Roles for Stress Response and Cell Wall Biosynthesis Pathways in Caspofungin Tolerance in Cryptococcus neoformans.

Limited antifungal diversity and availability are growing problems for the treatment of fungal infections in the face of increasing drug resistance. The echinocandins, one of the newest classes of antifungal drugs, inhibit production of a crucial cell wall component. However, these compounds do not...

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Published in:Genetics Vol. 213; no. 1; pp. 213 - 228
Main Authors: Pianalto, Kaila M., Blake Billmyre, R., Telzrow, Calla L., Andrew Alspaugh, J.
Format: Journal Article
Published: Oxford University Press / USA Sep2019
Online Access:View this record in EBSCOhost
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      dt: Sep2019
      vid: 213
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      pub: Oxford University Press / USA
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        138471914
        10.1534/genetics.119.302290
        138471914
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        atl: Roles for Stress Response and Cell Wall Biosynthesis Pathways in Caspofungin Tolerance in Cryptococcus neoformans.
      aug:
        au:
          Pianalto, Kaila M.
          Blake Billmyre, R.
          Telzrow, Calla L.
          Andrew Alspaugh, J.
        affil: Department of Medicine and Duke University School of Medicine, Durham, North Carolina 27710
      sug:
        subj:
          Genetic Screening
          Cryptococcus Analysis
          Caspofungin Analysis
          Stress, Physiological Metabolism
          Cellular Structures Metabolism
          Drug Tolerance Evaluation
          Animal Studies
          Mutation
          Signal Transduction
          Polysaccharides Analysis
          Hydrolases Analysis
          Phenotype Evaluation
      ab: Limited antifungal diversity and availability are growing problems for the treatment of fungal infections in the face of increasing drug resistance. The echinocandins, one of the newest classes of antifungal drugs, inhibit production of a crucial cell wall component. However, these compounds do not effectively inhibit the growth of the opportunistic fungal pathogen Cryptococcus neoformans, despite potent inhibition of the target enzyme in vitro. Therefore, we performed a forward genetic screen to identify cellular processes that mediate the relative tolerance of this organism to the echinocandin drug caspofungin. Through these studies, we identified 14 genetic mutants that enhance caspofungin antifungal activity. Rather than directly affecting caspofungin antifungal activity, these mutations seem to prevent the activation of various stress-induced compensatory cellular processes. For example, the pfa4D mutant has defects in the palmitoylation and localization of many of its target proteins, including the Ras1 GTPase and the Chs3 chitin synthase, which are both required for caspofungin tolerance. Similarly, we have confirmed the link between caspofungin treatment and calcineurin signaling in this organism, but we suggest a deeper mechanism in which caspofungin tolerance is mediated by multiple pathways downstream of calcineurin function. In summary, we describe here several pathways in C. neoformans that contribute to the complex caspofungin tolerance phenotype in this organism.
      pubtype: Academic Journal
      doctype: Journal Article
      ougenre: Article
    language: English
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