The role of mitochondria and sensory neurons in the longevity of C. elegans

Seung-Jae Lee
Seung-Jae Lee
11:10~12:00, November 22nd, 2013


Many genetic factors that regulate organismal aging have been identified by using C. elegans as a model system. For example, reduced mitochondrial respiration or inhibition of sensory neurons confers longevity in C. elegans. Remarkably, these factors have been shown to influence lifespan in other species such as D.melanogaster and/or mammals as well. Here, I will present our latest work on genetic pathways that mediate the effectsof mitochondrial respiration and sensory neurons on the lifespan of C. elegans. First, I will discuss how inhibition of mitochondrial respiration promotes longevity and immunity via a feedback circuit involving ROS (reactive oxygen species), AMPK (AMP-activated protein kinase)and HIF-1 (hypoxia-inducible factor 1). Second, I will focus on neuroendocrine pathways that transmit lifespan-regulatory signals from sensory neurons to other tissues. Because many findings on aging regulation in C. eleganshave been shown to be evolutionarily conserved, it is possible that homologous mechanisms exist in mammals including humans.


Research Interests:

My laboratory aims to elucidate molecular mechanisms that regulate aging using C. elegans genetics. Specific research topics include sensory influence on aging, role of mitochondrial respiration in longevity, and the effects of glucose-enriched diet on metabolism and aging


Awards and Honors:

  • 2013 Member of Faculty of 1000
  • 2011 Blue Ribbon Lecture Award, The Korean Society for Molecular and Cellular Biology
  • 2010-2012TJ Park Professor Fellowship, POSCO TJ Park foundation
  • 2008-2009Postdoctoral fellowship, American Heart Association