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1. Summary Candida albicans is an opportunistic human fungal pathogen that causes a variety of infections, ranging from superficial mucosal to deep-seated systemic infections, especially in immunocompromised patients. Although the ability of C.albicans to cause disease largely depends on the immune status of the host, the fungus also exhibits specific characteristics that facilitate colonization, dissemination, and adaptation to different host niches and thereby turn C.albicans from a harmless commensal to an aggressive pathogen. In response to various environmental stimuli C.albicans switches from growth as a budding yeast to invasive filamentous growth, and this morphogenetic switch plays an important role in C.albicans pathogenesis. Nitrogen limitation is one of the signals that induce filamentous growth in C.albicans, and the control of the morphogenetic transition by nitrogen availability was studied in detail in the present work. Ammonium is a preferred nitrogen source for yeasts that is taken up into the cells by specific transporters. It was found in this study that C.albicans possesses two major ammonium transporters, encoded by the CaMEP1 and CaMEP2 genes, expression of which is induced by nitrogen starvation. Whereas mep1 or mep2 single mutants grew as well as the wild-type strain on limiting concentrations of ammonium, deletion of both transporters rendered C.albicans unable to grow at ammonium concentrations below 5 mM. In contrast to mep1 mutants, mep2 mutants failed to filament and grew only in the yeast form under nitrogen starvation conditions, indicating that in addition to its role as an ammonium transporter CaMep2p also has a signaling function in the induction of filamentous growth. CaMep2p was found to be a less efficient ammonium transporter than CaMep1p and to be expressed at much higher levels, a distinguishing feature important for its signaling function. By the construction and analysis of serially truncated versions of CaMep2p, the C-terminal cytoplasmic tail of the protein was shown to be essential for signaling but dispensable for ammonium transport, demonstrating that these two functions of CaMep2p are separable. In C.albicans at least two signal transduction pathways, a MAP kinase cascade and a cAMP-dependent pathway ending in the transcriptional regulators Cph1p and Efg1p, respectively, control filamentous growth, and mutants defective in either one of these pathways are defective for filamentation under nitrogen starvation conditions. A hyperactive CaMEP2 allele rescued the filamentation defect of a cph1 or a efg1 mutant, but not of a cph1 efg1 double mutant or a mutant deleted for RAS1, which acts upstream of and activates both signaling pathways. Conversely, a dominant active RAS1 allele or addition of exogenous cAMP rescued the filamentation defect of mep2 mutants. These results suggest that CaMep2p activates both the MAP kinase and the cAMP pathway in a Ras1p dependent manner to promote filamentous growth under nitrogen starvation conditions. At sufficiently high concentrations, ammonium repressed filamentous growth even when the signaling pathways were artificially activated. Therefore, C.albicans has established a regulatory circuit in which a preferred nitrogen source, ammonium, serves as an inhibitor of morphogenesis that is taken up into the cell by the same transporter that induces filamentous growth in response to nitrogen starvation. Although a detailed understanding of virulence mechanisms of C.albicans may ultimately lead to novel approaches to combat infections caused by this pathogen, the identification and characterization of essential genes as potential targets for the development of antifungal drugs is a strategy favoured by most pharmaceutical companies. Therefore, C.albicans homologs of three genes that are essential in other fungi were selected in collaboration with an industrial partner and functionally characterized in this work. RAP1 encodes the repressor/activator protein 1, a transcription factor and telomere binding protein that is essential for viability in the budding yeast Saccharomyces cerevisiae. However, deletion of the C.albicans RAP1 homolog did not affect viability or growth of the mutants, suggesting that it is not a promising target. CBF1 (centromere binding factor 1) is necessary for proper chromosome segregation and transcriptional activation of methionine biosynthesis genes in S.cerevisiae and is essential for viability in the related yeasts Kluyveromyces lactis and Candida glabrata. Deletion of CBF1 in C.albicans did not result in an increased frequency of chromosome loss, indicating that it has no role in chromosome segregation in this organism. However, the C.albicans cbf1 mutants exhibited severe growth impairment, temperature sensitivity at 42°C, and auxotrophy for sulphur amino acids, suggesting that Cbf1p is a transcription factor that is important for normal growth of C.albicans. YIL19 is an essential gene in S.cerevisiae that is involved in 18S rRNA maturation. YIL19 was found to be an essential gene also in C.albicans. Conditional mutants in which the YIL19 gene could be excised from the genome by inducible, FLP-mediated recombination were non-viable and accumulated rRNA precursors, demonstrating that YIL19 is essential for this important cellular process and for viability of C.albicans and could serve as a target for the development of antifungal drugs.