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A conserved transcriptional regulator governs fungal morphology in widely diverged species [expression data]

ABSTRACT: In this paper, we examine orthologs of a transcriptional regulator in three fungal species, Saccharomyces cerevisiae, Candida albicans, and Histoplasma capsulatum. We show that, despite an estimated 600 million years since those species diverged from a common ancestor, Wor1 in C. albicans, Ryp1 in H. capsulatum, and Mit1 in S. cerevisiae recognize the same DNA motif. Previous work established that Wor1 regulates white-opaque switching in C. albicans and that its ortholog Ryp1 regulates the yeast to mycelial transition in H. capsulatum. Here we show that the ortholog Mit1 in S. cerevisiae also regulates a morphological transition, in this case pseudohyphal growth. Full genome chromatin immunoprecipitation experiments show that Mit1 binds to the control regions of approximately 94 genes including the previously known regulators of pseudohyphal growth. Through a comparison of full genome chromatin immunoprecipitation experiments for Mit1 in S. cerevisiae, Wor1 in C. albicans, and Wor1 ectopically expressed in S. cerevisiae, we conclude that genes controlled by the orthologous regulators overlap only slightly between these two species. We suggest that the ancestral Wor1/Mit1/Ryp1 protein controlled aspects of cell morphology and that evolutionary movement of genes in and out of the Wor1/Mit1/Ryp1 regulon is responsible, in part, for the differences of morphological forms among these species. Consistent with this idea, ectopic expression of C. albicans Wor1 or H. capsulatum Ryp1 can drive the pseudohyphal growth program in S. cerevisiae.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE32550 | GEO | 2011/10/04

SECONDARY ACCESSION(S): PRJNA154461

REPOSITORIES: GEO

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A conserved transcriptional regulator governs fungal morphology in widely diverged species [ChIP-chip, Transcriptional regulation by Mit1 and orthologs]

Project description:In this paper, we examine orthologs of a transcriptional regulator in three fungal species, Saccharomyces cerevisiae, Candida albicans, and Histoplasma capsulatum. We show that, despite an estimated 600 million years since those species diverged from a common ancestor, Wor1 in C. albicans, Ryp1 in H. capsulatum, and Mit1 in S. cerevisiae recognize the same DNA motif. Previous work established that Wor1 regulates white-opaque switching in C. albicans and that its ortholog Ryp1 regulates the yeast to mycelial transition in H. capsulatum. Here we show that the ortholog Mit1 in S. cerevisiae also regulates a morphological transition, in this case pseudohyphal growth. Full genome chromatin immunoprecipitation experiments show that Mit1 binds to the control regions of approximately 94 genes including the previously known regulators of pseudohyphal growth. Through a comparison of full genome chromatin immunoprecipitation experiments for Mit1 in S. cerevisiae, Wor1 in C. albicans, and Wor1 ectopically expressed in S. cerevisiae, we conclude that genes controlled by the orthologous regulators overlap only slightly between these two species. We suggest that the ancestral Wor1/Mit1/Ryp1 protein controlled aspects of cell morphology and that evolutionary movement of genes in and out of the Wor1/Mit1/Ryp1 regulon is responsible, in part, for the differences of morphological forms among these species. Consistent with this idea, ectopic expression of C. albicans Wor1 or H. capsulatum Ryp1 can drive the pseudohyphal growth program in S. cerevisiae. IP strains were compared to untagged or deletion control strains

2011-10-03 | E-GEOD-32557 | biostudies-arrayexpress

A conserved transcriptional regulator governs fungal morphology in widely diverged species [ChIP-chip, Transcriptional regulation by Mit1 and orthologs]

2011-10-04 | GSE32557 | GEO

A conserved transcriptional regulator governs fungal morphology in widely diverged species [expression data]

