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Certain yeasts secrete peptides known as killer toxins or mycocins with a deleterious effect on sensitive yeasts or filamentous fungi, a common phenomenon in environmental species. In a recent work, different  Debaryomyces hansenii  ( Dh ) strains isolated from a wide variety of cheeses were identified as producing killer toxins active against  Candida albicans  and  Candida tropicalis . We have analyzed the killer activity of these toxins in  C. albicans  mutants defective in MAPK signaling pathways and found that the lack of the MAPK Hog1 (but not Cek1 or Mkc1) renders cells hypersensitive to  Dh  mycocins while mutants lacking other upstream elements of the pathway behave as the wild type strain. Point mutations in the phosphorylation site (T174A-176F) or in the kinase domain (K52R) of  HOG1  gene showed that both activities were relevant for the survival of  C. albicans  to  Dh  killer toxins. Moreover, Hog1 phosphorylation was also required to sense and adapt to osmotic and oxidative stress while the kinase activity was somehow dispensable. Although the addition of supernatant from the killer toxin- producing  D. hansenii  242 strain ( Dh -242) induced a slight intracellular increase in Reactive Oxygen Species (ROS), overexpression of cytosolic catalase did not protect  C. albicans  against this mycocin. This supernatant induced an increase in intracellular glycerol concentration suggesting that this toxin triggers an osmotic stress. We also provide evidence of a correlation between sensitivity to  Dh -242 killer toxin and resistance to Congo red, suggesting cell wall specific alterations in sensitive strains.

Non-canonical Activities of Hog1 Control Sensitivity of Candida albicans to Killer Toxins From Debaryomyces hansenii