ArticleScientific reports2018
Iron chelation increases the tolerance of Escherichia coli to hyper-replication stress.
Article in Scientific reports, 2018. 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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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- The iron-sulfur accelerator YgfZ modulates genome-wide IHF-binding dynamics to regulate replication initiation inFrontiers in microbiology · 2026Article
- Griseolutein T from Streptomyces seoulensis, newly identified via combined-culture with Tsukamurella pulmonis, as an efficacious therapeutic agent against multidrug-resistant bacteria.The Journal of antibiotics · 2025Article
- Dispensability of extrinsic DnaA regulators inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Targeting synthesis of the Chromosome Replication Initiator Protein DnaA by antisense PNA-peptide conjugates inFrontiers in antibiotics · 2024Article
- Inhibition of Replication Fork Formation and Progression: Targeting the Replication Initiation and Primosomal Proteins.International journal of molecular sciences · 2023Review
- Blocking the Trigger: Inhibition of the Initiation of Bacterial Chromosome Replication as an Antimicrobial Strategy.Antibiotics (Basel, Switzerland) · 2019Review
- Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In Escherichia coli, an increase in the frequency of chromosome replication is lethal. In order to identify compounds that affect chromosome replication, we screened for molecules capable of restoring the viability of hyper-replicating cells. We made use of two E. coli strains that over-initiate DNA replication by keeping the DnaA initiator protein in its active ATP bound state. While viable under anaerobic growth or when grown on poor media, these strains become inviable when grown in rich media. Extracts from actinomycetes strains were screened, leading to the identification of deferoxamine (DFO) as the active compound in one of them. We show that DFO does not affect chromosomal replication initiation and suggest that it was identified due to its ability to chelate cellular iron. This limits the formation of reactive oxygen species, reduce oxidative DNA damage and promote processivity of DNA replication. We argue that the benzazepine derivate (±)-6-Chloro-PB hydrobromide acts in a similar manner.
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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.