Postdoctoral position in nutrient sensing and aging - Kapahi laboratory

The focus of the Kapahi Laboratory is to identify and characterize the genetic pathways that mediate effects on lifespan, age-related diseases and metabolism. This is being achieved by using an interdisciplinary approach combining genetic, biochemical and genomic techniques in invertebrate model systems D. melanogaster, C. elegans, and mammalian cells. In particular the lab is following their discoveries that TOR pathway, fat metabolism, modulation of mRNA translation, mitochondrial function and ER stress, modulate lifespan. The broader significance of this research is to help uncover the role of nutrition in the etiology of age-related human diseases like diabetes, obesity, cancer and neurodegeneration. The lab is interested in developing models of age-related diseases and host microbiome interactions using invertebrate and cell culture model systems. The candidate will receive training in specific area(s) of research with the aim of progressing towards an independent career. For more questions regarding this position please e mail Pkapahi@buckinstitute.org.

Selected publications

  1. Katewa D, Demontis F, Kolipinski M, Hubbard A, Gill M, Perrimon N, Melov S, & Kapahi P (2012) Intra-myocellular triglyceride turnover plays a critical role in mediating responses to dietary restriction in Drosophila melanogaster. Cell Metabolism 2012
  2. Rogers AN, Chen D, Czerwieniec G, McColl G, Felkey K, Melov S, Gibson B, Hubbard A, Lithgow GJ, Kapahi P. Post-transcriptional remodeling of longevity and stress response gene expression by inhibition of eIF-4G. Cell Metabolism. 2011
  3. Kapahi P, Rogers A, Chen D. Katewa SD, Li P, Kockel L. ‘With TOR, less is more: The emerging role of the TOR pathway in aging.’ Cell Metabolism, 2011
  4. Zid BM, Rogers A, Katewa SD, Au Lu T, Benzer S, Kapahi P. 4E-BP modulates lifespan and mitochondrial translation upon dietary restriction in Drosophila. Cell (2009).
  5. Chen, D; Thomas E L; Kapahi P. HIF-1 Modulates Dietary Restriction-mediated Lifespan Extension via IRE-1 in C. elegans. PLOS Genetics; 2009
  6. Chen D, Pan KZ, Palter JE, Kapahi P. Longevity determined by developmental arrest genes in Caenorhabditis elegans. Aging Cell, 2007
  7. Pan KZ, Palter JE, Rogers AN, Olsen A, Chen D, Lithgow GJ, Kapahi P. Inhibition of mRNA translation extends lifespan in C. elegans. Aging Cell 2007
  8. Kapahi P, Zid BM, Harper T, Koslover D, Sapin V, & Benzer S. Regulation of lifespan in Drosophila by modulation of genes in the TOR signaling pathway. Curr Biol. 2004

The Buck Institute for Age Research is a non-profit biomedical research institute in Novato, located 20 miles north of San Francisco & Berkeley. The Buck Institute is the only independent institute in the U.S. devoted solely to research on aging and age-related diseases. Our mission is to increase the healthspan, the healthy years of life. Awarded a federal grant to establish interdisciplinary research in a new field called Geroscience, Buck scientists work in a unique, collaborative environment that allows scientists to initiate studies quickly and respond to new opportunities in fields such as stem cell research and regenerative medicine. The Buck Institute has excellent in-house proteomic, genomic and microscopy facilities. Our scientists represent a variety of complementary fields, including genetics, epigenetics, biochemistry, molecular biology, bioenergetics, age-associated disease; and technological disciplines such as genomics, proteomics, protein interaction networks and bio-informatics. The Buck Institute has an excellent postdoctoral research program. There are currently 200 employees, and plans to grow to 550 over the next decade. We offer competitive salaries, excellent benefits, dynamic work environment, and new state-of-the-art facilities. For more information www.buckinstitute.org