ArticleGenetics2011
Pathways of resistance to thymineless death in Escherichia coli and the function of UvrD.
Article in Genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Enterocyte-like differentiation defines metabolic gene signatures of CMS3 colorectal cancers and provides therapeutic vulnerability.Nature communications · 2025Article
- Intracellular acidification is a hallmark of thymineless death in E. coli.PLoS genetics · 2022Article
- Oxidative Damage Blocks Thymineless Death and Trimethoprim Poisoning in Escherichia coli.Journal of bacteriology · 2022Article
- Electron Microscopy Reveals Unexpected Cytoplasm and Envelope Changes during Thymineless Death in Escherichia coli.Journal of bacteriology · 2021Article
- An interbacterial DNA deaminase toxin directly mutagenizes surviving target populations.eLife · 2021Article
- Exopolysaccharide defects cause hyper-thymineless death inProceedings of the National Academy of Sciences of the United States of America · 2020Article
- 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
- Contribution of reactive oxygen species to thymineless death in Escherichia coli.Nature microbiology · 2017Article
- 5-Fluorouracil targets thymidylate synthase in the selective suppression of TH17 cell differentiation.Oncotarget · 2016Article
- Thymineless death, at the origin.Frontiers in microbiology · 2015Review
- Tolerance of Escherichia coli to fluoroquinolone antibiotics depends on specific components of the SOS response pathway.Genetics · 2013Article
- Thymineless death is inhibited by CsrA in Escherichia coli lacking the SOS response.DNA repair · 2013Article
- Metabolic and functional genomic studies identify deoxythymidylate kinase as a target in LKB1-mutant lung cancer.Cancer discovery · 2013Article
- Disintegration of nascent replication bubbles during thymine starvation triggers RecA- and RecBCD-dependent replication origin destruction.The Journal of biological chemistry · 2012Article
- The mechanistic basis of Myxococcus xanthus rippling behavior and its physiological role during predation.PLoS computational biology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Thymineless death (TLD) is the rapid loss of viability in bacterial, yeast, and human cells starved of thymine. TLD is the mode of action of common anticancer drugs and some antibiotics. TLD in Escherichia coli is accompanied by blocked replication and chromosomal DNA loss and recent work identified activities of recombination protein RecA and the SOS DNA-damage response as causes of TLD. Here, we examine the basis of hypersensitivity to thymine deprivation (hyper-TLD) in mutants that lack the UvrD helicase, which opposes RecA action and participates in some DNA repair mechanisms, RecBCD exonuclease, which degrades double-stranded linear DNA and works with RecA in double-strand-break repair and SOS induction, and RuvABC Holliday-junction resolvase. We report that hyper-TLD in uvrD cells is partly RecA dependent and cannot be attributed to accumulation of intermediates in mismatch repair or nucleotide-excision repair. These data imply that both its known role in opposing RecA and an additional as-yet-unknown function of UvrD promote TLD resistance. The hyper-TLD of ruvABC cells requires RecA but not RecQ or RecJ. The hyper-TLD of recB cells requires neither RecA nor RecQ, implying that neither recombination nor SOS induction causes hyper-TLD in recB cells, and RecQ is not the sole source of double-strand ends (DSEs) during TLD, as previously proposed; models are suggested. These results define pathways by which cells resist TLD and suggest strategies for combating TLD resistance during chemotherapies.
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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.