@article{PaligeLindeMartinetal.2013,
  author    = {Palige, Katja and Linde, J{\"o}rg and Martin, Ronny and B{\"o}ttcher, Bettina and Citiulo, Francesco and Sullivan, Derek J. and Weber, Johann and Staib, Claudia and Rupp, Steffen and Hube, Bernhard and Morschh{\"a}user, Joachim and Staib, Peter},
  title     = {Global Transcriptome Sequencing Identifies Chlamydospore Specific Markers in Candida albicans and Candida dubliniensis},
  series = {PLoS ONE},
  volume    = {8},
  journal   = {PLoS ONE},
  number    = {4},
  doi       = {10.1371/journal.pone.0061940},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-131007},
  pages     = {e61940},
  year      = {2013},
  abstract  = {Candida albicans and Candida dubliniensis are pathogenic fungi that are highly related but differ in virulence and in some phenotypic traits. During in vitro growth on certain nutrient-poor media, C. albicans and C. dubliniensis are the only yeast species which are able to produce chlamydospores, large thick-walled cells of unknown function. Interestingly, only C. dubliniensis forms pseudohyphae with abundant chlamydospores when grown on Staib medium, while C. albicans grows exclusively as a budding yeast. In order to further our understanding of chlamydospore development and assembly, we compared the global transcriptional profile of both species during growth in liquid Staib medium by RNA sequencing. We also included a C. albicans mutant in our study which lacks the morphogenetic transcriptional repressor Nrg1. This strain, which is characterized by its constitutive pseudohyphal growth, specifically produces masses of chlamydospores in Staib medium, similar to C. dubliniensis. This comparative approach identified a set of putatively chlamydospore-related genes. Two of the homologous C. albicans and C. dubliniensis genes (CSP1 and CSP2) which were most strongly upregulated during chlamydospore development were analysed in more detail. By use of the green fluorescent protein as a reporter, the encoded putative cell wall related proteins were found to exclusively localize to C. albicans and C. dubliniensis chlamydospores. Our findings uncover the first chlamydospore specific markers in Candida species and provide novel insights in the complex morphogenetic development of these important fungal pathogens.},
  language  = {en}
}
@article{MorschhaeuserRamirezZavalaWeyleretal.2013,
  author    = {Morschh{\"a}user, Joachim and Ram{\´i}rez-Zavala, Bernardo and Weyler, Michael and Gildor, Tsvia and Schmauch, Christian and Kornitzer, Daniel and Arkowitz, Robert},
  title     = {Activation of the Cph1-Dependent MAP Kinase Signaling Pathway Induces White-Opaque Switching in Candida albicans},
  series = {PLoS Pathogens},
  journal   = {PLoS Pathogens},
  doi       = {10.1371/journal.ppat.1003696},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-97281},
  year      = {2013},
  abstract  = {Depending on the environmental conditions, the pathogenic yeast Candida albicans can undergo different developmental programs, which are controlled by dedicated transcription factors and upstream signaling pathways. C. albicans strains that are homozygous at the mating type locus can switch from the normal yeast form (white) to an elongated cell type (opaque), which is the mating-competent form of this fungus. Both white and opaque cells use the Ste11-Hst7-Cek1/Cek2 MAP kinase signaling pathway to react to the presence of mating pheromone. However, while opaque cells employ the transcription factor Cph1 to induce the mating response, white cells recruit a different downstream transcription factor, Tec1, to promote the formation of a biofilm that facilitates mating of opaque cells in the population. The switch from the white to the opaque cell form is itself induced by environmental signals that result in the upregulation of the transcription factor Wor1, the master regulator of white-opaque switching. To get insight into the upstream signaling pathways controlling the switch, we expressed all C. albicans protein kinases from a tetracycline-inducible promoter in a switching-competent strain. Screening of this library of strains showed that a hyperactive form of Ste11 lacking its N-terminal domain (Ste11ΔN467) efficiently stimulated white cells to switch to the opaque phase, a behavior that did not occur in response to pheromone. Ste11ΔN467-induced switching specifically required the downstream MAP kinase Cek1 and its target transcription factor Cph1, but not Cek2 and Tec1, and forced expression of Cph1 also promoted white-opaque switching in a Wor1-dependent manner. Therefore, depending on the activation mechanism, components of the pheromone-responsive MAP kinase pathway can be reconnected to stimulate an alternative developmental program, switching of white cells to the mating-competent opaque phase.},
  language  = {en}
}