Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Antifungal agent 4-AN changes the genome-wide expression profile, down-regulates virulence-associated genes, and induces necrosis in Candida albicans cells

ABSTRACT: Antifungal agent 4-AN changes the genome-wide expression profile, down-regulates virulence-associated genes, and induces necrosis in Candida albicans cells

PROVIDER: PRJNA633813 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11811454_1.fastq.gz	Fastqsanger.gz
	SRR11811454_2.fastq.gz	Fastqsanger.gz
	SRR11811455_1.fastq.gz	Fastqsanger.gz
	SRR11811455_2.fastq.gz	Fastqsanger.gz
	SRR11811456_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Antifungal agent 4-AN changes the genome-wide expression profile, down-regulates virulence-associated genes, and induces necrosis in Candida albicans cells

Project description:In the light of the increasing occurrence of antifungal resistance, there is an urgent need to search for new therapeutic strategies to overcome this phenomenon. One of the applied approaches is the synthesis of small-molecule compounds showing antifungal properties. Here we present a continuation of the research on the recently discovered anti-Candida albicans agent 4-AN. Using next generation sequencing and transcriptional analysis, we revealed that the treatment of C. albicans with 4-AN can change the expression profile of a large number of genes. The highest up-regulation was observed in the case of genes involved in cell stress, while the highest down-regulation was shown for genes coding sugar transporters. Real-time PCR analysis revealed 4-AN mediated reduction of the relative expression of genes engaged in fungal virulence (ALS1, ALS3, BCR1, CPH1, ECE1, EFG1, HWP1, HYR1, and SAP1). The determination of the fractional inhibitory concentration index (FICI) showed that the combination of 4-AN with Amphotericin B is synergistic. Finally, flow cytometry analysis revealed that the compound induces mainly necrosis in Candida albicans cells.

2020-05-20 | GSE150837 | GEO

Antifungal Activity of Mammalian Serum amyloid A1 against Candida albicans

Project description:Human serum amyloid A (SAA) is a major acute phase protein and shows a massive increase of concentration in plasma during inflammation. In the current study, we report that recombinant human and mouse SAA1 (rhSAA1 and rmSAA1) have a potent antifungal activity against the major fungal pathogen Candida albicans. rhSAA1 binds to the cell surface of C. albicans and promotes cell aggregation. At high concentrations, rhSAA1 disrupts the membrane integrity and induces rapid cell death of C. albicans. Further investigation demonstrates that rhSAA1 targets on the cell wall adhesin Als3 of C. albicans. Inactivation of ALS3 in C. albicans leads to remarkably decreased cell aggregation and death upon rhSAA1 treatment, implying that Als3 plays a critical role in SAA1 sensing. Moreover, deletion of the ALS3 transcriptional regulators such as AHR1, BCR1, and EFG1 in C. albicans results in a similar effect on cell responses to that of the als3/als3 mutant upon rhSAA1 treatment. Global gene expression profiling analysis indicates that rhSAA1 has a remarkable impact on the expression of cell wall- and metabolism-related genes in C. albicans. Our finding of the antifungal activity of rhSAA1 against C. albicans expands the function of this protein and would provide new insights into the understanding of the host-Candida interaction during infections.

2019-09-01 | GSE128598 | GEO

Candida albicans exposure to antifungal polymers

Project description:Candida albicans exposure to antifungal polymers

| PRJEB65085 | ENA

Microarray of Candida albicans treated with sublethal concentrations of the antifungal Jagaricin

Project description:Candida albicans were treated with a sublethal concentration of the antifungal Jagaricin for either a short time (30 min) or until an OD of 0.5 (indicating log growth) was reached. Controls were grown without any antifungal to determine cellular reactions to the compound.

