Bacterial infection elicits the Aedes aegypti unfolded protein response.

The unfolded protein response (UPR) is an ancient, highly conserved homeostatic cellular stress response pathway with diverse functions that include, but are not limited to, alleviating stress resulting from the presence of unfolded proteins in the endoplasmic reticulum of cells. Maintaining homeostasis and managing stress are critical to infection tolerance (i.e. host ability to mitigate infection-induced disease independently of strategies involving pathogen elimination). Stress responses such as the UPR are general mediators of tolerance, and the UPR may be activated during infections to promote host health. Understanding tolerance is an emerging priority in animal immunity, and there is unique motivation to understand how disease vectors tolerate infections because tolerance has implications for the efficiency of human pathogen transmission. However, stress responses are scarcely studied in arthropods, and the UPR has not been investigated in the context of a systemic mosquito infection. Herein, we characterize the trajectories of mortality and UPR transcript abundance in Aedes aegypti in response to infection with the opportunistic bacterial pathogen Serratia marcescens. We reveal that, with the exception of atf6, which displayed comparatively delayed activation, transcript levels of all UPR genes we measured harmoniously activate, peak, then diminish prior to the advent of appreciable infection-induced mortality.