Acute stress causes genome-wide transcriptional shifts resulting in global changes in proteostasis. Successfully responding to acute stress and adapting to chronic stress are critical to survival and healthy aging. However, because stress responses are energetically demanding and do not prioritize normal, healthy physiological function, organisms are constantly shifting the equilibrium between stress responses and normal growth/development and reproduction. I study humans and C. elegans to determine what shifts in the transcriptome occur during acute stress and recovery and over long-term adaptation to repeated stressors. Our aim is to identify conserved mechanisms that promote resilience to stress and healthy aging with hopes that we can find ways to manipulate and optimize these mechanisms.
Exercise competition and training in stressful environments under different diet and dehydration conditions is one model we use to study how humans respond to stress. In our collaboration with RNAseq for the Next Generation, we are analyzing RNAseq datasets from: (1) 2012 Kona Ironman World Championship Triathlon, (2) studies from our Human Performance Laboratory on the effect of diet in stress responses of elite ultraendurance (50-100 mile runners) athletes, and (3) studies in our lab on the effects of dehydration on cellular transcriptomes. The tractability of the conserved animal model C. elegans allows us to pursue mechanistic research into genes potentially significant for stress resilience and reduced stress- or age-induced protein damage.
Materials are under development.
Materials are under development.