Project description:In this paper, we examine orthologs of a transcriptional regulator in three fungal species, Saccharomyces cerevisiae, Candida albicans, and Histoplasma capsulatum. We show that, despite an estimated 600 million years since those species diverged from a common ancestor, Wor1 in C. albicans, Ryp1 in H. capsulatum, and Mit1 in S. cerevisiae recognize the same DNA motif. Previous work established that Wor1 regulates white-opaque switching in C. albicans and that its ortholog Ryp1 regulates the yeast to mycelial transition in H. capsulatum. Here we show that the ortholog Mit1 in S. cerevisiae also regulates a morphological transition, in this case pseudohyphal growth. Full genome chromatin immunoprecipitation experiments show that Mit1 binds to the control regions of approximately 94 genes including the previously known regulators of pseudohyphal growth. Through a comparison of full genome chromatin immunoprecipitation experiments for Mit1 in S. cerevisiae, Wor1 in C. albicans, and Wor1 ectopically expressed in S. cerevisiae, we conclude that genes controlled by the orthologous regulators overlap only slightly between these two species. We suggest that the ancestral Wor1/Mit1/Ryp1 protein controlled aspects of cell morphology and that evolutionary movement of genes in and out of the Wor1/Mit1/Ryp1 regulon is responsible, in part, for the differences of morphological forms among these species. Consistent with this idea, ectopic expression of C. albicans Wor1 or H. capsulatum Ryp1 can drive the pseudohyphal growth program in S. cerevisiae. Replicate experiments for each of four strains compared with reference sample - WT, a Mit1 deletion haploid A strain, a Yhr177w deletion haploid A strain, and a double deletion haploid A strain. All were in the sigma 2000 background.

2011-10-03 | E-GEOD-32550 | biostudies-arrayexpress

Regulation of filamentation in the human fungal pathogen Candida tropicalis

Project description:The yeast-filament transition is essential for the virulence of a variety of fungi that are pathogenic to humans. N-acetylglucosamine (GlcNAc), a ubiquitous molecule in both the environment and host, is one of the most potent inducers of filamentation in Candida albicans and thermally dimorphic fungi such as Histoplasma capsulatum and Blastomyces dermatitidis. However, GlcNAc suppresses rather than promotes filamentation in Candida tropicalis, a fungal species that is closely related to C. albicans. Furthermore, we discover that glucose induces filamentous growth in C. tropicalis. Mutation and overexpression assays demonstrate that the conserved cAMP signaling pathway plays a central role in the regulation of filamentation in C. tropicalis. Activation of this pathway promotes filamentation in C. tropicalis, while inactivation of this pathway results in a serious growth defect in filamentation. By screening an overexpression library of 154 transcription factors, we have identified approximately 40 regulators of filamentous growth in C. tropicalis. Although most of the regulators (e.g., Tec1, Gat2, Nrg1, Sfl1, Sfl2, and Ash1) demonstrate a conserved role in the regulation of filamentation, similar to their homologs in C. albicans or S. cerevisiae, some of them are specific to C. tropicalis. For example, Czf1 and Efh1 repress filamentation, while Wor1, Zcf3, and Hcm1 promote filamentation in C. tropicalis. Bcr1, Aaf1, and Csr1 play a specific role in the process of GlcNAc-regulated filamentation. Our findings indicate that multiple interconnected signaling pathways are involved in the regulation of filamentation in C. tropicalis. These mechanisms have conserved and divergent features among different Candida species. Total RNA profiles of cells grown in Lee's glucose or Lee's GlcNAc medium.

2016-07-01 | E-GEOD-73340 | biostudies-arrayexpress

Regulation of filamentation in the human fungal pathogen Candida tropicalis

2016-07-01 | GSE73340 | GEO

A Genome-wide Transcriptional Analysis of Morphology Determination in Candida albicans

Project description:Candida albicans, the most common cause of human fungal infections, undergoes a reversible morphological transition from yeast to pseudohyphal and hyphal filaments, which is required for virulence. For many years, the relationship between global gene expression patterns associated with determination of specific C. albicans morphologies has remained obscure. Using a strain that can be genetically manipulated to sequentially transition from yeast to pseudohyphae to hyphae in the absence of complex environmental cues and upstream signaling pathways, we demonstrate by whole-genome transcriptional profiling that genes associated with pseudohyphae represent a subset of those associated hyphae and are generally expressed at lower levels; interestingly, no genes appeared to be expressed exclusively in pseudohyphae. Our results also strongly suggest that in addition to dosage, extended duration of filament-specific gene expression is sufficient to drive the C. albicans yeast-pseudohyphal-hyphal transition. Finally, we describe the first transcriptional profile of the C. albicans reverse hyphal-pseudohyphal-yeast transition and demonstrate that this transition not only involves down-regulation of known hyphal-specific genes but also differential expression of additional genes which have not previously been associated with the forward transition, including many involved in protein synthesis. These findings provide new insight into genome-wide mechanisms important for determining fungal morphology and suggest that in addition to similarities, there are also fundamental differences in global gene expression as pathogenic filamentous fungi undergo forward and reverse morphological transitions.

