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SUMMARY:ATP Citrate Lyase: Novel Regulator of Skeletal Muscle Metabolism &
  Myofiber Differentiation
DTSTART:20190830T110000
DTEND:20190830T120000
DTSTAMP:20260916T005331Z
UID:858c8981f620d7739d4761c1be8f8933b65ef340c9f221a1694409f1
CATEGORIES:Conferences - Seminars
DESCRIPTION:Dr. Suman DAS\, Chemical Biology and Therapeutics\, NIBR\, Nov
 artis\, Basel (CH)\nSEMINAR of the LAUSANNE INTEGRATIVE METABOLISM and NUT
 RITION ALLIANCE (LIMNA)\n\nAbstract:\nAn intricate balance between metabol
 ic regulators\, signalling pathways and gene expression is essential for h
 ealthy skeletal muscle. Disruptions of this balance by extrinsic and/or ex
 trinsic factors lead to skeletal muscle pathology which results in loss o
 f muscle function and/or mass. During our investigations\, we found that A
 TP citrate lyase (ACL)\, a cytosolic enzyme that catalyzes mitochondria-de
 rived citrate into oxaloacetate and acetyl-CoA\, plays key role regulating
  mitochondrial function\, lipid metabolism as well as myogenesis in skelet
 al muscle. IGF1 through PI3K-AKT phosphorylates ACL thus inducing its acti
 vity. ACL activation and/or overexpression of ACL lead to increased cardio
 lipin levels\, thus increasing mitochondrial complexes as well as supercom
 plexes. Concomitant increase in oxygen consumption and ATP levels were obs
 erved. Moreover\, ACL silencing impaired myoblast and satellite cell diffe
 rentiation specially a significant decrease fast myosin heavy chain as wel
 l as MYOD. We identified that ACL regulates availability of acetyl groups 
 leading to alterations in acetylation of (K9/14) and H3(K27) at the MYOD l
 ocus\, thus increasing MYOD expression. ACL overexpresion led to improved 
 muscle regeneration following cardiotoxin mediated damage. Altogether\, ou
 r results suggest that ACL plays an important role in skeletal muscle meta
 bolism as well as in myofiber differentiation.\n \n 
LOCATION:AI 1153 https://plan.epfl.ch/?room=AI1153
STATUS:CONFIRMED
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