Regulation of Candida glabrata oxidative stress resistance is adapted to host environment

The human fungal pathogen Candida glabrata is related to Saccharomyces cerevisiae but has developed high resistance against reactive oxygen species. We find that induction of conserved genes encoding antioxidant functions is dependent on the transcription factors CgYap1 and CgSkn7 which cooperate fo...

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Autores principales: Roetzer, Andreas, Klopf, Eva, Gratz, Nina, Marcet-Houben, Marina, Hiller, Ekkehard, Rupp, Steffen, Gabaldón, Toni, Kovarik, Pavel, Schüller, Christoph
Formato: Texto
Lenguaje:English
Publicado: Elsevier Science B.V 2011
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022126/
https://www.ncbi.nlm.nih.gov/pubmed/21156173
http://dx.doi.org/10.1016/j.febslet.2010.12.006
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author Roetzer, Andreas
Klopf, Eva
Gratz, Nina
Marcet-Houben, Marina
Hiller, Ekkehard
Rupp, Steffen
Gabaldón, Toni
Kovarik, Pavel
Schüller, Christoph
author_facet Roetzer, Andreas
Klopf, Eva
Gratz, Nina
Marcet-Houben, Marina
Hiller, Ekkehard
Rupp, Steffen
Gabaldón, Toni
Kovarik, Pavel
Schüller, Christoph
author_sort Roetzer, Andreas
collection PubMed
description The human fungal pathogen Candida glabrata is related to Saccharomyces cerevisiae but has developed high resistance against reactive oxygen species. We find that induction of conserved genes encoding antioxidant functions is dependent on the transcription factors CgYap1 and CgSkn7 which cooperate for promoter recognition. Superoxide stress resistance of C. glabrata is provided by superoxide dismutase CgSod1, which is not dependent on CgYap1/Skn7. Only double mutants lacking both CgSod1 and CgYap1 were efficiently killed by primary mouse macrophages. Our results suggest that in C. glabrata the regulation of key genes providing stress protection is adopted to meet a host–pathogen situation.
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spelling pubmed-30221262011-02-11 Regulation of Candida glabrata oxidative stress resistance is adapted to host environment Roetzer, Andreas Klopf, Eva Gratz, Nina Marcet-Houben, Marina Hiller, Ekkehard Rupp, Steffen Gabaldón, Toni Kovarik, Pavel Schüller, Christoph FEBS Lett Article The human fungal pathogen Candida glabrata is related to Saccharomyces cerevisiae but has developed high resistance against reactive oxygen species. We find that induction of conserved genes encoding antioxidant functions is dependent on the transcription factors CgYap1 and CgSkn7 which cooperate for promoter recognition. Superoxide stress resistance of C. glabrata is provided by superoxide dismutase CgSod1, which is not dependent on CgYap1/Skn7. Only double mutants lacking both CgSod1 and CgYap1 were efficiently killed by primary mouse macrophages. Our results suggest that in C. glabrata the regulation of key genes providing stress protection is adopted to meet a host–pathogen situation. Elsevier Science B.V 2011-01-21 /pmc/articles/PMC3022126/ /pubmed/21156173 http://dx.doi.org/10.1016/j.febslet.2010.12.006 Text en © 2011 Elsevier B.V. https://creativecommons.org/licenses/by-nc-nd/3.0/ Open Access under CC BY-NC-ND 3.0 (https://creativecommons.org/licenses/by-nc-nd/3.0/) license
spellingShingle Article
Roetzer, Andreas
Klopf, Eva
Gratz, Nina
Marcet-Houben, Marina
Hiller, Ekkehard
Rupp, Steffen
Gabaldón, Toni
Kovarik, Pavel
Schüller, Christoph
Regulation of Candida glabrata oxidative stress resistance is adapted to host environment
title Regulation of Candida glabrata oxidative stress resistance is adapted to host environment
title_full Regulation of Candida glabrata oxidative stress resistance is adapted to host environment
title_fullStr Regulation of Candida glabrata oxidative stress resistance is adapted to host environment
title_full_unstemmed Regulation of Candida glabrata oxidative stress resistance is adapted to host environment
title_short Regulation of Candida glabrata oxidative stress resistance is adapted to host environment
title_sort regulation of candida glabrata oxidative stress resistance is adapted to host environment
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022126/
https://www.ncbi.nlm.nih.gov/pubmed/21156173
http://dx.doi.org/10.1016/j.febslet.2010.12.006
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