Project description:The experiment was designed to study the transcriptional profiling of Candida albicans wild-type CAI-4 strains and corresponding Histatin 5 treated strains. Since Histatin 5 will kill Candida albicans, the focus will be on how many and which genes are significantly affected with the treatment of Histatin 5. Currently, we only conducted the microarray experiments at one concentration of Histatin 5 and one time point of treatment. Keywords: cell type comparison
Project description:We perform microarray analysis of HUVECs upon stimulation with virulent wildtype C. albicans strain SC5314 or its efg1/efg1 cph1/cph1 hyphal-deficient derivative strain CAN34 to compare the gene expression profiles elicited from HUVECs in response to these strains. In addition, these responses are compared to that of TNF-alpha induced responses to determine which responses are Candida-specific. Keywords: comparison of host response to different Candida albicans morphologies
Project description:Transcriptional profiling of Candida albicans cells grown under planktonic and biofilm-inducing conditions, comparing SN76 and sfl1Δ/sfl1Δ strains. Goal was to study the effect of SFL1 deletion on the transcriptomic profile of C. albicans planktonic and biofilm cells under acidic conditions, in order to reveal the function of the Sfl1 transcription factor in C. albicans biofilm development.
Project description:Transcriptomic analysis of wild type and GCN5-deficient Candida albicans cells prior to and after treatment with Caspofungin 15 min and 45 min was done to determine the transcriptional changes in these strains
Project description:Candida yeasts causing human infections are spread across the yeast phylum with Candida glabrata being related to Saccharomyces cerevisiae, Candida krusei grouping to Pichia spp., and Candida albicans, Candida parapsilosis and Candida tropicalis belonging to the CTG-clade. The latter lineage contains yeasts with an altered genetic code translating CUG codons as serine using a serine-tRNA with a mutated anticodon. It has been suggested that the CTG-clade CUG codons are mistranslated to a small extent as leucine due to mischarging of the serine-tRNA(CAG). The mistranslation was suggested to result in variable surface proteins explaining fast host adaptation and pathogenicity. Here, we re-assessed this potential mistranslation by high-resolution mass spectrometry-based proteogenomics of multiple CTG-clade yeasts, various C. albicans strains, isolated from colonized and from infected human body sites, and C. albicans grown in yeast and hyphal forms.
Project description:Aneuploidy and the evolution of aneuploid karyotypes of Candida albicans strains was identified using aCGH. Whole chromosome and segmental aneuploidies, (specifically on the left arm of chromosome 5 - shown to be due to isochromosome formation) are associated with the appearance of resistance to the antifungal drug fluconazole. Keywords: Comparative Genomic Hybridization
Project description:We performed DNA microarray analyses and compared the difference in the transcriptome between B6 and DBA/2 mice with modest or dramatic sensitivity to CAWS-vasculitis, respectively. Candida albicans water-soluble fraction (CAWS), a mannoprotein-β-glucan complex obtained from the culture supernatant of C. albicans NBRC1385, causes CAWS mediated vasculitis (CAWS-vasculitis) with distinct sensitivity among mouse strains.
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.
Project description:The purpose of this review is to describe the tools used to detect genome changes, to highlight recent advances in our understanding of large scale chromosome changes that arise in C. albicans and to discuss the role of specific stresses in eliciting these genome changes. The types of genomic diversity that have been characterized suggest C. albicans can undergo extreme genomic changes in order to survive stresses in the human host. We propose that C. albicans and other pathogens may have evolved mechanisms not only to tolerate, but also to generate, large-scale genetic variation as a means of adaptation. Strains included in this series are described in a Eukaryotic Cell review of genomic plasticity of Candida albicans. These strains are well-characterized and some of them are frequently utilized by the Candida community to generate mutant strains. Each strain was analyzed once and all strains were competed against the same reference strain, SC5314 (the first sequenced C. albicans strain).