In their natural habitat, fungi are constantly exposed to mycopredators, which exert evolutionary pressure that drives the development of survival strategies. To investigate these defensive attributes fungi use against such biotic threats, often overlapping with virulence traits responsible for human infections, this study employed the obligate fungivorous amoeba Protostelium aurantium as a model mycopredator. In this context, we focused on the important opportunistic human pathogen Aspergillus fumigatus and conducted a comparative genomic analysis on 18 strains from 13 different Aspergillus species. Our results revealed over 1700 genes with differing evolutionary rates between pathogens and non-pathogens. Out of these 1700 genes, I functionally tested 17 transcription factor deletion mutants, discovering four transcription factors whose deletion significantly enhanced fungal survival during P. aurantium predation of swollen spores. Furthermore, the role of the antifungal mycotoxin sphingofungin in amoeba predation of A. fumigatus was examined. Sphingofungins inhibit the biosynthesis of serine palmitoyl transferases and thus impair the growth of certain eukaryotic cells. However, in this study, the strain lacking sphingofungin biosynthesis did not show a significant difference in sensitivity to amoeba predation compared to the wild type. Despite P. aurantium's intriguing ability to feed on certain opportunistic human fungal pathogens, including Aspergillus, Candida, and Cryptococcus species, it cannot sustain feeding on members of the Saccharomyces clade. This observation prompted us to investigate the molecular basis of fungal prey discrimination by P. aurantium. Our findings revealed that the length of the polyprenyl side chain in coenzyme Q (CoQ) determines whether a fungal species is classified as prey or non-prey. Overall, these results suggest that P. aurantium is a valuable model organism for studying fungal virulence traits that helps to fungal evade better.
Nauman Saeed (Wed,) studied this question.