ArticlePLoS genetics2022
Intracellular acidification is a hallmark of thymineless death in E. coli.
Article in PLoS genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- Generation of Interstrand DNA Cross-Links under Conditions of Acid Stress.Chemical research in toxicology · 2026Article
- Cyclic di-AMP inhibitsmBio · 2026Article
- Defects in the central metabolism prevent thymineless death in Escherichia coli, while still allowing significant protein synthesis.Genetics · 2024Article
- TisB protein is the single molecular determinant underlying multiple downstream effects of ofloxacin inScience advances · 2024Article
- Exploitation of microbial activities at low pH to enhance planetary health.FEMS microbiology reviews · 2024Article
- Antibacterial effects of vinegar N6 and UV-C light-emitting diodes against Shiga toxin-producing and enterohemorrhagicFood science and biotechnology · 2023Article
- Regulation of phosphate starvation-specific responses inMicrobiology (Reading, England) · 2023Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Thymidine starvation causes rapid cell death. This enigmatic process known as thymineless death (TLD) is the underlying killing mechanism of diverse antimicrobial and antineoplastic drugs. Despite decades of investigation, we still lack a mechanistic understanding of the causal sequence of events that culminate in TLD. Here, we used a diverse set of unbiased approaches to systematically determine the genetic and regulatory underpinnings of TLD in Escherichia coli. In addition to discovering novel genes in previously implicated pathways, our studies revealed a critical and previously unknown role for intracellular acidification in TLD. We observed that a decrease in cytoplasmic pH is a robust early event in TLD across different genetic backgrounds. Furthermore, we show that acidification is a causal event in the death process, as chemical and genetic perturbations that increase intracellular pH substantially reduce killing. We also observe a decrease in intracellular pH in response to exposure to the antibiotic gentamicin, suggesting that intracellular acidification may be a common mechanistic step in the bactericidal effects of other antibiotics.
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Registered trials
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