Aspergillus fumigatus is an environmental mould that propagates itself by the release into the air of high concentrations of conidia (spores), which are unavoidably inhaled. Patients who are immunosuppressed, such as cancer or transplant patients, are at increased risk for infection with these conidia. Despite some advances in therapy, invasive aspergillosis continues to have a poor outcome, emphasizing the need for more information on fungal pathways that are essential to the growth of the organism in vivo. The ability of A. fumigatus to thrive in the host environment requires the secretion of abundant degradative enzymes. This exerts stress on the endoplasmic reticulum (ER) of the fungus, which is countered by the activation of a stress response pathway termed the unfolded protein response (UPR).
Our lab is currently interested in understanding how A. fumigatus harnesses the UPR and associated pathways to meet the demands of a high capacity secretory system, with the long term goal of developing new antifungal therapies that can interrupt ER homeostasis.
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