Iron chelation increases the tolerance of Escherichia coli to hyper-replication stress

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Standard

Iron chelation increases the tolerance of Escherichia coli to hyper-replication stress. / Charbon, Godefroid; Klitgaard, Rasmus Nielsen; Liboriussen, Charlotte Dahlmann; Thulstrup, Peter Waaben; Maffioli, Sonia Ilaria; Donadio, Stefano; Løbner-Olesen, Anders.

I: Scientific Reports, Bind 8, Nr. 1, 10550, 2018.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Charbon, G, Klitgaard, RN, Liboriussen, CD, Thulstrup, PW, Maffioli, SI, Donadio, S & Løbner-Olesen, A 2018, 'Iron chelation increases the tolerance of Escherichia coli to hyper-replication stress', Scientific Reports, bind 8, nr. 1, 10550. https://doi.org/10.1038/s41598-018-28841-9

APA

Charbon, G., Klitgaard, R. N., Liboriussen, C. D., Thulstrup, P. W., Maffioli, S. I., Donadio, S., & Løbner-Olesen, A. (2018). Iron chelation increases the tolerance of Escherichia coli to hyper-replication stress. Scientific Reports, 8(1), [10550]. https://doi.org/10.1038/s41598-018-28841-9

Vancouver

Charbon G, Klitgaard RN, Liboriussen CD, Thulstrup PW, Maffioli SI, Donadio S o.a. Iron chelation increases the tolerance of Escherichia coli to hyper-replication stress. Scientific Reports. 2018;8(1). 10550. https://doi.org/10.1038/s41598-018-28841-9

Author

Charbon, Godefroid ; Klitgaard, Rasmus Nielsen ; Liboriussen, Charlotte Dahlmann ; Thulstrup, Peter Waaben ; Maffioli, Sonia Ilaria ; Donadio, Stefano ; Løbner-Olesen, Anders. / Iron chelation increases the tolerance of Escherichia coli to hyper-replication stress. I: Scientific Reports. 2018 ; Bind 8, Nr. 1.

Bibtex

@article{9499f23d34cc4595838bf64dd8f5a7a4,
title = "Iron chelation increases the tolerance of Escherichia coli to hyper-replication stress",
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.",
author = "Godefroid Charbon and Klitgaard, {Rasmus Nielsen} and Liboriussen, {Charlotte Dahlmann} and Thulstrup, {Peter Waaben} and Maffioli, {Sonia Ilaria} and Stefano Donadio and Anders L{\o}bner-Olesen",
year = "2018",
doi = "10.1038/s41598-018-28841-9",
language = "English",
volume = "8",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

T1 - Iron chelation increases the tolerance of Escherichia coli to hyper-replication stress

AU - Charbon, Godefroid

AU - Klitgaard, Rasmus Nielsen

AU - Liboriussen, Charlotte Dahlmann

AU - Thulstrup, Peter Waaben

AU - Maffioli, Sonia Ilaria

AU - Donadio, Stefano

AU - Løbner-Olesen, Anders

PY - 2018

Y1 - 2018

N2 - 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.

AB - 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.

U2 - 10.1038/s41598-018-28841-9

DO - 10.1038/s41598-018-28841-9

M3 - Journal article

C2 - 30002429

VL - 8

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

M1 - 10550

ER -

ID: 199630940