Candida albicans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA176392 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The transcription regulators HMS1, RTG1, RTG3, ZCF21, LYS14 and LYS144 play roles in the proliferation of C. albicans in a mammalian host. Chromatin immunoprecipitation (ChIP) of HMS1-MYC, RTG1-MYC, RTG3-MYC, GFP-ZCF21, GFP-LYS14, GFP-LYS144 followed by array hybridization (Agilent) uncovered a network of target genes required for C. albicans to thrive in the host.
2012-10-02 | GSE41237 | GEO
Project description:The transcription regulators HMS1, RTG1, RTG3, ZCF21, LYS14 and LYS144 play roles in the proliferation of C. albicans in a mammalian host. Chromatin immunoprecipitation (ChIP) of HMS1-MYC, RTG1-MYC, RTG3-MYC, GFP-ZCF21, GFP-LYS14, GFP-LYS144 followed by array hybridization (Agilent) uncovered a network of target genes required for C. albicans to thrive in the host. Comparison of IP/input in tagged strains to untagged cells immuniprecipitated with the same antibody.
2012-10-02 | E-GEOD-41237 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE34255: Pho85, Pcl1, and Hms1 Signaling Governs Candida albicans Morphogenesis Induced by Elevated Temperature or Hsp90 Compromise [mRNA] GSE34938: Pho85, Pcl1, and Hms1 Signaling Governs Candida albicans Morphogenesis Induced by Elevated Temperature or Hsp90 Compromise [ChIP-chip] Refer to individual Series
2012-03-20 | E-GEOD-34939 | biostudies-arrayexpress
Project description:Goal: We employed RNA-seq to identify targets of regulation of the Candida albicans SREBP transcription regulators Cph2 and Hms1.
2018-11-05 | GSE118414 | GEO
Project description:ChIP-chip from Candida albicans cells with GFP-LYS142, GFP-LYS143, GFP-LYS14, and GFP-LYS144
| PRJNA227154 | ENA
Project description:Candida albicans is associated with humans as both a harmless commensal organism and a pathogen. Cph2 is a transcription factor whose DNA binding domain is similar to mammalian sterol response element binding proteins (SREBPs). SREBPs are master regulators of cellular cholesterol levels, and are highly conserved from fungi to mammals. However, ergosterol biosynthesis is regulated by the zinc finger transcription factor Upc2 in C. albicans and several other yeasts. Cph2 is not necessary for ergosterol biosynthesis, but important for colonization in the murine gastrointestinal tract. Here we demonstrate that Cph2 is a membrane-associated transcription factor that is processed to release the N-terminal DNA binding domain like SREBPs; but its cleavage is not regulated by cellular levels of ergosterol or oxygen. ChIP-Seq shows that Cph2 binds to the promoters of HMS1 and other components of the regulatory circuit for GI tract colonization. In addition, 50% of Cph2 targets are also bound by Hms1 and other factors of the regulatory circuit. Several common targets function at the head of the glycolysis pathway. Thus, Cph2 is an integral part of the regulatory circuit for GI colonization that regulates glycolytic flux. RNA-seq shows a significant overlap in genes differentially regulated by Cph2 and hypoxia, and Cph2 is important for optimal expression of some hypoxia-responsive genes in glycolysis and the citric acid cycle. We suggest that Cph2 and Upc2 regulate hypoxia-responsive expression in different pathways, consistent with a synthetic lethal defect of the cph2 upc2 double mutant in hypoxia. Genome binding/occupancy profiling by high throughput sequencing. ChIP-seq of Cph2 was carried out in a wild-type strain carrying N-terminal myc-tagged Cph2 under the MAL2 promoter (MAL2-myc-Cph2N). IP and INPUT samples from 2 independent experiments, as well as a sample of untagged wild-type control, were sequenced.
2015-08-05 | E-GEOD-71728 | biostudies-arrayexpress
Project description:Pho85, Pcl1, and Hms1 Signaling Governs Candida albicans Morphogenesis Induced by Elevated Temperature or Hsp90 Compromise [ChIP-chip]
| PRJNA156143 | ENA
Project description:The capacity to sense and transduce temperature signals pervades all aspects of biology, and temperature exerts powerful control over the development and virulence of diverse pathogens. In the leading fungal pathogen of humans, Candida albicans, temperature has a profound impact on morphogenesis, a key virulence trait. Many cues that induce the transition from yeast to filamentous growth are contingent on a minimum temperature of 37ºC, while further elevatation to 39ºC serves as an independent inducing cue. The molecular chaperone Hsp90 is a key regulator of C. albicans temperature-dependent morphogenesis, as induction of filamentous growth requires relief from Hsp90-mediated repression of the morphogenetic program. Compromise of Hsp90 function genetically, pharmacologically, or by elevated temperature induces filamentation in a manner that depends on protein kinase A (PKA) signaling, but is independent of the terminal transcription factor, Efg1. Here, we determine that despite morphological and regulatory differences, inhibition of Hsp90 induces a transcriptional profile similar to that induced by other filamentation cues, and does so in a manner that is independent of Efg1. Further, we identify Hms1 as a transcriptional regulator required for morphogenesis induced by elevated temperature or compromise of Hsp90 function. Hms1 functions downstream of the cyclin Pcl, and the cyclin-dependent kinase Pho85, both of which are required for temperature-dependent filamentation. Upon Hsp90 inhibition, Hms1 binds to DNA elements involved in filamentous growth, including UME6 and RBT5, and regulates their expression, providing a mechanism through which Pho85, Pcl1, and Hms1 govern morphogenesis. Consistent with the importance of morphogenetic flexibility with virulence, deletion of C. albicans HMS1 attenuates virulence in a metazoan model of infection. Thus, we establish a new mechanism through which Hsp90 orchestrates C. albicans morphogenesis, and define novel regulatory circuitry governing a temperature-dependent developmental program, with broad implications for temperature sensing and virulence of microbial pathogens.
2012-03-20 | GSE34938 | GEO
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