency in PolIV-proficient and -deficient backgrounds. We found that PolIV performs an error-free bypass of DNA damage that accumulates in the alkA tag genetic background. This result indicates that PolIV is involved in the error-free bypass of cytotoxic alkylating DNA lesions. When the amount of cytotoxic alkylating DNA lesions is increased by the treatment with chemical alkylating agents, PolIV is required for survival in an alkA tag-proficient genetic background as well. Our study, together with the reported involvement of the mammalian PolIV homolog, Polkappa, in similar activity, indicates that Y-family DNA polymerases from the DinB branch can be added to the list of evolutionarily conserved molecular mechanisms that counteract cytotoxic effects of DNA alkylation. This activity is of major biological relevance because alkylating agents are continuously produced endogenously in all living cells and are also present in the environment.
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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.