2012-12-12 | GSE39677 | GEO

Modulation of the complex regulatory network for methionine biosynthesis in fungi

Project description:In this study, C. albicans regulates its methionine biosynthetic pathways using the transcription factors Met4 and Cbf1. This circuitry appears more complex than that of filamentous fungi, which use orthologs of the Met4 transcription factor, but lack versions of Cbf1, but is considerably less complex than that of S. cerevisiae, which 2 requires two transcription complexes, involving Cbf1 and Met31/32 as DNA binding modules, and Met4 and the Met4 ortholog Met28 as co-activators, to regulate Met biosynthesis. Although C. albicans contains Met31/32 and Met28 orthologs, they do not appear to be linked to regulation of the methionine circuit. Thus, the phylogenetic progression from filamentous fungi to S. cerevisiae is characterized by increasing complexity of the regulators, although the structural elements of the pathways are fundamentally the same.

2020-11-26 | GSE162171 | GEO

Passage through the mammalian gut triggers a phenotypic switch required for Candida albicans commensalism

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

The gray phenotype in the human fungal pathogen Candida tropicalis

Project description:Phenotypic plasticity, the ability to switch between different morphological types, plays critical roles in environmental adaptation, leading to infections, and allowing for sexual reproduction in pathogenic Candida species. Candida tropicalis, which is both an emerging human fungal pathogen and an environmental fungus, can switch between two heritable cell types termed white and opaque. In this study, we report the discovery of a novel phenotype in C. tropicalis, named the gray phenotype. Similar to Candida albicans and Candida dubliniensis, white, gray, and opaque cell types of C. tropicalis also form a tristable switching system, where gray cells are relatively small and elongated. In C. tropicalis, gray cells exhibit intermediate levels of mating competency and virulence in a mouse systemic infection model compared to the white and opaque cell types, express a set of cell type-enriched genes, and exhibit both common and species-specific biological features. The key regulators of white-opaque transitions, Wor1 and Efg1, are not required for the gray phenotype. A comparative study of the gray phenotypes in C. tropicalis, C. albicans, and C. dubliniensis provides clues to explain the species differences in terms of virulence, ecological niches, and prevalence among these three species.

2017-01-30 | GSE81514 | GEO

Expression analysis of Candida albicans following a block in mitotic exit

Project description:Candida albicans demonstrates three main growth morphologies yeast, pseudohyphal and true hyphal forms. Cell separation is distinct in these morphological forms and the process of separation is closely linked to the completion of mitosis and cytokinesis. In Saccharomyces cerevisiae the small GTPase Tem1 is known to initiate the mitotic exit network, a signalling pathway involved in signalling the end of mitosis and initiating cytokinesis and cell separation. We have characterised the role of Tem1 in C. albicans, and demonstrate that it is essential for mitotic exit and cytokinesis, and that this essential function is signalled through the kinase Cdc15. Consistent with its role in activating the mitotic exit network Tem1 localised to spindle pole bodies in a cell cycle dependent manner. Cells depleted of Tem1 displayed highly polarised growth but ultimately fail to complete cytokinesis and re-enter the cell cycle following nuclear division. At the transcriptional level genes downregulated following the depletion of Tem1 where significantly enriched for genes whose expression peaks early in the cell cycle and for those associated with glycolysis. For expression analysis triplicate RNA samples were generated from exponentially growing C. albicans yeast cells and from cells following 8 h inhibition of TEM1 expression. Gene expression was determined using RNA-seq on the Illumina HiSeq 2000 platform.

2014-01-01 | E-GEOD-48650 | biostudies-arrayexpress

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