Candida albicans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA104147 | ENA |
REPOSITORIES: ENA
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Project description:We have used DNA microarray technology to compare the expression of over 6000 genes between C. albicans WT and ACE2 knockout strains in the hyphal form. Keywords: Gene expression comparison
2007-02-23 | GSE7100 | GEO
Project description:Our genetic screen reveals that deletion of CTM1, which abolishes the lysine trimethylation of cytochrome c (Cyc1), results in inhibition of hyphal morphogenesis in Candida albicans. Similar results are observed in the unmethylatable Cyc1 mutant (cyc1K79A). To elucidate how unmethylated Cyc1 inhibits hyphal growth, we performed RNA-Seq analysis by comparing WT (BWP17), ctm1∆/∆, and cyc1K79A cells grown in yeast and hyphal condition. Consistent with previous published data, many hyphal specific genes (HSGs), such as ALS3, ECE1, HWP1, and UME6, are upregulated while three major hyphal suppressor genes, TUP1, NRG1, and RFG1, are downregulated when WT cells switch from yeast to hyphal growth. Similar changes are observed in ctm1Δ/Δ and cyc1K79A cells upon hyphal induction, even though most mutant cells maintain yeast morphology throughout the induction. Further comparisons reveal that the basal transcriptional levels of HSGs are much lower in ctm1Δ/Δ and cyc1K79A cells than those in WT cells. Upon hyphal induction, the levels of HSGs in ctm1Δ/Δ and cyc1K79A cells increase but still remain lower than their basal levels in WT cells. In contrast, the hyphal suppressor genes (especially NRG1) exhibit much higher basal transcriptional levels in ctm1Δ/Δ and cyc1K79A cells than in WT cells. Their transcriptional levels reduce upon hyphal induction but still remain higher than the basal levels in WT cells. Together, these data suggest that unmethylated Cyc1 inhibits hyphal morphogenesis via transcriptional regulation of HSGs and hyphal suppressor genes.
2024-01-01 | GSE243813 | GEO
Project description:Sfl1p and Sfl2p are two homologous heat shock factor-type transcriptional regulators that antagonistically control morphogenesis in Candida albicans, while being required for full pathogenesis and virulence. To understand how Sfl1p and Sfl2p exert their function, we combined genome-wide location and expression analyses to reveal their transcriptional targets in vivo together with the associated changes of the C. albicans transcriptome. We show that Sfl1p and Sfl2p bind to the promoter of at least 113 common targets through divergent binding motifs and modulate directly the expression of key transcriptional regulators of C. albicans morphogenesis and/or virulence. Surprisingly, we found that Sfl2p additionally binds to the promoter of 75 specific targets, including a high proportion of hyphal-specific genes (HSGs; HWP1, HYR1, ECE1, others), revealing a direct link between Sfl2p and hyphal development. Data mining pointed to a regulatory network in which Sfl1p and Sfl2p act as both transcriptional activators and repressors. Sfl1p directly represses the expression of positive regulators of hyphal growth (BRG1, UME6, TEC1, SFL2), while upregulating both yeast form-associated genes (RME1, RHD1,YWP1) and repressors of morphogenesis (SSN6, NRG1). On the other hand, Sfl2p directly upregulates HSGs and activators of hyphal growth (UME6, TEC1), while downregulating yeast form-associated genes and repressors of morphogenesis (NRG1, RFG1, SFL1). Using genetic interaction analyses, we provide further evidences that Sfl1p and Sfl2p antagonistically control C. albicans morphogenesis through direct modulation of the expression of important regulators of hyphal growth. Bioinformatic analyses suggest that binding of Sfl1p and Sfl2p to their targets occurs with the co-binding of Efg1p and/or Ndt80p. Indeed, we show that Sfl1p and Sfl2p targets are bound by Efg1p and that both Sfl1p and Sfl2p associate in vivo with Efg1p. Taken together, our data suggest that Sfl1p and Sfl2p act as central M-bM-^@M-^\switch on/offM-bM-^@M-^] proteins to coordinate the regulation of C. albicans morphogenesis. ChIP was performed in 2 independently grown C. albicans sfl1 or sfl2 homozygous mutant strains expressing (sfl1-CaEXP-SFL1-HA or sfl2-CaEXP-SFL2-HA, respectively) or not (sfl1-CaEXP or sfl2-CaEXP, respectively) SFL1-HA or SFL2-HA (-HA, 3'-triple-HA-tagged alleles of SFL1 or SFL2) under the control of a methionine-repressible promoter (Total samples = 8; 2xCaEXP-SFL1-HA, 2xCaEXP-SFL2-HA, 2xCaEXP control for SFL1-HA ChIP and 2xCaEXP control for SFL2-HA ChIP).
