Hog1 regulates stress tolerance and virulence in the emerging fungal pathogen Candida auris

Alison M. Day*, Megan M. McNiff, Alessandra da Silva Dantas, Neil A.R. Gow, Janet Quinn

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

59 Citations (Scopus)
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Candida auris has recently emerged as an important, multidrug-resistant fungal pathogen of humans. Comparative studies indicate that despite high levels of genetic divergence, C. auris is as virulent as the most pathogenic member of the genus, Candida albicans. However, key virulence attributes of C. albicans, such as morphogenetic switching, are not utilized by C. auris, indicating that this emerging pathogen employs alternative strategies to infect and colonize the host. An important trait required for the pathogenicity of many fungal pathogens is the ability to adapt to host-imposed stresses encountered during infection. Here, we investigated the relative resistance of C. auris and other pathogenic Candida species to physiologically relevant stresses and explored the role of the evolutionarily conserved Hog1 stress-activated protein kinase (SAPK) in promoting stress resistance and virulence. In comparison to C. albicans, C. auris is relatively resistant to hydrogen peroxide, cationic stress, and cell-wall-damaging agents. However, in contrast to other Candida species examined, C. auris was unable to grow in an anaerobic environment and was acutely sensitive to organic oxidative-stress-inducing agents. An analysis of C. auris hog1? cells revealed multiple roles for this SAPK in stress resistance, cell morphology, aggregation, and virulence. These data demonstrate that C. auris has a unique stress resistance profile compared to those of other pathogenic Candida species and that the Hog1 SAPK has pleiotropic roles that promote the virulence of this emerging pathogen.

Original languageEnglish
Article numbere00506-18
Issue number5
Publication statusPublished - 24 Oct 2018

Bibliographical note

We thank Elizabeth Johnson and Adrien Szekely from the Mycology Reference Laboratory, Public Health England, for the clinical C. auris isolates used in this study. We also thank Katharina Trunk for comments on the manuscript.

This work was funded by the BBSRC (BB/K016393/1, BB/P020119/1) and the Wellcome Trust (097377/101873).

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.


  • Candida auris
  • Pathogenesis
  • Stress adaptation
  • Stress kinases


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