ArticleMolecular cell2007
UmuD and RecA directly modulate the mutagenic potential of the Y family DNA polymerase DinB.
Article in Molecular cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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Who cites it
66 citing papers in PubMed, 121 citations in OpenAlex.
- Should I stay or should I go? DNA damage thresholds drive stay-or-go decisions inJournal of bacteriology · 2026Review
- Mechanistic divergence between SOS response activation and antibiotic-induced plasmid conjugation inMicrobiology spectrum · 2025Article
- SOS genes are rapidly induced while translesion synthesis polymerase activity is temporally regulated.Frontiers in microbiology · 2024Article
- Modeling the Homologous Recombination Process: Methods, Successes and Challenges.International journal of molecular sciences · 2023Review
- Regulation of phosphate starvation-specific responses inMicrobiology (Reading, England) · 2023Review
- 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
- Sending out an SOS - the bacterial DNA damage response.Genetics and molecular biology · 2022Article
- Building Biological Relevance Into Integrative Modelling of Macromolecular Assemblies.Frontiers in molecular biosciences · 2022Article
- Single-molecule live-cell imaging reveals RecB-dependent function of DNA polymerase IV in double strand break repair.Nucleic acids research · 2020Article
- New insights into the structures and interactions of bacterial Y-family DNA polymerases.Nucleic acids research · 2019Article
- Residues in the fingers domain of the translesion DNA polymerase DinB enable its unique participation in error-prone double-strand break repair.The Journal of biological chemistry · 2019Article
- The SOS system: A complex and tightly regulated response to DNA damage.Environmental and molecular mutagenesis · 2019Review
- Translesion and Repair DNA Polymerases: Diverse Structure and Mechanism.Annual review of biochemistry · 2018Review
- DNA polymerase IV primarily operates outside of DNA replication forks in Escherichia coli.PLoS genetics · 2018Article
- Single-molecule imaging reveals multiple pathways for the recruitment of translesion polymerases after DNA damage.Nature communications · 2017Article
- A Small-Molecule Inducible Synthetic Circuit for Control of the SOS Gene Network without DNA Damage.ACS synthetic biology · 2017Article
- Altering the N-terminal arms of the polymerase manager protein UmuD modulates protein interactions.PloS one · 2017Article
- RNA Primer Extension Hinders DNA Synthesis byFrontiers in microbiology · 2017Article
- Mutations for Worse or Better: Low-Fidelity DNA Synthesis by SOS DNA Polymerase V Is a Tightly Regulated Double-Edged Sword.Biochemistry · 2016Review
6 more citing papers are in PubMed but not listed here.
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
Abstract
DinB is the only translesion Y family DNA polymerase conserved among bacteria, archaea, and eukaryotes. DinB and its orthologs possess a specialized lesion bypass function but also display potentially deleterious -1 frameshift mutagenic phenotypes when overproduced. We show that the DNA damage-inducible proteins UmuD(2) and RecA act in concert to modulate this mutagenic activity. Structural modeling suggests that the relatively open active site of DinB is enclosed by interaction with these proteins, thereby preventing the template bulging responsible for -1 frameshift mutagenesis. Intriguingly, residues that define the UmuD(2)-interacting surface on DinB statistically covary throughout evolution, suggesting a driving force for the maintenance of a regulatory protein-protein interaction at this site. Together, these observations indicate that proteins like RecA and UmuD(2) may be responsible for managing the mutagenic potential of DinB orthologs throughout evolution.
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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.