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The stress response gene  DDR48  has been characterized in  Saccharomyces cerevisiae  and  Candida albicans  to be involved in combating various cellular stressors, from oxidative agents to antifungal compounds. Surprisingly, the biological function of  DDR48  has yet to be identified, though it is likely an important part of the stress response. To gain insight into its function, we characterized  DDR48  in the dimorphic fungal pathogen  Histoplasma capsulatum . Transcriptional analyses showed preferential expression of  DDR48  in the mycelial phase. Induction of  DDR48  in  Histoplasma  yeasts developed after treatment with various cellular stress compounds. We generated a  ddr48∆  deletion mutant to further characterize  DDR48  function. Loss of  DDR48  alters the transcriptional profile of the oxidative stress response and membrane synthesis pathways. Treatment with ROS or antifungal compounds reduced survival of  ddr48∆  yeasts compared to controls, consistent with an aberrant cellular stress response. In addition, we infected RAW 264.7 macrophages with  DDR48 -expressing and  ddr48∆  yeasts and observed a 50% decrease in recovery of  ddr48∆  yeasts compared to wild-type yeasts. Loss of  DDR48  function results in numerous negative effects in  Histoplasma  yeasts, highlighting its role as a key player in the global sensing and response to cellular stress by fungi.

journal of fungi

Deletion of the Stress Response Gene DDR48 from Histoplasma capsulatum Increases Sensitivity to Oxidative Stress, Increases Susceptibility to Antifungals, and Decreases Fitness in Macrophages