Aspergillus fumigatus is a filamentous fungus that is the most common cause of life-threatening invasive mould infections in immunosuppressed individuals. A. fumigatus produces a sialidase enzyme that shows a preference for 2-keto-3-deoxy-D-glycero-D-galacto-nononic acid, (KDN). Sialidases break the glycosidic bond between terminal sialic acids and an underlying glycan chain. The purpose of my research was to create and characterize the KDNase knockout and complemented strains in A. fumigatus. Both strains were successfully generated. Growth in the presence of cell wall stressors (hyperosmolarity, antifungal agents, Congo Red dye) showed that the KDNase gene deletion affected morphology and cell wall integrity. Treatment of A. fumigatus conidia with endogenous AfKDNase enzyme resulted in conidial clumping and damage, an effect not observed when conidia were treated with a bacterial sialidase. The Δkdnase strain remained virulent in an immunosuppressed murine model of invasive aspergillosis.
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Thesis advisor: Moore, Margo
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