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Mistranslation accelerates the adaptation of Candida albicans to Fluconazole

ABSTRACT: Mistranslation accelerates the adaptation of Candida albicans to Fluconazole

PROVIDER: PRJEB8387 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR753552_1.fastq.gz	Fastqsanger.gz
	ERR753552_2.fastq.gz	Fastqsanger.gz
	ERR753553_1.fastq.gz	Fastqsanger.gz
	ERR753553_2.fastq.gz	Fastqsanger.gz
	ERR753554_1.fastq.gz	Fastqsanger.gz

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Mistranslation accelerates the adaptation of Candida albicans to Fluconazole

Project description:The leucine CUG codon was reassigned to serine in the fungal pathogen Candida albicans. To clarify the biological role of this tuneable codon ambiguity on drug resistance, we evolved C. albicans strains that were engineered to mistranslate the CUG codon at constitutively elevated levels, in the presence and absence of the antifungal drug fluconazole. Elevated levels of mistranslation resulted in the rapid acquisition of resistance to fluconazole.

2016-10-27 | E-SYBR-13 | biostudies-arrayexpress

Mistranslation accelerates the evolution of antifungal drug resistance in Candida albicans [CGH]

Project description: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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Mistranslation accelerates the evolution of antifungal drug resistance in Candida albicans

Project description:Mistranslation accelerates the evolution of antifungal drug resistance in Candida albicans

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Mistranslation accelerates the evolution of antifungal drug resistance in Candida albicans [Gene expression]

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Differential gene expression of Candida albicans under no stress conditions or fluconazole stress

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Potential Role of Lysine Acetylation in the Stepwise Adaptation of Candida albicans to Fluconazole

Project description:Candida albicans is an opportunistic fungal pathogen capable of causing superficial mucosal and systemic infections, sometimes leading to life-threatening conditions. The increasing resistance of C. albicans to azole antifungals has become a significant challenge in clinical treatment. Lysine acetylation (Kac) is a well-studied post-translational modification that plays crucial roles in various biological processes. However, its impact on antifungal resistance in C. albicans remains poorly understood. Five strains of C. albicans isolated from the same patient, representing different stages of acquired fluconazole resistance in vivo, were used in this study to investigate the potential regulatory mechanism of Kac on the development of azole resistance in C. albicans. Quantitative proteomic analysis using tandem mass tag (TMT) labeling, acetylation enrichment, and liquid chromatography-mass spectrometry (LC-MS) was conducted on these five strains. We divided all strains into four comparison groups and identified a total of 1796 lysine acetylation sites across 938 proteins, with quantitative data available for 1314 acetylation sites in 712 proteins. Analysis of 155 significantly differentially modified sites revealed that the acetylation levels of key proteins involved in the conversion of pyruvate to acetyl-CoA for entry into the tricarboxylic acid (TCA) cycle for energy production were initially downregulated and then upregulated during the acquisition of fluconazole resistance. Additionally, the acetylation levels of proteins involved in ribosome synthesis, translation processes, and amino acid synthesis were found to increase. Therefore, lysine acetylation in C. albicans may contribute to azole resistance by regulating energy metabolism and protein synthesis.

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Candida albicans

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The early transcriptional and post-transcriptional responses to fluconazole in sensitive and resistant Candida albicans (5P-Seq)

Project description:Candida albicans is a leading cause of fungal infections in immunocompromised patients. Management of candidemia relies on a few antifungal agents, with fluconazole being first line therapy. The emergence of fluconazole-resistant strains highlights the pressing need to improve our molecular understanding of the drug response mechanisms. By sequencing the 5’P mRNA degradation intermediates, we show that co-translational mRNA decay is common in C. albicans and characterize how in vivo 5´-3´ exonuclease degradation trails the last translating ribosome. Thus, the study of the 5'P mRNA degradome (5PSeq) offers a simple and affordable way to measure ribosome dynamics and identify codon specific ribosome stalls in response to drugs and amino acid deprivation. Building upon this, we combine RNA-Seq and 5PSeq to study the early response of sensitive and resistant C. albicans isolates to fluconazole. Our results highlight that transcriptional responses, rather than changes in ribosome dynamics, are the main driver of Candida resistance to fluconazole.

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