Impact of secreted glucanases upon the cell surface and fitness of during colonisation and infection.

Host recognition of the pathogen-associated molecular pattern (PAMP), β-1,3-glucan, plays a major role in antifungal immunity. β-1,3-glucan is an essential component of the inner cell wall of the opportunistic pathogen . Most β-1,3-glucan is shielded by the outer cell wall layer of mannan fibrils, but some can become exposed at the cell surface. In response to host signals such as lactate, shaves the exposed β-1,3-glucan from its cell surface, thereby reducing the ability of innate immune cells to recognise and kill the fungus. We have used sets of barcoded and mutants to compare the impacts of the secreted β-glucanases Xog1 and Eng1 upon and . Flow cytometry of Fc-dectin-1-stained strains revealed that Eng1 plays the greater role in lactate-induced β-1,3-glucan masking. Transmission electron microscopy and stress assays showed that neither Eng1 nor Xog1 are essential for cell wall maintenance, but the inactivation of either enzyme compromised fungal adhesion to gut and vaginal epithelial cells. Competitive barcode sequencing suggested that neither Eng1 nor Xog1 strongly influence fitness during systemic infection or vaginal colonisation in mice. However, the deletion of enhanced fitness during gut colonisation. We conclude that both Eng1 and Xog1 exert subtle effects on the cell surface that influence fungal adhesion to host cells and that affect fungal colonisation in certain host niches.