Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression of C. albicans genes during GI tract colonization and influence of efg1, efh1 and cph1 mutations

ABSTRACT: The goals of this study were to identify the Efg1p-regulon during GI tract colonization and to compare C. albicans gene expression during colonization of different organs of the GI tract. Our results identified significant differences in gene expression between cells colonizing the cecum and ileum. In addition, during laboratory growth, efg1- null mutant cells grew to a higher density than WT cells. The efg1- null mutant grew in depleted medium, while WT cells could only grow if the depleted medium was supplemented with carnitine, a compound that promotes the metabolism of fatty acids. During colonization, efg1- null mutant cells expressed higher levels of genes involved in lipid catabolism, carnitine biosynthesis and carnitine utilization in comparison to colonizing WT cells. This altered gene expression supports the ability of efg1- cells to hypercolonize naïve mice.

ORGANISM(S): Candida albicans

PROVIDER: GSE41771 | GEO | 2013/02/08

SECONDARY ACCESSION(S): PRJNA178150

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression of C. albicans genes during GI tract colonization and influence of efg1, efh1 and cph1 mutations

Project description:The goals of this study were to identify the Efg1p-regulon during GI tract colonization and to compare C. albicans gene expression during colonization of different organs of the GI tract. Our results identified significant differences in gene expression between cells colonizing the cecum and ileum. In addition, during laboratory growth, efg1- null mutant cells grew to a higher density than WT cells. The efg1- null mutant grew in depleted medium, while WT cells could only grow if the depleted medium was supplemented with carnitine, a compound that promotes the metabolism of fatty acids. During colonization, efg1- null mutant cells expressed higher levels of genes involved in lipid catabolism, carnitine biosynthesis and carnitine utilization in comparison to colonizing WT cells. This altered gene expression supports the ability of efg1- cells to hypercolonize naïve mice. C. albicans cells (WT, efg1-, efg1- efh1- or efg1- cph1-) were inoculated into antibiotic-treated BALB/c mice by oral gavage. Contents of the cecum and ileum were collected and frozen in RNALater. Reference cells (WT C. albicans) were grown in YPD medium at 37oC to exponential phase. Total RNA was extracted from both all samples. Sample of C. albicans isolated from GI tract organs was compared to reference on microarray. Between 4 and 7 microarray hybridizations, with dye swaps, were performed for each sample.

2013-02-08 | E-GEOD-41771 | biostudies-arrayexpress

Candida albicans

Project description:Expression of C. albicans genes during GI tract colonization and influence of efg1, efh1 and cph1 mutations

| PRJNA178150 | ENA

Pseudomonas aeruginosa

Project description:Expression data from P. aeruginosa colonizing the Murine GI Tract

| PRJNA128003 | ENA

C. albicans white-opaque transcription factor binding recorded in the mammalian gut

Project description:Candida albicans is a central fungal component of the human gut microbiota and an opportunistic pathogen. Two C. albicans transcription factors, Wor1 and Efg1, control its ability to colonize the mammalian gut. They are also master regulators of an epigenetic switch required for mating. The mammalian gastrointestinal tract is a complex environment difficult to model in vitro. In C. albicans, it is known that environmental signals can dictate the binding targets of these transcription factors. To study the regulation of transcription factors of C. albicans in the GI tract, a Calling card-seq approach was adopted. This technique allowed us to directly record transcription factor binding that occurred in the mammalian gut.

2020-06-01 | GSE150856 | GEO

Differential roles of nuclear and cytosolic GI in regulating plant circadian system

Project description:GIGANTEA (GI) is an important modulator of plant circadian system. Recent studies have reported that protein GI is localized in both nucleus and cytosol, and nuclear and cytosolic GI exert differential effect on plant circadian clock. We first generated GI-null mutants and transgenic Arabidopsis plants that expressed GI fused to green fluorescent protein gene (GIpro::GI-GFP) and GI-GFP with a nuclear localization signal (GIpro::GI-GFP-NLS) or with a nuclear export signal (GIpro::GI-GFP-NES) under the control of native promoter in GI-null mutants. To investigate differential roles of nuclear and cytosolic GI in regulating plant circadian clock, we performed genome-wide gene expression profiling for wild-type plants and the GI-transgenic plants at morning and evening, and analyzed complementation patterns of gi-2 lesion by nuclear and cytosolic GI. As a result, we identified four complementation patterns representing genes affected by only nuclear GI (GIN) or cytosolic GI (GIC), those by either GIN or GIC, and those by the action of both GIN and GIC. Furthermore, we compared the transgenic plants expressing GIpro::GI-GFP with WT and the other GI-transgenic plants to confirm whether abnormally expressed genes by the gi-2 mutation can be complemented by restoring protein GI.

