ArticleJournal of bacteriology2010
Role of the DinB homologs Rv1537 and Rv3056 in Mycobacterium tuberculosis.
Article in Journal of bacteriology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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Who cites it
32 citing papers in PubMed, 65 citations in OpenAlex.
- Desiccation promotes DNA damage and rifampin resistance in Mycobacterium tuberculosis.Nature microbiology · 2026Article
- Article
- A nucleoid-associated protein is involved in the emergence of antibiotic resistance by promoting the frequent exchange of the replicative DNA polymerase inbioRxiv : the preprint server for biology · 2024Article
- Article
- Distinctive roles of translesion polymerases DinB1 and DnaE2 in diversification of the mycobacterial genome through substitution and frameshift mutagenesis.Nature communications · 2022Article
- The Error-Prone Polymerase DnaE2 Mediates the Evolution of Antibiotic Resistance in Persister Mycobacterial Cells.Antimicrobial agents and chemotherapy · 2022Article
- Evolution ofFrontiers in cellular and infection microbiology · 2022Review
- Division of labor between SOS and PafBC in mycobacterial DNA repair and mutagenesis.Nucleic acids research · 2021Article
- Transcriptional Response ofFrontiers in microbiology · 2021Article
- Visualizing mutagenic repair: novel insights into bacterial translesion synthesis.FEMS microbiology reviews · 2020Review
- Mycobacterial DNA polymerase I: activities and crystal structures of the POL domain as apoenzyme and in complex with a DNA primer-template and of the full-length FEN/EXO-POL enzyme.Nucleic acids research · 2020Article
- Role of error-prone DNA polymerases in spontaneous mutagenesis in Caulobacter crescentus.Genetics and molecular biology · 2020Article
- Harnessing Biological Insight to Accelerate Tuberculosis Drug Discovery.Accounts of chemical research · 2019Review
- New insights into the structures and interactions of bacterial Y-family DNA polymerases.Nucleic acids research · 2019Article
- Ribonucleotide discrimination by translesion synthesis DNA polymerases.Critical reviews in biochemistry and molecular biology · 2018Review
- DNA Replication in Mycobacterium tuberculosis.Microbiology spectrum · 2017Review
- A DinB Ortholog Enables Mycobacterial Growth under dTTP-Limiting Conditions Induced by the Expression of a Mycobacteriophage-Derived Ribonucleotide Reductase Gene.Journal of bacteriology · 2016Article
- Mycobacterium smegmatis DinB2 misincorporates deoxyribonucleotides and ribonucleotides during templated synthesis and lesion bypass.Nucleic acids research · 2014Article
- Molecular dissection of phage endolysin: an interdomain interaction confers host specificity in Lysin A of Mycobacterium phage D29.The Journal of biological chemistry · 2014Article
- Characterization of three mycobacterial DinB (DNA polymerase IV) paralogs highlights DinB2 as naturally adept at ribonucleotide incorporation.Nucleic acids research · 2014Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
The environment encountered by Mycobacterium tuberculosis during infection is genotoxic. Most bacteria tolerate DNA damage by engaging specialized DNA polymerases that catalyze translesion synthesis (TLS) across sites of damage. M. tuberculosis possesses two putative members of the DinB class of Y-family DNA polymerases, DinB1 (Rv1537) and DinB2 (Rv3056); however, their role in damage tolerance, mutagenesis, and survival is unknown. Here, both dinB1 and dinB2 are shown to be expressed in vitro in a growth phase-dependent manner, with dinB2 levels 12- to 40-fold higher than those of dinB1. Yeast two-hybrid analyses revealed that DinB1, but not DinB2, interacts with the beta-clamp, consistent with its canonical C-terminal beta-binding motif. However, knockout of dinB1, dinB2, or both had no effect on the susceptibility of M. tuberculosis to compounds that form N(2)-dG adducts and alkylating agents. Similarly, deletion of these genes individually or in combination did not affect the rate of spontaneous mutation to rifampin resistance or the spectrum of resistance-conferring rpoB mutations and had no impact on growth or survival in human or mouse macrophages or in mice. Moreover, neither gene conferred a mutator phenotype when expressed ectopically in Mycobacterium smegmatis. The lack of the effect of altering the complements or expression levels of dinB1 and/or dinB2 under conditions predicted to be phenotypically revealing suggests that the DinB homologs from M. tuberculosis do not behave like their counterparts from other organisms.
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Registered trials
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