2019-06-14 | E-MTAB-7718 | biostudies-arrayexpress

Metabolomic-based investigation on the effects of antifungal agents in Candida albicans

Project description:Our aim is to determine the metabolic effects of increasing doses of an antifungal agent on C. albicans metabolism (untargeted, steady state metabolomics). We will culture in vitro Candida cells to the mid-logarithmic growth in liquid media (RPMI-1640) at 37°C and then inoculate biological replicates (1ml) onto 22mm nitrocellulose filters under vocuum filtration in sterile conditions. Subsequently, isolates will be cultivated to midlogarithmic phase of growth on the same agar (RPMI-1640) to which the antifungal agent has been added at a range of concentrations to achieve doses equivalent to 0 MIC (no drug), 0.0625 MIC, 0.125 MIC, 0.25 MIC, 0.5 MIC and 1.0 MIC at 37°C. At mid-logarithmic phase of growth (12h) replicates will be metabolically quenched by immersion into a solvent mixture of 40% acetonitrile: 40% methanol: 20% water precooled at -40°C. The resulting quenched isolate/solvent mixtrue will be mechanically lysed by bead-beating with 0.1mm Zirconia beads in a tissue homogenizer and then centrifuged to seperate out cell wall components. Supernatants will be removed and stored at -80°C until they will be sent to SECIM facility.

2015-02-10 | ST000243 | MetabolomicsWorkbench

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

2017-07-18 | GSE60120 | GEO

Gene expression response to the antifungal compound sampangine in C. albicans

Project description:Sampangine, a plant-derived alkaloid found in the Annonaceae family, exhibits strong inhibitory activity against the opportunistic fungal pathogens Candida albicans, Cryptococcus neoformans and Aspergillus fumigatus. In the present study, transcriptional profiling experiments coupled with the analysis of mutants were performed in an effort to elucidate its mechanism of action. Using Saccharomyces cerevisiae as a model organism, we show that sampangine produces a transcriptional response indicative of hypoxia, altering the expression of genes known to respond to low oxygen conditions. Several additional lines of evidence obtained suggest that these responses could involve effects on heme. First, the hem1 deletion mutant lacking the first enzyme in the heme biosynthetic pathway showed increased sensitivity to sampangine, and exogenously supplied hemin partially rescued the inhibitory activity of sampangine in wild-type cells. In addition, heterozygous mutants with deletions in genes involved in five out of eight steps in the heme biosynthetic pathway showed increased susceptibility to sampangine. Furthermore, spectral analysis of pyridine extracts indicated significant accumulation of free porphyrins in sampangine-treated cells. Transcriptional profiling experiments were also performed in C. albicans to investigate the response of a pathogenic fungal species to sampangine. Taking into account the known differences in the physiological responses of C. albicans and S. cerevisiae to low oxygen, significant correlations were observed between the two transcription profiles suggestive of heme-related defects. Our results indicate that the antifungal activity of the plant alkaloid sampangine is due, at least in part, to perturbations in the biosynthesis or metabolism of heme. Keywords: antifungal compound, transcriptional profiling, C. albicans

2008-01-09 | GSE10075 | GEO

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

2017-07-18 | GSE60121 | GEO

Antifungal agent tempol

Project description:Stable Redox-Cycling Nitroxide Tempol has Antifungal and Immune-modulatory Properties

| PRJEB31969 | ENA

Transcriptome profile of tra1 mutant in C. albicans in response to the antifungal caspofungin

Project description:The emergence of drug-resistant fungal strains is a threat to human health. Identifying targets that increase the susceptibility of fungal pathogens to current therapies will significantly improve outcomes. Tra1 is an essential component of the SAGA and NuA4 transcriptional co-activator complexes and is linked to multiple cellular processes associated with the yeast response to antifungal drugs. This submission contains RNA sequencing data from Candida albicans strain expressing a Tra1 mutant with three arginine to glutamine mutations in the PI3K domain (tra1Q3; Berg et al., 2018) treated with or without the antifungal caspofungin. Our goal was to identify genes regulated by Tra1 in C. albicans and identify genes with differential responses in the mutant tra1 strain upon capsofungin relative to the wild-type strain. We identified 68 genes that were differentially expressed when the tra1Q3 strain was treated with caspofungin, as compared to gene expression changes induced by either tra1Q3 or caspofungin alone. Included in this set were genes involved in cell wall maintenance, adhesion and filamentous growth. As a critical component of both SAGA and NuA4, Tra1 is uniquely positioned to regulate the yeast antifungal response and emerges, through targeting its PI3K domain, as a promising new therapeutic target for fungal infections.

2021-03-17 | GSE168988 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data