Aspergillus aff. fumigatus
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ABSTRACT:
PROVIDER: PRJNA1234068 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptome analysis of Aspergillus section Fumigati
| PRJDB7496 | ENA
Project description:Biological Relevance and Intent: Cryptic species within the Aspergillus section Fumigati, such as the Aspergillus viridinutans species complex, are increasingly recognized as important opportunistic pathogens in both human and veterinary medicine. These species often exhibit an intrinsic reduction in susceptibility to standard azole antifungals. The intent of this experiment was to determine how the tolerant veterinary isolate Aspergillus felis CCF5624 responds to acute azole stress (tolerance is transient state, not genetically determined like mutations). This study aimed to map the active cellular survival pathways and identify regulatory networks that could be targeted to bypass this protective tolerance machinery. Experimental Workflow Overview: Conidia suspensions of Aspergillus felis CCF5624 were inoculated onto pure RPMI medium covered with sterile cellophane and cultivated for 40 hours at 37 °C to establish vegetative colonies. To capture the immediate transcriptomic shifts associated with drug tolerance, the grown biomass was transferred directly to new RPMI plates supplemented with either a control solvent (DMSO) [abbreviated as \"A\"] or one of three clinical azole compounds (itraconazole, voriconazole, or posaconazole) [abbreviated as B, C,D, respectively] at concentrations corresponding to EUCAST resistance breakpoints. Following an acute 4-hour exposure, fungal biomass was harvested and flash-frozen in liquid nitrogen. Total RNA was isolated using a combined TRI reagent and spin-column methodology. High-throughput RNA sequencing (RNA-seq) was performed by Novogene Limited UK. Poly-A enriched mRNA libraries were prepared and sequenced on the Illumina NovaSeq X Plus platform using a 150 bp paired-end (PE150) strategy, yielding a minimum sequencing depth of 3 Gb (approximately 10 million paired-end reads) per individual sample. Reference gemone Aspergillus pseudoviridinutans IFM_55266 https://ftp.ncbi.nlm.nih.gov/genomes/all/GCF/018/340/605/GCF_018340605.1_Asppvi_assembly01/GCF_018340605.1_Asppvi_assembly01_genomic.fna.gz https://ftp.ncbi.nlm.nih.gov/genomes/all/GCF/018/340/605/GCF_018340605.1_Asppvi_assembly01/GCF_018340605.1_Asppvi_assembly01_genomic.gtf.gz
2026-07-15 | E-MTAB-17342 | biostudies-arrayexpress
Project description:As a major fungal pathogen, Aspergillus fumigatus can induce chronic, allergic or severe invasive infections, meanwhile its escalating resistance to azole antifungals has emerged as a global public health menace. Squalene, an essential molecule in the sterol biosynthesis pathway, can be cyclized by squalene hopene cyclase (SHC) to produce hopanoids and affect probably sterol biosynthesis modifying azole resistance; however, the physiological function of SHC in A. fumigatus pathogenesis is poorly understood.
2026-02-03 | GSE317610 | GEO
Project description:Draft genome sequences of the strains in Aspergillus section Fumigati
| PRJDB8156 | ENA
Project description:Azole-resistant Aspergillus fumigatus isolated from tulip bulbs
| PRJDB19701 | ENA
Project description:Genome sequence data results are reported from experimental and bioinfomatic work using the technique 'Bulk Segregant Analysis' to determine the genetic basis of observed resistance to the azole antifungal compound itraconazole in the opportunistic fungal pathogen Aspergillus fumigatus.
2022-05-11 | GSE193956 | GEO
Project description:Phenotype of azole-resistant Aspergillus fumigatus with a HapE mutation
| PRJDB10244 | ENA
Project description:Whole genome analysis of azole-resistant Aspergillus fumigatus Isolates from Taiwan
| PRJDB20599 | ENA
Project description:Azole-resistant Aspergillus infections are a source of serious concern, as only three classes of drugs are available for treatment. However, as most infections are still caused by azole-sensitive AF strains, there is a need to better understand fungal response to azole drugs. Here, we have identified a long non-coding RNA, afu-182, as a major regulator of erg11-independent fungal azole recalcitrant colony growth (ARC), without an apparent change in azole’s minimum inhibitory concentration. As strains are currently classified in a binary system of resistant or susceptible to drugs, we show that afu-182 is a negative regulator of azole drug response, leading to azole recalcitrant biofilms and poor disease outcomes in an animal model upon azole treatment. Furthermore, overexpression of afu-182 significantly reduced fungal burden in animals treated with azole drugs, showing a genetic basis of action. Whole transcriptome analysis revealed that azole drugs lead to upregulation of 7-transmembrane domain proteins of the RTA1 family, and these proteins are negatively regulated by afu-182. Here, we characterized two RTA1 family genes downstream of afu-182 and showed their individual and additive effects in regulating fungal ARC. Taken together, our data show a trans-acting role of long non-coding RNA afu-182 in regulating fungal response to azole drugs both in vitro and in vivo. This provides a promising novel approach to determine the treatment outcomes, given that MIC alone is a poor predictor for treatment outcomes in infections caused by ASAF strains.
2026-02-26 | GSE309441 | GEO
Project description:Newer fungal pathogens have emerged recently, attributed to their adaptation to higher environmental temperatures. With increasing earth’s temperatures, many existing fungal pathogens are adapting and show changes in host-pathogen interactions, disease pattern, and response to the antimicrobial drugs. Here, we show that thermal adaptation to 42C leads to reversible changes in fungal colony size, appearance, and azole drug response in human pathogenic fungus Aspergillus fumigatus. Importantly, this adaptation is mediated by a lncRNA, afu-182, whose RNA levels negatively correlate with temperature. Either growth back at lower temperature or ectopically increasing afu-182 RNA levels reverses the temperature adaptation. Global transcriptomic analyses show enrichment of pathogenesis associated genes at 37C and 42C compared to 25C. Interestingly, we show that small heat shock proteins and chaperones, but not ATP dependent heat-shock proteins are negatively regulated by afu-182 at 37C and 42C. Previously, we have shown that delta afu-182 strain produce worse disease outcomes in a murine model of invasive pulmonary aspergilllosis. Here, more importantly, we show that overexpression of afu-182 in clinically azole resistant isolates increased survival in a murine model of invasive pulmonary aspergillosis. Taken together, fungal adaptation to increased temperature leads to decrease in afu-182 RNA levels that is associated with worse disease outcomes upon azole treatment and an increase in MIC. This provides a framework, to take temperature into account when analyzing the rise in azole MIC in environmental and clinical isolates.
2026-03-02 | GSE319853 | GEO