ArticleMolecular microbiology2012
Chromosome demise in the wake of ligase-deficient replication.
Article in Molecular microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 28 citations in OpenAlex.
- UV induces codirectional replication-transcription conflicts and an alternative DnaA-dependent replication origin in the rnhAB mutants of Escherichiacoli.Nucleic acids research · 2025Article
- Unrepaired base excision repair intermediates in template DNA strands trigger replication fork collapse and PARP inhibitor sensitivity.The EMBO journal · 2023Article
- rRNA operon multiplicity as a bacterial genome stability insurance policy.Nucleic acids research · 2022Article
- Robust linear DNA degradation supports replication-initiation-defective mutants in Escherichia coli.G3 (Bethesda, Md.) · 2022Article
- Catastrophic chromosome fragmentation probes the nucleoid structure and dynamics in Escherichia coli.Nucleic acids research · 2022Article
- Thymine-starvation-induced chromosomal fragmentation is not required for thymineless death in Escherichia coli.Molecular microbiology · 2022Article
- Thymineless Death inJournal of bacteriology · 2019Article
- Sources of thymidine and analogs fueling futile damage-repair cycles and ss-gap accumulation during thymine starvation in Escherichia coli.DNA repair · 2019Article
- Near-continuously synthesized leading strands inProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways.Microbial cell (Graz, Austria) · 2019Review
- Replication Fork Breakage and Restart in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2018Review
- The Importance of Poly(ADP-Ribose) Polymerase as a Sensor of Unligated Okazaki Fragments during DNA Replication.Molecular cell · 2018Article
- Degradation of RNA during lysis of Escherichia coli cells in agarose plugs breaks the chromosome.PloS one · 2017Article
- Prompt repair of hydrogen peroxide-induced DNA lesions prevents catastrophic chromosomal fragmentation.DNA repair · 2016Article
- Static and Dynamic Factors Limit Chromosomal Replication Complexity in Escherichia coli, Avoiding Dangers of Runaway Overreplication.Genetics · 2016Article
- Temperature Sensitivity Conferred by ligA Alleles from Psychrophilic Bacteria upon Substitution in Mesophilic Bacteria and a Yeast Species.Applied and environmental microbiology · 2016Article
- Bactericidal Antibiotics Induce Toxic Metabolic Perturbations that Lead to Cellular Damage.Cell reports · 2015Article
- Cyanide enhances hydrogen peroxide toxicity by recruiting endogenous iron to trigger catastrophic chromosomal fragmentation.Molecular microbiology · 2015Article
- Replication fork inhibition in seqA mutants of Escherichia coli triggers replication fork breakage.Molecular microbiology · 2014Article
- The precarious prokaryotic chromosome.Journal of bacteriology · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Bacterial DNA ligases, NAD⁺-dependent enzymes, are distinct from eukaryotic ATP-dependent ligases, representing promising targets for broad-spectrum antimicrobials. Yet, the chromosomal consequences of ligase-deficient DNA replication, during which Okazaki fragments accumulate, are still unclear. Using ligA251(Ts), the strongest ligase mutant of Escherichia coli, we studied ligase-deficient DNA replication by genetic and physical approaches. Here we show that replication without ligase kills after a short resistance period. We found that double-strand break repair via RecA, RecBCD, RuvABC and RecG explains the transient resistance, whereas irreparable chromosomal fragmentation explains subsequent cell death. Remarkably, death is mostly prevented by elimination of linear DNA degradation activity of ExoV, suggesting that non-allelic double-strand breaks behind replication forks precipitate DNA degradation that enlarge them into allelic double-strand gaps. Marker frequency profiling of synchronized replication reveals stalling of ligase-deficient forks with subsequent degradation of the DNA synthesized without ligase. The mechanism that converts unsealed nicks behind replication forks first into repairable double-strand breaks and then into irreparable double-strand gaps may be behind lethality of any DNA damaging treatment.
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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.