[2014 Spring Life Sciences & IBB Regular Seminar]
 
   
▶Subject: Molecular Mechanisms of Pro-Longevity ROS Signaling in the Nematode C. elegans
       
 
▶Speaker: Prof. Siegfried Hekimi (Department of Biology, McGill University)
        
 
▶Date: 4:00PM/May/9(Fri)/2014
       
  
▶Place: Auditorium(1F), Postech Biotech Center
       
 
      *Abctract
       The oxidative stress theory of aging postulates that aging results from the accumulation of molecular damage caused by mitochondrial reactive oxygen species (ROS) generated during normal metabolism. In the nematode C. elegans several mutations in mitochondrial proteins lead to a substantial increase in longevity. Examples include isp-1 and nuo-6, which encode subunits of mitochondrial respiratory chain complexes, and sod-2, which encodes the main mitochondrial superoxide dismutase. We have investigated the involvement of ROS metabolism in the mechanisms of longevity of these mutants. Our findings indicate that the longevity of these mutants is not the result of lower accumulation of oxidative damage. Rather we find that their mitochondria display an enhanced generation of superoxide, a property that we find to be necessary and sufficient for their increased longevity. We propose a general model that suggests that the level of ROS generation increases with aging because the signalling function of ROS is protective and is stimulated by age-dependent damage and cellular dysfunction. We have investigated the signal transduction mechanisms by which mitochondrial ROS (mtROS) induce longevity. We find the mtROS signal is relayed by the conserved, mitochondria-associated, intrinsic apoptosis signalling pathway, in a manner completely independent of apoptosis per se. In vertebrates, mtROS stimulate apoptosis through the intrinsic pathway to protect from severely damaged cells. Our observations in nematodes demonstrate that sensing of mtROS by the apoptotic pathway can, independently of apoptosis, elicit protective mechanisms that keep the organism alive under stressful conditions. This results in extended longevity when mtROS generation is inappropriately elevated, as in the mitochondrial mutants we have been studying. We believe that our findings help to clarify the relationships between mitochondria, ROS, apoptosis, and aging.
 
 
 ▶Inquiry: Prof.Lee, Seung-Jae (279-2351)
      
 
 * This seminar will be given in English