[2014 Spring Life Sciences & IBB Regular Seminar]
 
   
▶Subject: Transcriptional regulators of aging in worms and humans
       
 
▶Speaker: Prof. Stuart Kim (Dept. of Developmental Biology and Genetics, Stanford University)
        
 
▶Date: 5:00PM/May/13(Tue)/2014
       
  
▶Place: Auditorium(1F), Postech Biotech Center
       
 
      *Abctract
       We are studying the process of aging in C. elegans (which age in two weeks) and humans, particularly the kidney.  Is there an underlying intrinsic clock for aging that determines our lifespan?  What are the regulatory factors that control our rate of aging and specify our lifespan?  
  In C. elegans, we have discovered that aging is partly caused by a suite of developmental transcription factors.  In middle age, expression of these key developmental regulators begins to decline.  This leads to a cascade of changes in expression of genes in the skin and intestine, which leads to dysfunction and physiological breakdown of these two organs.  Resetting the expression level of the aging transcription factors in old worms to the young state (by overexpression) rejuvenates the aging transcriptome and increases lifespan.  Conversely, resetting the expression of the aging transcription factors in young worms to the old state (by RNAi inhibition) results in a transcriptome with premature aging and decreases lifespan.  These results indicate that key developmental regulators play a role in driving the aging process in C. elegans. 
  In humans, we have found that the STAT3 and NFKB transcription factors are key drivers of kidney aging.  Both of these transcription factors are known to mediate the inflammation response.  We have found that there is a gradual activation of both transcription factors during aging of the kidney, leading to a chronic inflammatory response.  We can mimic the aging process in tissue culture experiments by using growth factors that activate STAT3 or NFKB.  Interestingly, inhibition of STAT3 activity with a drug leads to changes in gene expression in tissue culture cells that resemble expression changes seen in young kidneys; that is, inhibition of STAT3 activity appears to rejuvenate the kidney aging transcriptome

 
 ▶Inquiry: Prof.Lee, Seung-Jae (279-2351)
      
 
 * This seminar will be given in English