Candida parapsilosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA246482 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1278970_1.fastq.gz | Fastqsanger.gz | |||
| SRR1278970_2.fastq.gz | Fastqsanger.gz | |||
| SRR1278980_1.fastq.gz | Fastqsanger.gz | |||
| SRR1278980_2.fastq.gz | Fastqsanger.gz | |||
| SRR1278990_1.fastq.gz | Fastqsanger.gz |
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Project description:Abstract: Candida parapsilosis and Candida albicans are human fungal pathogens that belong to the CUG clade in the Saccharomycotina. In contrast to C. albicans, relatively little is known about the virulence properties of C. parapsilosis, a pathogen particularly associated with infections of premature neonates. We describe here the construction of >200 C. parapsilosis strains carrying double allele deletions of transcription factors, protein kinases and species-specific genes. Two independent deletions were constructed for each target gene. Growth in > 40 conditions was tested, including carbon source, temperature, and the presence of antifungal drugs. The phenotypes were compared to C. albicans strains with deletions of orthologous transcription factors. We found that many phenotypes are shared between the two species, such as the role of Upc2 as a regulator of azole resistance. Others are unique. For example, Cph2 plays a role in the hypoxic response in C. parapsilosis and not in C. albicans. We found extensive divergence between the biofilm regulators of the two species. We identified 7 transcription factors and one protein kinase that are required for biofilm development in C. parapsilosis. Only three (Efg1, Bcr1, and Ace2) have similar effects on C. albicans biofilms, whereas Cph2, Czf1, Gzf3 and Ume6 have major roles in C. parapsilosis only. In addition, two transcription factors (Brg1 and Tec1) with well-characterized roles in biofilm formation in C. albicans do not have the same function in C. parapsilosis. We also compared the transcription profile of C. parapsilosis and C. albicans biofilms. Our analysis suggests the processes shared between the two species are predominantly metabolic.
2014-07-21 | GSE57451 | GEO
Project description:Abstract: Candida parapsilosis and Candida albicans are human fungal pathogens that belong to the CUG clade in the Saccharomycotina. In contrast to C. albicans, relatively little is known about the virulence properties of C. parapsilosis, a pathogen particularly associated with infections of premature neonates. We describe here the construction of >200 C. parapsilosis strains carrying double allele deletions of transcription factors, protein kinases and species-specific genes. Two independent deletions were constructed for each target gene. Growth in > 40 conditions was tested, including carbon source, temperature, and the presence of antifungal drugs. The phenotypes were compared to C. albicans strains with deletions of orthologous transcription factors. We found that many phenotypes are shared between the two species, such as the role of Upc2 as a regulator of azole resistance. Others are unique. For example, Cph2 plays a role in the hypoxic response in C. parapsilosis and not in C. albicans. We found extensive divergence between the biofilm regulators of the two species. We identified 7 transcription factors and one protein kinase that are required for biofilm development in C. parapsilosis. Only three (Efg1, Bcr1, and Ace2) have similar effects on C. albicans biofilms, whereas Cph2, Czf1, Gzf3 and Ume6 have major roles in C. parapsilosis only. In addition, two transcription factors (Brg1 and Tec1) with well-characterized roles in biofilm formation in C. albicans do not have the same function in C. parapsilosis. We also compared the transcription profile of C. parapsilosis and C. albicans biofilms. Our analysis suggests the processes shared between the two species are predominantly metabolic. C. parapsilosis mRNA profiles of wild type (WT) at 37 degree celcius in planktonic growth conditions and ace2-/-, cph2-/-, efg1-/-, czf1-/-, ume6-/-, bcr1-/- and WT in biofilm conditions were generated by deep sequencing, in triplicate, using Illumina HiSeq2000.
2014-07-21 | E-GEOD-57451 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE33460: Transcriptional profile of Candida albicans bcr1 knockout. GSE33461: Transcriptional profile of Candida parapsilosis bcr1 knockout. GSE33462: Transcriptional profile of Candida parapsilosis CLIB214 culture in low iron conditions Refer to individual Series
2011-11-05 | E-GEOD-33490 | biostudies-arrayexpress
Project description:In Candida albicans the Efg1 transcription factor (a member of the APSES family) is an important regulator of hyphal growth, and of the white-to-opaque transition. In contrast, we show that the Efg1 ortholog in Candida parapsilosis is a major regulator of a different morphological switch at the colony level, from a concentric to smooth morphology. The rate of switching is at least 100-fold increased in an efg1 knockout relative to wild type. Deleting efg1 also reduces biofilm formation, and results in increased sensitivity to SDS, Congo red, caspofungin and calcofluor white in cells of both morphologies. Biofilm reduction is more dramatic in in vitro than in in vivo models. We use ChIP-seq to show that Efg1 binds to 502 promoter regions, including 70 potential transcription factors or regulatory proteins. Several of the transcription factors belong to networks that regulate biofilm development and white-opaque switching in C. albicans. Efg1 also binds to its own promoter. The binding site for C. parapsilosis Efg1 resembles that of orthologs in other fungi. Many Efg1 targets are probably also regulated by the Ndt80 transcription factor. We show that a paralog of Efg1 (Efh1) is restricted to Candida species. Efh1 does not regulate concentric-smooth phenotype switching, biofilm formation or stress response in C. parapsilosis. Our analysis supports the hypothesis that Efg1 has an ancient role as regulator of development in fungi, but we have identified a new role in C. parapsilosis as a regulator of colony switching that is distinct from the white-opaque switch in C. albicans.
