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Status |
Public on Jul 18, 2017 |
Title |
Mistranslation accelerates the evolution of antifungal drug resistance in Candida albicans [CGH] |
Platform organism |
Candida albicans SC5314 |
Sample organism |
Candida albicans |
Experiment type |
Genome variation profiling by array
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Summary |
The fungal pathogen Candida albicans and other pathogens of the CTG clade reassigned the leucine CUG codon to serine and tolerate highly variable levels of both serine and leucine at CUG positions in response to environmental cues. Previous studies found that increased leucine misincorporation levels enhance resistance to drugs but the underlying mechanisms are not known. To clarify the biological role of this tuneable codon ambiguity, we evolved C. albicans strains engineered to mistranslate CUG at elevated levels, in the presence and absence of the antifungal drug fluconazole
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Overall design |
CGH analysis was performed on evolved C.albicans strains grown in presence of fluconazole and the parental strain not subjected to fluconazole.
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Contributor(s) |
Weil T, SantamarĂa R |
Citation(s) |
28808688 |
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Submission date |
Aug 05, 2014 |
Last update date |
Oct 17, 2017 |
Contact name |
Tobias Weil |
E-mail(s) |
tobias.weil@fmach.it
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Organization name |
Fondazione Edmund Mach
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Street address |
Via E. Mach, 1
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City |
S. Michele all'Adige (TN) |
ZIP/Postal code |
38010 |
Country |
Italy |
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Platforms (1) |
GPL19026 |
Agilent-038464 CaSC5314_SnpCgh_v1_Santos 033626 |
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Samples (3) |
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This SubSeries is part of SuperSeries: |
GSE60122 |
Mistranslation accelerates the evolution of antifungal drug resistance in Candida albicans |
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Relations |
BioProject |
PRJNA257517 |