Bacterial viruses enable their host to acquire antibiotic resistance genes from neighbouring cells

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Standard

Bacterial viruses enable their host to acquire antibiotic resistance genes from neighbouring cells. / Haaber, Jakob Krause; Leisner, Jørgen; Cohn, Marianne Thorup; Catalan Moreno, Arancha; Nielsen, Jesper Boye; Westh, Henrik T.; Penadés, José R.; Ingmer, Hanne.

I: Nature Communications, Bind 7, 13333, 2016.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Haaber, JK, Leisner, J, Cohn, MT, Catalan Moreno, A, Nielsen, JB, Westh, HT, Penadés, JR & Ingmer, H 2016, 'Bacterial viruses enable their host to acquire antibiotic resistance genes from neighbouring cells', Nature Communications, bind 7, 13333. https://doi.org/10.1038/ncomms13333

APA

Haaber, J. K., Leisner, J., Cohn, M. T., Catalan Moreno, A., Nielsen, J. B., Westh, H. T., Penadés, J. R., & Ingmer, H. (2016). Bacterial viruses enable their host to acquire antibiotic resistance genes from neighbouring cells. Nature Communications, 7, [13333]. https://doi.org/10.1038/ncomms13333

Vancouver

Haaber JK, Leisner J, Cohn MT, Catalan Moreno A, Nielsen JB, Westh HT o.a. Bacterial viruses enable their host to acquire antibiotic resistance genes from neighbouring cells. Nature Communications. 2016;7. 13333. https://doi.org/10.1038/ncomms13333

Author

Haaber, Jakob Krause ; Leisner, Jørgen ; Cohn, Marianne Thorup ; Catalan Moreno, Arancha ; Nielsen, Jesper Boye ; Westh, Henrik T. ; Penadés, José R. ; Ingmer, Hanne. / Bacterial viruses enable their host to acquire antibiotic resistance genes from neighbouring cells. I: Nature Communications. 2016 ; Bind 7.

Bibtex

@article{8fcf174691ce45808dda9709dbda3f87,
title = "Bacterial viruses enable their host to acquire antibiotic resistance genes from neighbouring cells",
abstract = "Prophages are quiescent viruses located in the chromosomes of bacteria. In the human pathogen, Staphylococcus aureus, prophages are omnipresent and are believed to be responsible for the spread of some antibiotic resistance genes. Here we demonstrate that release of phages from a subpopulation of S. aureus cells enables the intact, prophage-containing population to acquire beneficial genes from competing, phage-susceptible strains present in the same environment. Phage infection kills competitor cells and bits of their DNA are occasionally captured in viral transducing particles. Return of such particles to the prophage-containing population can drive the transfer of genes encoding potentially useful traits such as antibiotic resistance. This process, which can be viewed as {\textquoteleft}auto-transduction{\textquoteright}, allows S. aureus to efficiently acquire antibiotic resistance both in vitro and in an in vivo virulence model (wax moth larvae) and enables it to proliferate under strong antibiotic selection pressure. Our results may help to explain the rapid exchange of antibiotic resistance genes observed in S. aureus.",
author = "Haaber, {Jakob Krause} and J{\o}rgen Leisner and Cohn, {Marianne Thorup} and {Catalan Moreno}, Arancha and Nielsen, {Jesper Boye} and Westh, {Henrik T.} and Penad{\'e}s, {Jos{\'e} R.} and Hanne Ingmer",
year = "2016",
doi = "10.1038/ncomms13333",
language = "English",
volume = "7",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Bacterial viruses enable their host to acquire antibiotic resistance genes from neighbouring cells

AU - Haaber, Jakob Krause

AU - Leisner, Jørgen

AU - Cohn, Marianne Thorup

AU - Catalan Moreno, Arancha

AU - Nielsen, Jesper Boye

AU - Westh, Henrik T.

AU - Penadés, José R.

AU - Ingmer, Hanne

PY - 2016

Y1 - 2016

N2 - Prophages are quiescent viruses located in the chromosomes of bacteria. In the human pathogen, Staphylococcus aureus, prophages are omnipresent and are believed to be responsible for the spread of some antibiotic resistance genes. Here we demonstrate that release of phages from a subpopulation of S. aureus cells enables the intact, prophage-containing population to acquire beneficial genes from competing, phage-susceptible strains present in the same environment. Phage infection kills competitor cells and bits of their DNA are occasionally captured in viral transducing particles. Return of such particles to the prophage-containing population can drive the transfer of genes encoding potentially useful traits such as antibiotic resistance. This process, which can be viewed as ‘auto-transduction’, allows S. aureus to efficiently acquire antibiotic resistance both in vitro and in an in vivo virulence model (wax moth larvae) and enables it to proliferate under strong antibiotic selection pressure. Our results may help to explain the rapid exchange of antibiotic resistance genes observed in S. aureus.

AB - Prophages are quiescent viruses located in the chromosomes of bacteria. In the human pathogen, Staphylococcus aureus, prophages are omnipresent and are believed to be responsible for the spread of some antibiotic resistance genes. Here we demonstrate that release of phages from a subpopulation of S. aureus cells enables the intact, prophage-containing population to acquire beneficial genes from competing, phage-susceptible strains present in the same environment. Phage infection kills competitor cells and bits of their DNA are occasionally captured in viral transducing particles. Return of such particles to the prophage-containing population can drive the transfer of genes encoding potentially useful traits such as antibiotic resistance. This process, which can be viewed as ‘auto-transduction’, allows S. aureus to efficiently acquire antibiotic resistance both in vitro and in an in vivo virulence model (wax moth larvae) and enables it to proliferate under strong antibiotic selection pressure. Our results may help to explain the rapid exchange of antibiotic resistance genes observed in S. aureus.

U2 - 10.1038/ncomms13333

DO - 10.1038/ncomms13333

M3 - Journal article

C2 - 27819286

VL - 7

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 13333

ER -

ID: 169284968