Investigating a Link between Intestinal Cell-to-Cell Communication and Aging in C. elegans

Science Center, Bent Corridor

Live organisms must balance energy usage with their available energy stores. In stressful situations, such as low food availability, organisms will prioritize survival of self, over their ability to reproduce. In Caenorhabditis elegans (C. elegans) reduction in caloric intake correlates with decreases in progeny number, and increases in lifespan. A key transcription factor, DAF-16, orchestrates the cellular response to limited caloric intake. C. elegans with lower caloric intake typically have higher DAF-16 activation levels, resulting in lower brood sizes and longer lifespans. Recent studies suggest that effective digestion, caloric absorption, and defecation may be linked (Sheng, 2015). Worms with intestinal problems resulting in constipation also have lower fat stores. This reduction in fat, an important energy source, suggests possible deficiencies in nutrient uptake. Our lab has extensively studied the INX-16 gap junction protein found in the C. elegans intestine. Mutants lacking INX-16 are constipated. We hypothesize that the INX-16 mutation disrupts the nutrient uptake, lifespan and brood size of the organism through the activation of DAF-16. INX-16 mutant worms have a significant reduction in number of progeny compared to normal, wild type animals. Preliminary results of INX-16 lifespan analysis show significantly increased longevity. To test whether the DAF-16 transcription factor is activated in the INX-16 mutant, fluorescently tagged DAF-16 molecules were introduced into the mutant. Imaging of the fluorescent DAF-16 will be performed in the near future. Future experiments will allow us to understand how intestinal disruption affects caloric intake and DAF-16 activity.