ArticleJournal of bacteriology2008
Synthetic lethality with the dut defect in Escherichia coli reveals layers of DNA damage of increasing complexity due to uracil incorporation.
Article in Journal of bacteriology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Synthetic lethal mutants inJournal of bacteriology · 2023Pooled it
- Tripleknock: predicting lethal effect of three-gene knockout in bacteria by deep learning.Scientific reports · 2026Article
- Uracil-DNA Glycosylase fromInternational journal of molecular sciences · 2025Article
- Structural and Functional Insights into UDGs.Protein and peptide letters · 2025Review
- Defects in the central metabolism prevent thymineless death in Escherichia coli, while still allowing significant protein synthesis.Genetics · 2024Article
- Robust linear DNA degradation supports replication-initiation-defective mutants in Escherichia coli.G3 (Bethesda, Md.) · 2022Article
- Article
- Role for DNA double strand end-resection activity of RecBCD in control of aberrant chromosomal replication initiation in Escherichia coli.Nucleic acids research · 2022Article
- A New Class of Uracil-DNA Glycosylase Inhibitors Active against Human and Vaccinia Virus Enzyme.Molecules (Basel, Switzerland) · 2021Article
- Ultraviolet-induced RNA:DNA hybrids interfere with chromosomal DNA synthesis.Nucleic acids research · 2021Article
- Diverse roles of nucleoside diphosphate kinase in genome stability and growth fitness.Current genetics · 2020Review
- Sources of thymidine and analogs fueling futile damage-repair cycles and ss-gap accumulation during thymine starvation in Escherichia coli.DNA repair · 2019Article
- Phenotypes ofJournal of bacteriology · 2017Article
- Potentiation of hydrogen peroxide toxicity: From catalase inhibition to stable DNA-iron complexes.Mutation research. Reviews in mutation research · 2017Review
- SeqA structures behind Escherichia coli replication forks affect replication elongation and restart mechanisms.Nucleic acids research · 2017Article
- Article
- Chromosome demise in the wake of ligase-deficient replication.Molecular microbiology · 2012Article
- Replication fork reversal after replication-transcription collision.PLoS genetics · 2012Article
- Article
- Structure and activity of the Saccharomyces cerevisiae dUTP pyrophosphatase DUT1, an essential housekeeping enzyme.The Biochemical journal · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Synthetic lethality is inviability of a double-mutant combination of two fully viable single mutants, commonly interpreted as redundancy at an essential metabolic step. The dut-1 defect in Escherichia coli inactivates dUTPase, causing increased uracil incorporation in DNA and known synthetic lethalities [SL(dut) mutations]. According to the redundancy logic, most of these SL(dut) mutations should affect nucleotide metabolism. After a systematic search for SL(dut) mutants, we did identify a single defect in the DNA precursor metabolism, inactivating thymidine kinase (tdk), that confirmed the redundancy explanation of synthetic lethality. However, we found that the bulk of mutations interacting genetically with dut are in DNA repair, revealing layers of damage of increasing complexity that uracil-DNA incorporation sends through the chromosomal metabolism. Thus, we isolated mutants in functions involved in (i) uracil-DNA excision (ung, polA, and xthA); (ii) double-strand DNA break repair (recA, recBC, and ruvABC); and (iii) chromosomal-dimer resolution (xerC, xerD, and ftsK). These mutants in various DNA repair transactions cannot be redundant with dUTPase and instead reveal "defect-damage-repair" cycles linking unrelated metabolic pathways. In addition, two SL(dut) inserts (phoU and degP) identify functions that could act to support the weakened activity of the Dut-1 mutant enzyme, suggesting the "compensation" explanation for this synthetic lethality. We conclude that genetic interactions with dut can be explained by redundancy, by defect-damage-repair cycles, or as compensation.
Indexed as
Identifiers
What OpenQuestion holds
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.