2013-06-20 | GSE41064 | GEO
Project description:Candidiasis is an infection caused by yeasts of the genus Candida that ranges in severity from debilitating mucosal infections to disseminated disease with high mortality rates. C. albicans is the most common cause of infection, but non-albicans species collectively represent a significant disease burden. Disseminated disease rarely affects immunocompetent individuals, largely due to the action of innate immune cells, including macrophages, in controlling infection. The interaction of C. albicans with macrophages has been subject to extensive study, but there has been little investigation of the macrophage response to non-albicans Candida species. Here, we used RNA-seq to investigate global transcriptional changes within primary murine macrophages after one hour in response to four species: C. albicans, C. parapsilosis, C. tropicalis and Clavispora lusitaniae. We identified a strong pro-inflammatory response to C. albicans that was largely independent of fungal variability and found that this was highly correlated with the response to C. parapsilosis and C. tropicalis. In contrast, C. lusitaniae elicited a broadly weaker response, including reduced induction of cytokine genes. Several chemokine genes also showed weaker induction in response to both C. lusitaniae and C. parapsilosis than to C. albicans, although significantly reduced secretion of CCL3 protein was only evident in response to C. lusitaniae. These data indicate a high degree of similarity in early macrophage recognition of multiple important Candida pathogens, but also suggest that weaker recognition of C. lusitaniae by immune cells may aid immune evasion by this species.
2021-11-28 | GSE152700 | GEO
Project description:Candidiasis affects a wide variety of immunocompromised individuals, including HIV/AIDS patients and cancer patients on chemotherapy. Candida albicans, a major human fungal pathogen, accounts for about 50% of all cases, while the remainder are caused by the less pathogenic non-albicans Candida species (NACS). These species are believed to be less pathogenic, in part, because they do not filament as readily or robustly as C. albicans, although definitive evidence is lacking. To address this question, we used strains for two NACS, Candida tropicalis and Candida parapsilosis, that are genetically engineered to constitutively express the key transcriptional regulator UME6 and drive strong filamentation both in vitro and during infection in vivo. Unexpectedly, both strains showed a dramatic reduction in organ fungal burden and clearance of infection in response to UME6 expression. Consistent with these findings, we observed that a C. tropicalis hyperfilamentous mutant was significantly reduced and a filamentation-defective mutant was slightly increased for organ fungal burden. Comprehensive immune profiling did not reveal any significant changes in the host immune response to UME6 expression in the NACS. Interestingly, however, whole-genome transcriptional profiling indicated that while genes important for filamentation were induced by UME6 expression in C. tropicalis and C. parapsilosis, other genes involved in a variety of processes important for pathogenesis were strongly down-regulated. Our findings are significant because they suggest fundamental evolutionary differences in the relationship between morphology and pathogenicity among Candida species and that NACS do not necessarily possess the same virulence properties as C. albicans.
2019-10-01 | GSE134321 | GEO
Project description:Predatory interactions among microbes are a major evolutionary driving force for biodiversity. The fungivorous amoeba Protostelium aurantium has a wide fungal food spectrum including major pathogenic members of the genus Candida. Phagocytic feeding by P. aurantium is highly effective with C. parapsilosis, a major pathogenic yeast. Here we show that upon ingestion by the amoeba C. parapsilosis is confronted with an oxidative burst and undergoes phagosomal lysis within minutes. On the fungal side, a functional genomic approach identified the fungal copper and redox homeostasis as primary targets of amoeba predation with the highly expressed copper exporter Crp1 and the peroxiredoxin Prx1 contributing to survival when encountering P. aurantium. The fungolytic activity was largely retained in intracellular vesicles of the amoebae. Following their isolation, the content of these vesicles induced immediate killing and lysis of C. parapsilosis. A proteomic analyses identified 56 vesicular proteins. Although fully unknown proteins were dominant, many of them could be categorized as hydrolytic enzymes presumably targeting the fungal cell wall, indicating that fungal cell wall structures are under predatory selection pressure in natural environments.
2021-12-01 | PXD023816 | Pride
Project description:In Candida albicans the Efg1 transcription factor (a member of the APSES family) is an important regulator of hyphal growth, and of the white-to-opaque transition. In contrast, we show that the Efg1 ortholog in Candida parapsilosis is a major regulator of a different morphological switch at the colony level, from a concentric to smooth morphology. The rate of switching is at least 100-fold increased in an efg1 knockout relative to wild type. Deleting efg1 also reduces biofilm formation, and results in increased sensitivity to SDS, Congo red, caspofungin and calcofluor white in cells of both morphologies. Biofilm reduction is more dramatic in in vitro than in in vivo models. We use ChIP-seq to show that Efg1 binds to 502 promoter regions, including 70 potential transcription factors or regulatory proteins. Several of the transcription factors belong to networks that regulate biofilm development and white-opaque switching in C. albicans. Efg1 also binds to its own promoter. The binding site for C. parapsilosis Efg1 resembles that of orthologs in other fungi. Many Efg1 targets are probably also regulated by the Ndt80 transcription factor. We show that a paralog of Efg1 (Efh1) is restricted to Candida species. Efh1 does not regulate concentric-smooth phenotype switching, biofilm formation or stress response in C. parapsilosis. Our analysis supports the hypothesis that Efg1 has an ancient role as regulator of development in fungi, but we have identified a new role in C. parapsilosis as a regulator of colony switching that is distinct from the white-opaque switch in C. albicans. RNA was isolated from C. parapsilosis wild type (three biological replicates, concentric phenotype), and from efg1 deletion strains (three biological replicates from both concentric and smooth phenotype). Gene expression was determined using strand-specific RNA-seq.
2013-06-20 | E-GEOD-41064 | biostudies-arrayexpress