2013-09-01 | GSE47169 | GEO

Differential roles of nuclear and cytosolic GI in regulating plant circadian system

2013-09-01 | E-GEOD-47169 | biostudies-arrayexpress

Ionizing radiation in GI tract of Tweak KO mice

Project description:TWEAK/Fn14 signaling may regulate the expression of genes involved in epithelial repair and mucosal inflammation. Comparing the gene signatures in WT and TWEAK KO mice will inform the biology of TWEAK/Fn14 pathway in the GI tract.

2011-07-01 | GSE25029 | GEO

Murine gastrointestinal bile acid profiles before and after antibiotics

Project description:Clostridium difficile infection (CDI) following antibiotic therapy is a major public health threat. While antibiotic disruption of the indigenous microbiota underlies the majority of cases of CDI, the early dynamics of infection in the disturbed intestinal ecosystem are poorly characterized. This study defines the dynamics of infection with C. difficile strain VPI 10463 throughout the gastrointestinal (GI) tract using a murine model of infection. After inducing susceptibility to C. difficile colonization via antibiotic administration, we followed the dynamics of spore germination, colonization, sporulation, toxin activity, and disease progression throughout the GI tract. C. difficile spores were able to germinate within 6 h postchallenge, resulting in the establishment of vegetative bacteria in the distal GI tract. Spores and cytotoxin activity were detected by 24 h postchallenge, and histopathologic colitis developed by 30 h. Within 36 h, all infected mice succumbed to infection. We correlated the establishment of infection with changes in the microbiota and bile acid profile of the small and large intestines. Antibiotic administration resulted in significant changes to the microbiota in the small and large intestines, as well as a significant shift in the abundance of primary and secondary bile acids. Ex vivo analysis suggested the small intestine as the site of spore germination. This study provides an integrated understanding of the timing and location of the events surrounding C. difficile colonization and identifies potential targets for the development of new therapeutic strategies. Research is published: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4333439/

2015-06-09 | ST000196 | MetabolomicsWorkbench

Function and regulation of Cph2 in Candida albicans [RNA-Seq]

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. Expression profiling by high throughput sequencing. RNA sequencing was performed on wild type and cph2 deletion strains. 2 biological replicates were sequenced for each strain.

2015-08-10 | E-GEOD-71902 | biostudies-arrayexpress

Integration of the tricarboxylic acid (TCA) cycle with cAMP signaling and Sfl2 pathways in the regulation of CO2 sensing, filamentation, and virulence in Candida albicans

Project description:Candida albicans is the most common opportunistic fungal pathogen of humans and is also a benign member of the gastrointestinal (GI) tract microbiota. Morphological transitions and metabolic regulation are critical for C. albicans to adapt to the changing host environment. We generated a library of central metabolic pathway mutants in the tricarboxylic acid (TCA) cycle, and investigated the functional consequences of these gene deletions on C. albicans biology. Inactivation of the TCA cycle impairs the ability of C. ablicans to utilize non-fermentable carbon sources and dramatically attenuates cell growth rates under several culture conditions. Through integrations with the Ras1-cAMP signaling pathway and the heat shock factor-type transcription regulator Sfl2, we found that the TCA cycle plays fundamental roles in the regulation of CO2 sensing and filamentation. The TCA cycle and cAMP signaling pathways form a regulatory feedback loop, in which ATP and CO2 may function as molecular linkers. We further demonstrate that inactivation of the TCA cycle leads to lowered intracellular ATP and cAMP levels and thus affects the activation of the Ras1-regulated cAMP signaling pathway. In turn, the Ras1-cAMP signaling pathway controls the TCA cycle through both Efg1- and Sfl2-mediated transcriptional regulation in response to elevated CO2 levels. The protein kinase A (PKA) catalytic subunit Tpk1, but not Tpk2, may play a major role in this regulation. Sfl2 specifically binds to several TCA cycle and filamentation-associated genes under high CO2 conditions. Global transcriptional profiling experiments indicate that Sfl2 is indeed required for the gene expression changes occurring in response to these elevated CO2 levels. Finally, we also demonstrate that several key genes of the TCA cycle are essential for virulence and successful colonization of the GI tract in two mouse infection models.

2017-10-04 | GSE102039 | 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