2013-06-15 | E-GEOD-42886 | biostudies-arrayexpress
Project description:The Regulation of Ace2 and Morphogenesis (RAM) pathway is an important regulatory network in the human fungal pathogen Candida albicans. The RAM pathway’s two most well-studied components, the NDR/Lats kinase Cbk1 and its putative substrate, the transcription factor Ace2, have a wide range of phenotypes and functions. It is not clear, however, which of these functions are specifically due to the phosphorylation of Ace2 by Cbk1. To address this question, we first compared the transcriptional profiles of CBK1 and ACE2 deletion mutants. This analysis indicates that, of the large number of genes whose expression is affected by deletion of CBK1 and ACE2, only 5.5% of those genes are concordantly regulated. Our data also suggest that Ace2 directly or indirectly represses a large set of genes during hyphal morphogenesis. Second, we generated strains containing ACE2 alleles with alanine mutations at the Cbk1 phosphorylation sites. Phenotypic and transcriptional analysis of these ace2 mutants indicates that, as in Saccharomyces cerevisiae, Cbk1 regulation is important for daughter cell localization of Ace2 and cell separation during yeast phase growth. In contrast, Cbk1 phosphorylation of Ace2 plays a minor role in C. albicans yeast-to-hyphae transition. We have, however, discovered a new function for the Cbk1-Ace2 axis. Specifically, Cbk1 phosphorylation of Ace2 prevents the hyphae-to-yeast transition. To our knowledge, this is one of the first regulators of the C. albicans hyphae-to-yeast transition to be described. Finally, we present an integrated model for the role of Cbk1 in the regulation of hyphal morphogenesis in C. albicans.
2020-08-26 | GSE155450 | GEO
Project description:Sfl1p and Sfl2p are two homologous heat shock factor-type transcriptional regulators that antagonistically control morphogenesis in Candida albicans, while being required for full pathogenesis and virulence. To understand how Sfl1p and Sfl2p exert their function, we combined genome-wide location and expression analyses to reveal their transcriptional targets in vivo together with the associated changes of the C. albicans transcriptome. We show that Sfl1p and Sfl2p bind to the promoter of at least 113 common targets through divergent binding motifs and modulate directly the expression of key transcriptional regulators of C. albicans morphogenesis and/or virulence. Surprisingly, we found that Sfl2p additionally binds to the promoter of 75 specific targets, including a high proportion of hyphal-specific genes (HSGs; HWP1, HYR1, ECE1, others), revealing a direct link between Sfl2p and hyphal development. Data mining pointed to a regulatory network in which Sfl1p and Sfl2p act as both transcriptional activators and repressors. Sfl1p directly represses the expression of positive regulators of hyphal growth (BRG1, UME6, TEC1, SFL2), while upregulating both yeast form-associated genes (RME1, RHD1,YWP1) and repressors of morphogenesis (SSN6, NRG1). On the other hand, Sfl2p directly upregulates HSGs and activators of hyphal growth (UME6, TEC1), while downregulating yeast form-associated genes and repressors of morphogenesis (NRG1, RFG1, SFL1). Using genetic interaction analyses, we provide further evidences that Sfl1p and Sfl2p antagonistically control C. albicans morphogenesis through direct modulation of the expression of important regulators of hyphal growth. Bioinformatic analyses suggest that binding of Sfl1p and Sfl2p to their targets occurs with the co-binding of Efg1p and/or Ndt80p. Indeed, we show that Sfl1p and Sfl2p targets are bound by Efg1p and that both Sfl1p and Sfl2p associate in vivo with Efg1p. Taken together, our data suggest that Sfl1p and Sfl2p act as central “switch on/off” proteins to coordinate the regulation of C. albicans morphogenesis.
2013-06-15 | GSE42886 | GEO
Project description:Ace2 transcription factor family genes are found in many fungal genomes and are required for regulation of expression of genes involved in cell separation. We used transcriptional profiling to identify the targets of Ace2 in Candida albicans, and we show that these include several cell wall components, such as glucanases and glycosylphosphatidylinositol-anchored proteins. Expression is downregulated in ace2 deletion mutants in both yeast and hyphal cells. In addition, deleting ace2 results in dramatic changes in expression of metabolic pathways. Expression of glycolytic enzymes is reduced, while expression of respiratory genes (including those involved in the tricarboxylic acid cycle, oxidative phosphorylation, and ATP synthesis) is increased. Similar changes occur in both yeast and hyphal cells. In contrast, genes required for acetyl-coenzyme A and lipid metabolism are upregulated in an ace2 deletion mutant grown predominantly as yeast cells but are downregulated in hyphae. These results suggest that in wild-type strains, Ace2 acts to increase glycolysis and reduce respiration. This is supported by the observation that deleting ace2 results in increased resistance to antimycin A, a drug that inhibits respiration. We also show that Ace2 is required for filamentation in response to low oxygen concentrations (hypoxia). We suggest that filamentation is induced in wild-type cells by reducing respiration (using low oxygen or respiratory drugs) and that mutants with increased respiratory activity fail to undergo filamentation under these conditions. This SuperSeries is composed of the SubSeries listed below.
2007-02-23 | GSE7105 | GEO
Project description:RNA-Seq of Candida albicans WT vs zcf13 mutant
| PRJNA1074308 | ENA
Project description:Candida albicans TRKO rbf1Δ/hfl1Δ/dpb4Δ vs WT transcriptome data
| PRJNA234493 | ENA
Project description:Candida wildtype cells control vs. Candida QDR1/QDR2/QDR3 knockout cells test
| PRJNA177378 | ENA