News Release

Exploiting parasitic yeast to kill yeast pathogens

Peer-Reviewed Publication

PLOS

Exploiting Parasitic Yeast to Kill Yeast Pathogens

image: 

The mycoparasitic yeast Saccharomycopsis schoenii attacks and kills other yeast species, using penetration pegs (yellow arrows). The model prey species used in this study was A) Saccharomyces cerevisiae (H4-GFP), but the host range also include B) Candida albicans, C) C. auris, D) C. glabrata, E) C. lusitaniae, F) C. tropicalis and G) Schizosaccharomyces pombe (1). Dead prey cells are stained red with propidium iodide. Scale bar 5 μm.

1. Junker, K. et al. The mycoparasitic yeast Saccharomycopsis schoenii predates and kills multi-drug resistant Candida auris. Sci. Rep. 8, 14959 (2018). view more 

Credit: Images taken by Klara Junker, using the PerkinElmer UltraVIEW VoX Spinning Disk Confocal Microscope at the Institute of Medical Sciences, University of Aberdeen

Insights into the genes and proteins involved in the predatory behavior of a parasitic yeast species could lead to new strategies for controlling yeast pathogens, according to a study published May 9 in the open-access journal PLOS Pathogens by Jürgen Wendland of the Carlsberg Research Laboratory in Denmark and Vrije Universiteit Brussel in Belgium, and colleagues.

Pathogenic yeasts and fungi are an increasing global healthcare burden, but the discovery of novel antifungal agents is slow. The parasitic yeast Saccharomycopsis schoenii was recently demonstrated to be able to kill the emerging multi-drug resistant yeast pathogen Candida auris. However, the molecular mechanisms involved in the predatory activity of S. schoenii have not been explored. To this end, the researchers sequenced, assembled and annotated a draft genome of S. schoenii. They integrated quantitative live-cell microscopy assays with genomic, transcriptomic and proteomic approaches to identify genes and proteins that are overexpressed by S. schoenii during its predation of the model prey cell Saccharomyces cerevisiae.

The researchers hypothesized that the need for organic sulfur compounds, especially methionine, play a central role in the predatory behavior of S. schoenii. Surprisingly, they found that a general nutrition limitation, not a specific methionine deficiency, triggered predatory activity. During predation, both proteomic and transcriptomic analyses revealed that S. schoenii highly upregulated and translated genes that encode enzymes called aspartic proteases, probably used to break down prey cell walls. According to the authors, these fundamental insights into the predatory behavior of S. schoenii open up new avenues to exploit this yeast as a biocontrol agent or source for novel antifungal agents.

The authors add, "With the combined efforts of big-data global analysis tools we were able to place Saccharomycopsis schoenii into a CTG clade and dissect predacious behavior of this yeast to identify genes and pathways that likely play a decisive role in the predation process. Additionally, with 'caught-in-the-act' in vivo time lapse microscopy we were able to monitor predacious behavior and prey cell death over time."

###

Research Article

Funding: This research was supported by the European Union Marie Curie Initial Training Network Fungibrain (Project ID: 607963). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing Interests: The authors have declared that no competing interests exist.

Citation: Junker K, Chailyan A, Hesselbart A, Forster J, Wendland J (2019) Multi-omics characterization of the necrotrophic mycoparasite Saccharomycopsis schoenii. PLoS Pathog 15(5): e1007692. https://doi.org/10.1371/journal.ppat.1007692

Author Affiliations:

Yeast & Fermentation, Carlsberg Research Laboratory, Copenhagen, Denmark
Functional Yeast Genomics, Vrije Universiteit Brussel, Brussels, Belgium

In your coverage please use this URL to provide access to the freely available paper: http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1007692


Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.