Seung-Jae Lee, Ph.D.

Assistant Professor
Division of Molecular and Life Sciences
Molecular Genetics

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Publications Abstract
E-mail seungjaelee1@gmail.com
Phone +82-54-279-2351(office)
          +82-54-279-8066(lab.)
Laboratory Molecular Genetics of Aging Laboratory

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Profile |  Research Interests  |  Selected Publications

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2003
2003-2004
2004-2008

Ph.D. The Johns Hopkins University, School of Medicine
Postdoctoral Fellow, The Johns Hopkins University, School of Medicine
Postdoctoral Fellow, University of California, San Francisco

 

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dia_red.gif Research Interests

Aging is a fundamental mystery in biology. Although a number of genetic and environmental factors that affect aging have been discovered, the mechanisms by which these factors influence aging are poorly understood. This is mainly due to the difficulty in studying complex aging processes at the organismal level. The roundworm C. elegans is an excellent model animal to overcome these complications because of its genetic tractability, ease of culture in controlled environments and very short lifespan. In our laboratory we plan to elucidate the molecular mechanisms by which these genetic and environmental factors regulate lifespan using C. elegans as a main model organism.
 

young (2 days old) worm

old (17 days old) worm


1. How can we dissect complex interactions between genetic and environmental factors that     affect aging?
We are working on how two important environmental factors, temperature and food, influence the lifespan of C. elegans. Our initial findings suggest that the effects on lifespan of both ambient temperature and a diet rich in glucose are under the control of endocrine signaling. Our discoveries represent novel departures from previously existing beliefs about how these two factors influence longevity. We plan to further investigate the interactions between each of these environmental factors and the endocrine signaling pathways that regulate lifespan.

2. What are the genes that regulate lifespan in response to environmental changes?
Despite the generally accepted notion that environmental factors can influence lifespan, only a handful of genes that mediate such effects are known. Therefore, the identification of additional genes will be crucial to gain mechanistic insights into how environmental changes affect aging. To this end, we are conducting large scale gene discovery efforts by employing DNA microarray analysis, RNAi screening and chemical mutagenesis screening. We plan to confirm the functional significance of the candidates from these experiments and to further characterize these genes.

3. Are our findings in C. elegans conserved in other organisms?
The ultimate goal of aging research using C. elegans is to provide more information to help understand general aging processes including those of human aging. Therefore, we plan to test whether our findings in C. elegans are conserved in other organisms such as Drosophila and mice. In particular, our laboratory has expertise in the molecular genetics of Drosophila as well as C. elegans. Our ability to utilize these two wonderful model animals in parallel will greatly aid our knowledge on how aging processes are conserved across phyla.

Since many findings on the regulation of aging in C. elegans have already been shown to be amazingly well conserved during evolution, we believe our research may eventually help us understand the secrets of human aging and improve the quality of old age.

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dia_red.gif Selected Publications 

  1. Murphy C.T.*, Lee S.J.*, and Kenyon C. (2007) Tissue entrainment by feedback regulation of insulin gene expression in the endoderm of Caenorhabditis elegans. Proc. Natl. Acad. Sci. USA 104: 19046-19050 (* equal contribution)
  2. Lee S.J., and Montell C. (2004). Suppression of constant-light-induced blindness but not retinal degeneration by inhibition of the rhodopsin degradation pathway. Curr. Biol. 14: 2076-2085
  3. Lee S.J., Xu H., and Montell C. (2004). Rhodopsin kinase activity modulates the amplitude of the visual response in Drosophila. Proc. Natl. Acad. Sci. USA 101: 11874-11879.
  4. Lee S.J., and Montell C. (2004). Light-dependent translocation of visual arrestin regulated by the NINAC myosin III. Neuron 43: 95-103.
  5. Lee S.J., Xu H., Kang L., Amzel L.M., and Montell C. (2003). Light adaptation through phosphoinositide-regulated translocation of Drosophila visual arrestin. Neuron 39: 121-132.

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Division of Molecular & Life Sciences| POSTECH