We use the roundworm, Caenorhabditis elegans, as a model system to investigate the effect of redox active molecules on stress resistance and aging. The most prevalent theory of aging postulates that the driving force of aging is reactive byproducts of cellular metabolism and respiration (free radicals) that damage cellular macromolecules. Paradoxically, however, small amounts of otherwise toxic oxidants extend the C. elegans lifespan. Our lab actively investigates the mechanisms of this phenomenon in the context of bacterial metabolism. Bacteria are not merely food for C. elegans, as they also colonize worms, and depending on the species, growth conditions, and dietary supplements, serve as a natural source of pro- and antioxidant molecules, thereby profoundly affecting host health and aging. For example, free radical nitric oxide generated by B. subtilis diffuses into the worm and activates cellular stress response programs, thus prolonging the animal’s lifespan. Similarly, billions of bacteria colonize the human digestive tract. We aim to use the highly defined worm-bacteria model and synthetic biology approaches to modify the production of beneficial and harmful bacterial molecules to enhance their positive effect on health and lifespan. We also utilize NGS and proteomics as applied to individual animals to identify specific markers and/or traits associated with longer lifespan.
- Mechanism of biofilm-mediated stress resistance and lifespan extension in C. elegans. Sci Rep. 02 Aug 2017. 7(1):7137
- Glycogen controls Caenorhabditis elegans lifespan and resistance to oxidative stress. Nat Commun. 19 Jun 2017. 8:15868
- Bacterial nitric oxide extends the lifespan of C. elegans. Cell. 14 Feb 2013. 152(4):818-30