Candida albicans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA263832 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Map ORC binding sites to identify replication origins in C. albicans by using polyclonal ORC antibodies (gift from Stephen Bell Lab). Due to the unsynchronized nature of Candida cells, log-phase cultures were taken to perfoem ChIP-chip experiments to find the genome-wide ORC binding sites.
2014-02-13 | GSE54923 | GEO
Project description:To elucidate the impact of IFU5 in Candida albicans, genome wide transcription profiling was performed in ifu5?/? mutant strain. Wild type and mutant cells were grown for 5 hours and RNA extracted from these cultures, followed by microarray profiling. Expression of six genes (EFG1, ALS3, SOD3, BMT4, COX2, NAD1) was validated by qPCR.
2019-02-01 | GSE110650 | GEO
Project description:Candida albicans is part of the human gastrointestinal (GI) microbiota. To better understand how C. albicans efficiently establishes GI colonisation, we competitively challenged growth of 572 signature-tagged strains (~10% genome coverage), each conditionally overexpressing a single gene, in the murine gut. We identified CRZ2, a transcription factor whose overexpression and deletion respectively increased and decreased early GI colonisation. Using clues from genome-wide expression and gene-set enrichment analyses, we found that the optimal activity of Crz2p occurs under hypoxia at 37°C, as evidenced by both phenotypic and transcriptomic analyses following CRZ2 genetic perturbation. Consistent with early colonisation of the GI tract, we show that CRZ2 overexpression confers resistance to acidic pH and bile salts, suggesting an adaptation to the upper sections of the gut. Genome-wide location analyses revealed that Crz2p directly modulates the expression of many mannosyltransferase- and cell-wall protein-encoding genes, suggesting a link with cell-wall function. We show that CRZ2 overexpression alters cell-wall phosphomannan abundance and increases sensitivity to tunicamycin, suggesting a role in protein glycosylation. Our study reflects the powerful use of gene overexpression as a complementary approach to gene deletion to identify relevant biological pathways involved in C. albicans interaction with the host environment.
2018-11-20 | GSE67233 | GEO
Project description:Genome-wide expression profiling of Candida albicans transcription factor Crz2p
| PRJNA279298 | ENA
Project description:Genome-wide expression profiling of Candida albicans transcription factor Skn7p
| PRJNA338060 | ENA
Project description:This data was generated to compare genome-wide expression differences between a major fungal pathogen of humans, Candida albicans and its less pathogenic relative, Candida dubliniensis, using interspecies hybrids to systematically identify cis-regulatory adaptations.
2021-03-31 | GSE168112 | GEO
Project description:Genome-wide transcriptional profiles of Candida albicans without and with inhibition of an analog sensitive Ssn3 using 3-MB-PP1.
2021-06-01 | GSE171859 | GEO
Project description:Transcriptional profiling of Candida albicans SC5314 comparing C. albicans grown in RPMI1640 or in RPMI1640 with 100ug/ml AAT. Goal was to determine the effects of AAT on global C. albicans gene expression.
2023-01-01 | GSE165326 | GEO
Project description:Candida albicans is an opportunistic yeast pathogen that causes a wide range of infections especially amongst immunocompromised patients. Aureobasidin A (AbA) has been shown to inhibit inositolphosphoryl ceramide synthase (IPCS), a key enzyme responsible for sphingolipid biosynthesis. There are limited studies exploring IPCS as a target molecule for antifungal treatment. It is hypothesized that the mechanism of AbA inhibition involves alteration of C. albicans phospholipid and sphingolipid profiles. The profiling of C. albicans phospholipid and sphingolipid upon exposure to 0.5-4 µg/ml of AbA were determined using Liquid chromatography-mass spectrometry (LC-MS).
2021-09-16 | ST001982 | MetabolomicsWorkbench
Project description:Biofilm formation is an important virulence trait of the pathogenic yeast Candida albicans. We have combined gene overexpression, strain barcoding and microarray profiling to screen a library of 531 C. albicans conditional overexpression strains (~10% of the genome) for genes affecting biofilm development in mixed-population experiments. The overexpression of 16 genes increased strain occupancy within a multi-strain biofilm, whereas overexpression of 4 genes decreased it. The set of 16 genes was significantly enriched for those encoding predicted glycosylphosphatidylinositol (GPI)-modified proteins, namely Ihd1/Pga36, Phr2, Pga15, Pga19, Pga22, Pga32, Pga37, Pga42 and Pga59; eight of which have been classified as pathogen-specific. Validation experiments using either individually- or competitively-grown overexpression strains revealed that the contribution of these genes to biofilm formation was variable and stage-specific. Deeper functional analysis of PGA59 and PGA22 at a single-cell resolution using atomic force microscopy showed that overexpression of either gene increased C. albicans ability to adhere to an abiotic substrate. However, unlike PGA59, PGA22 overexpression led to cell cluster formation that resulted in increased sensitivity to shear forces and decreased ability to form a single-strain biofilm. Within the multi-strain environment provided by the PGA22-non overexpressing cells, PGA22-overexpressing cells were protected from shear forces and fitter for biofilm development. Ultrastructural analysis, genome-wide transcript profiling and phenotypic analyses in a heterologous context suggested that PGA22 affects cell adherence through alteration of cell wall structure and/or function. Taken together, our findings reveal that several novel predicted GPI-modified proteins contribute to the cooperative behaviour between biofilm cells and are important participants during C. albicans biofilm formation. Moreover, they illustrate the power of using signature tagging in conjunction with gene overexpression for the identification of novel genes involved in processes pertaining to C. albicans virulence.
2014-03-31 | GSE48647 | GEO