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Lifespans across the animal kingdom exhibit huge variability, revealing that biological aging does not occur at a universal rate defined by physics. Rather, how we age is defined largely by our own physiology, which is shaped in turn by evolution (i.e., genes and the environment).


Through model systems ranging from single-cell organisms to primates, we have learned that single genetic, nutritional, and pharmacological interventions can extend lifespan and protect against multiple forms of age-onset pathology. Many of these interventions target mechanisms responsible for maintaining nutrient and energy homeostasis, revealing a common, evolutionarily-conserved theme: conditions of nutrient scarcity reprogram metabolism and physiology in a way that promotes slower and/or healthier aging. We want to understand how this works so that we can harness these mechanisms therapeutically against ‘diseases of old age.’


Using a foundation of molecular genetics and quantitative, live imaging in the transparent model C. elegans, we are striving to understand how triggering a low-energy physiological state translates into longevity, stress resistance and protection from age-related diseases. We are particularly interested in the roles that organelles like the ER and mitochondria play in these processes for two reasons. First, the architecture and behavior of these organelles begins to shift as animals age, and these aberrant organelle dynamics are correlated with the onset of multiple age-onset diseases—especially in neurons and muscle, tissues which are sensitive to age-related pathology. Second, these organelles are both key responders and controllers of cell and organismal metabolism. Fluctuating nutrient levels cause these organelles to remodel their form, thereby allowing them to optimize their function for the changing environment. Through cutting-edge genetic techniques such as CRISPR/Cas9 transgenesis, we will label organelles and  manipulate metabolic functions and the regulators of organelle dynamics to ask (i) how and why the dysregulation of organelle architecture occurs in aging animals, (ii) how long-lived animals are able to better protect organelle form and function, and (iii) can we target organelle dynamics therapeutically to prevent age-onset declines and pathology?