Abstract

The Sanabria lab is generally interested in studying the intersection between stress and aging. Exposure to stress can be detrimental to cellular health and fitness, and thus cells have adapted cellular stress responses that mitigate damage associated with stress exposure. Interestingly, cellular stress mechanisms decline during aging, such that aged organisms are more sensitive to stress. In fact, hyperactivating stress responses can promote resilience and improve general health and longevity. In the stress and aging, field, specific stress responses are studied in individual contexts: for example, the mitochondrial unfolded protein response (UPR^MT), a critical mechanism for preserving mitochondrial function under conditions of stress is studied solely for its impact on mitochondrial health. This proposal is unique in trying to understand how the UPR^MT and other functional roles of the mitochondria can impact other organelles, such as the actin cytoskeleton. We ask how seemingly compartmentalized stress responses can affect global cellular and organismal health through crosstalk between stress responses: that is, how can mitochondrial stress responses impact other organelles and vice versa. Put another way, we wonder whether our physiological response to heat stress (e.g., sweating, increased heart rate, etc.) will affect our capacity to respond to other stressors (e.g., infection, cold, emotional, etc.).