학회소개 
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이승재 (포항공과대학교 생명과학과) Dr. Seung-Jae V. Lee obtained his Ph. D. from Johns Hopkins University School of Medicine in 2003. After finishing his postdoctoral training at University of California, San Francisco, he joined POSTECH as an assistant professor in 2009. Dr. Lee has become a rising star in his research field, biology of aging. He has published many research papers in internationally leading journals, including Genes and Development, PNAS, and Current Biology as a corresponding author. Dr. Lee's research group has been focusing on how various regulatory genes influence animal aging by using the roundworm C. elegans as a model system. One important contribution is regarding a paradoxical phenomenon known in the field of aging research; mild impairment of mitochondrial respiration increases the lifespan of many organisms, including C. elegans and mice. Dr. Lee's research team demonstrated that inhibiting mitochondrial respiration elevates the level of reactive oxygen species (ROS), which in turn promote longevity via up-regulating the transcription factor, hypoxia-inducible factor 1 (HIF-1). Further, they showed that internal ROS levels are tightly regulated by HIF-1 and the protein kinase AMPK, via feedback mechanisms. Their findings are among pioneering ones answering the enigmatic question regarding how inhibited mitochondria can promote longevity. Most evolutionarily conserved aging-regulatory pathways, including insulin/IGF-1 signaling (IIS) and target of rapamycin (TOR) signaling pathways, actively monitor external signals to exert internal physiological responses. However, it remains incompletely understood how these signaling pathways modulate lifespan upon changes in environments. Dr. Lee's group found that upon detecting food cues chemosensory neurons shorten lifespan by inducing neuroendocrine factors that up-regulate IIS. They also demonstrated that under glucose-rich diet conditions SREBP transcription factor protects animals from accelerated aging via enhancing fat conversion processes. In addition, they showed that heat shock transcription factor 1 promotes IIS-mediated longevity through integrating signals from TOR and that RNA helicases lengthen lifespan through increasing cellular RNA homeostasis. Because all these factors are evolutionarily well conserved, similar mechanisms for longevity regulation may operate in mammals, including humans. Representative papers |