George Sutphin
Mentor: Matt KaeberleinBox: 357470
Phone: 425-478-3779
Email: lothos@u.washington.edu
http://www.kaeberleinlab.org/
A number of genetic and environmental interventions have been identified that extend life span in one or more model organisms. Interventions that extend life span in multiple highly-divergent organisms are of particular interest because they are likely to play a conserved role in humans. A collaborative effort between the Kaeberlein and Kennedy labs has identified a set of 25 genes that extend life span in both the nematode Caenorhabditis elegans and the budding yeast Saccharomyces cerevisiae. In terms of evolutionary distance, worms and yeast are separated by ~1.5 billion years while worms and humans are separated ~1 billion years, making these evolutionarily conserved genes of particular interest as potential modulators of human aging. Understanding the molecular mechanisms behind the action of these genes will thus provide insight into human aging and age-associated disease. George Sutphins's research is focused on uncovering the molecular mechanisms behind these genes. The first step will be to place each conserved aging gene into genetic pathways. Dietary restriction, insulin/IFG-1-like signaling, sir-2.1, mRNA translation, and mitochondrial function have all been identified as pathways that affect aging, though others will likely be discovered. Once the genes have been placed into pathways, specific genes of interested will be selected for follow-up studies to determine the specific molecular mechanisms behind their action on life span.
Publications
Steinkraus KA, Smith ED, Davis C, Carr D, Pendergrass WR, Sutphin GL, Kennedy BK, Kaeberlein M. Dietary restriction suppresses proteotoxicity and enhances longevity by an hsf-1-dependent mechanism in Caenorhabditis elegans. Aging Cell. 2008 Jun;7(3):394-404.
Sutphin GL, Kaeberlein M. Dietary restriction by bacterial deprivation increases life span in wild-derived nematodes. Exp Gerontol. 2008 Mar;43(3):130-5.