Candida albicans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1066548 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A unique iron homeostasis regulatory circuit with reciprocal roles in Candida albicans commensalism and pathogenesis [ChIP_chip]
| PRJNA154667 | ENA
Project description:A unique iron homeostasis regulatory circuit with reciprocal roles in Candida albicans commensalism and pathogenesis [Expression Array]
| PRJNA154669 | ENA
Project description:The study asked the question whether commensalism or pathogenicity of an opportunistic pathogen like Candida albicans, depend on strain specific traits or on the phenotypic and genomic plasticity of the genus as a whole. Transcriptional analysis performed upon different medium conditions (RPMI in presence or absence of FBS) indicated differentially expressed genes involved in adhesion, filamentous growth and biofilm formation. Both genome sequence and gene expression highlighted concordant changes in pathways related to invasiveness and filamentation. These results reflected marked differences in term of morphological features, environment adaptation and survival to phagocytosis. The results indicate that the genetic background of C. albicans may greatly affect its behaviour in terms of in vitro susceptibility to immune effector cells. Based on this approach, a more in depth understanding of fungal genetic makeup is achievable, thus allowing to establish the virulence potential of a given isolate and possibly to predict the outcome of C. albicans infection.
2018-02-14 | GSE85138 | GEO
Project description:Passage through the mammalian gut triggers a phenotypic switch required for Candida albicans commensalism
| PRJNA188306 | ENA
Project description:The ability to undergo heritable switching between cell states is well recognized in microbial species. In the human fungal pathogen Candida albicans, cells can stably exist in several alternative states that show differential interactions with the mammalian host. Here, we demonstrate that gene dosage of the master transcription factor, Efg1, controls access to distinct cell states in diploid C. albicans cells. Thus, cells that are hemizygous for EFG1 can stably differentiate into a cell state that is not available to cells with two functional copies of the EFG1 gene. Strikingly, we reveal that a number of clinical isolates of C. albicans encode polymorphisms that produce a hemizygous EFG1 genotype and that this enables access to the novel cell state. Furthermore, we show that C. albicans cells in different cell states each exhibit unique interactions with the mammalian host, with consequences for both commensalism and pathogenesis.
2019-01-31 | GSE105399 | GEO
Project description:Among ~5,000,000 fungal species on Earth, Candida albicans is exceptional in its lifelong association with humans, where it exists either as a benign component of the gastrointestinal microbiome or as an invasive pathogen. Although it is generally assumed that invasiveness results from a breakdown of host immunity , it is also possible that specific fungal programs control the transition between these divergent lifestyles. Here, we report that exposure of C. albicans to the mammalian gut triggers a developmental switch, driven by the Wor1 transcription factor, to a commensal cell type. Wor1 has been thought to occur only in unique genetic backgrounds, but we show that WOR1 expression is triggered when wild-type cells are propagated in a murine gastrointestinal infection model. Similar to Wor1’s role in a white-opaque switch for mating, WOR1 overexpression within the host induces a novel switch affecting cell and colony morphology and conferring commensal fitness. However, these hyperfit GUT (Gastrointestinally-IndUced Transition) cells lack the functional hallmarks of opaque cells, which they resemble morphologically, whereas bona fide opaque cells are defective for commensalism. Instead, the GUT cell transcriptome is optimized for the environment of the distal mammalian digestive tract. The GUT cell type switch illuminates how a single organism can utilize distinct genetic programs to transition between commensalism and invasive tissue pathogenesis Candida albicans strains including the Wild type strain (SN425), WOR1OE -White (a/a, SN1044), WOR1OE -GUT (a/a, SN1045), White (a/a, SN966) and Opaque (a/a, SN967) were grown at room temperature in SC medium supplemented with 100ug/ml adenine; 2-4 biological replicates were performed per strain. RNA was prepared from these strains and samples were hybridized on custom Agilent C. albicans ORF arrays (15,000 spots/array, 70-mer probes).
2013-07-28 | E-GEOD-43972 | biostudies-arrayexpress
Project description:A family of secreted pathogenesis-related proteins in Candida albicans
| PRJNA139659 | ENA
Project description:Among ~5,000,000 fungal species on Earth, Candida albicans is exceptional in its lifelong association with humans, where it exists either as a benign component of the gastrointestinal microbiome or as an invasive pathogen. Although it is generally assumed that invasiveness results from a breakdown of host immunity , it is also possible that specific fungal programs control the transition between these divergent lifestyles. Here, we report that exposure of C. albicans to the mammalian gut triggers a developmental switch, driven by the Wor1 transcription factor, to a commensal cell type. Wor1 has been thought to occur only in unique genetic backgrounds, but we show that WOR1 expression is triggered when wild-type cells are propagated in a murine gastrointestinal infection model. Similar to Wor1’s role in a white-opaque switch for mating, WOR1 overexpression within the host induces a novel switch affecting cell and colony morphology and conferring commensal fitness. However, these hyperfit GUT (Gastrointestinally-IndUced Transition) cells lack the functional hallmarks of opaque cells, which they resemble morphologically, whereas bona fide opaque cells are defective for commensalism. Instead, the GUT cell transcriptome is optimized for the environment of the distal mammalian digestive tract. The GUT cell type switch illuminates how a single organism can utilize distinct genetic programs to transition between commensalism and invasive tissue pathogenesis
2013-07-28 | GSE43972 | GEO
Project description:N-Acetylglucosamine-Induced Cell Death in Candida albicans and Its Implications for Adaptive Mechanisms of Nutrient Sensing in Yeasts
| PRJNA271586 | ENA
Project description:Cell cycle-independent phospho-regulation of Fkh2 during hyphal growth regulates Candida albicans pathogenesis.
| PRJNA270862 | ENA