White-Opaque Switching in Natural MTLa/alpha Isolates of Candida albicans: Evolutionary Implications for Roles in Host Adaptation, Pathogenesis and Sex
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ABSTRACT:
ORGANISM(S): Candida albicans
SUBMITTER: Jing Xie
PROVIDER: E-GEOD-43938 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The capacity of the commensal yeast Candida albicans to grow in several forms, referred to as phenotypic plasticity, is critical for its survival, and abilities to thrive and cause infection in the human host. In this study, we report a novel phenotype of C. albicans, referred as the “gray” phenotype. The gray cell type, together with the previously discovered “white” and “opaque” cell types, forms a tristable phenotypic switching system. The three phenotypes differ in cellular and colony appearance, global transcriptional profiles, secreted aspartyl proteinase (Sap) activities and virulence in different infection models. The addition of the gray cell type to the phenotypic transition systems may enhance fitness and confers an adaptive advantage for C. albicans in the host. We further demonstrate that two key regulators of white-opaque switching, Wor1 and Efg1, are not required for maintenance of the gray phenotype, suggesting that a different regulatory circuitry may be involved in the regulation of gray cell formation. Our study provides an example of multiple stable and heritable switching systems, indicating that the regulation of morphological forms to adapt to environmental changes could be much more elaborate than previously thought. total RNA profiles of 24h old white, gray and opaque cell types
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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.
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Project description:C. albicans white, opaque and white engineered cells were incubated on Spider medium for 8 hours. Crosses were between a and alpha cells of each phenotype, and a white cells alone or a opaque cells alone were also incubated as controls. White cells are no
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Project description:In Candida albicans, the a1-alpha2 complex represses white-opaque switching as well as mating. A ChIP-chip strategy was, therefore, used to screen for genes with a1-alpha2 binding sites and expression patterns consistent with a master switch gene (MSG). Of 51 genes identified with an a1-alpha2 binding site, one gene, TOS9, also referred to as EAP2, exhibited an expression pattern consistent with a MSG. TOS9 is expressed in opaque, not white a/a and alpha/alpha cells and Tos9p localizes to the opaque cell nucleus. Deletion of TOS9 blocks cells in the white phase, and misexpression in the white phase of the parent tos9+/tos9+ strain results in mass conversion to opaque. Expression of TOS9 under control of a MET promoter rescues the TOS9 null mutant tos9-/tos9- phenotype. Temperature-induced mass conversion of opaque to white in the parent strain results in the immediate cessation of TOS9 transcription, and loss of Tos9p prior to the point of commitment to white (the switch event), which occurs at the time of the second cell doubling. Misexpression of TOS9, as well as inhibition of the second round of DNA replication inhibits the temperature-induced switch from opaque to white. Based on these observations, a model is developed for the regulation and role of TOS9 in switching. Keywords: ChIP chip
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