Persistence and drug tolerance in pathogenic yeast

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Standard

Persistence and drug tolerance in pathogenic yeast. / Bojsen, Rasmus Kenneth; Regenberg, Birgitte; Folkesson, Anders.

I: Current Genetics, Bind 63, Nr. 1, 02.2017, s. 19-22.

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Harvard

Bojsen, RK, Regenberg, B & Folkesson, A 2017, 'Persistence and drug tolerance in pathogenic yeast', Current Genetics, bind 63, nr. 1, s. 19-22. https://doi.org/10.1007/s00294-016-0613-3

APA

Bojsen, R. K., Regenberg, B., & Folkesson, A. (2017). Persistence and drug tolerance in pathogenic yeast. Current Genetics, 63(1), 19-22. https://doi.org/10.1007/s00294-016-0613-3

Vancouver

Bojsen RK, Regenberg B, Folkesson A. Persistence and drug tolerance in pathogenic yeast. Current Genetics. 2017 feb;63(1):19-22. https://doi.org/10.1007/s00294-016-0613-3

Author

Bojsen, Rasmus Kenneth ; Regenberg, Birgitte ; Folkesson, Anders. / Persistence and drug tolerance in pathogenic yeast. I: Current Genetics. 2017 ; Bind 63, Nr. 1. s. 19-22.

Bibtex

@article{165d0894eae04ad3a5f603b279a23706,
title = "Persistence and drug tolerance in pathogenic yeast",
abstract = "In this review, we briefly summarize the current understanding of how fungal pathogens can persist antifungal treatment without heritable resistance mutations by forming tolerant persister cells. Fungal infections tolerant to antifungal treatment have become a major medical problem. One mechanism leading to drug recalcitrance is the formation of antifungal persister cells. These cells have wild-type genotype with the ability to survive exposure to antifungal agents due to changed membrane composition, upregulated stress response, and enhanced cell wall integrity. Knowledge of the mechanisms regulating entry and exit of the persister phenotype is limited, but it has recently been shown that the inhibition of the growth regulating TORC1 pathway induces fungal persistence. The phenotypic properties of persister cells and the involvement of the TORC1 pathway indicate that persister cells are quiescent in G0 of the cell cycle. This knowledge leads us to suggest that the identified shared drug-tolerance mechanisms of persister and quiescent cells may serve as a foundation for developing novel treatment strategies that are independent of growth mode against systemic fungal infections.",
author = "Bojsen, {Rasmus Kenneth} and Birgitte Regenberg and Anders Folkesson",
year = "2017",
month = "2",
doi = "10.1007/s00294-016-0613-3",
language = "English",
volume = "63",
pages = "19--22",
journal = "Current Genetics",
issn = "0172-8083",
publisher = "Springer",
number = "1",

}

RIS

TY - JOUR

T1 - Persistence and drug tolerance in pathogenic yeast

AU - Bojsen, Rasmus Kenneth

AU - Regenberg, Birgitte

AU - Folkesson, Anders

PY - 2017/2

Y1 - 2017/2

N2 - In this review, we briefly summarize the current understanding of how fungal pathogens can persist antifungal treatment without heritable resistance mutations by forming tolerant persister cells. Fungal infections tolerant to antifungal treatment have become a major medical problem. One mechanism leading to drug recalcitrance is the formation of antifungal persister cells. These cells have wild-type genotype with the ability to survive exposure to antifungal agents due to changed membrane composition, upregulated stress response, and enhanced cell wall integrity. Knowledge of the mechanisms regulating entry and exit of the persister phenotype is limited, but it has recently been shown that the inhibition of the growth regulating TORC1 pathway induces fungal persistence. The phenotypic properties of persister cells and the involvement of the TORC1 pathway indicate that persister cells are quiescent in G0 of the cell cycle. This knowledge leads us to suggest that the identified shared drug-tolerance mechanisms of persister and quiescent cells may serve as a foundation for developing novel treatment strategies that are independent of growth mode against systemic fungal infections.

AB - In this review, we briefly summarize the current understanding of how fungal pathogens can persist antifungal treatment without heritable resistance mutations by forming tolerant persister cells. Fungal infections tolerant to antifungal treatment have become a major medical problem. One mechanism leading to drug recalcitrance is the formation of antifungal persister cells. These cells have wild-type genotype with the ability to survive exposure to antifungal agents due to changed membrane composition, upregulated stress response, and enhanced cell wall integrity. Knowledge of the mechanisms regulating entry and exit of the persister phenotype is limited, but it has recently been shown that the inhibition of the growth regulating TORC1 pathway induces fungal persistence. The phenotypic properties of persister cells and the involvement of the TORC1 pathway indicate that persister cells are quiescent in G0 of the cell cycle. This knowledge leads us to suggest that the identified shared drug-tolerance mechanisms of persister and quiescent cells may serve as a foundation for developing novel treatment strategies that are independent of growth mode against systemic fungal infections.

U2 - 10.1007/s00294-016-0613-3

DO - 10.1007/s00294-016-0613-3

M3 - Review

VL - 63

SP - 19

EP - 22

JO - Current Genetics

JF - Current Genetics

SN - 0172-8083

IS - 1

ER -

ID: 162711683