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SUMMARY:Cell growth control by nutrients: focus on mTOR and class III PI3K
DTSTART:20170306T133000
DTEND:20170306T143000
DTSTAMP:20260510T155031Z
UID:25084ca4e84aa02baa84039323a7f345c9231ec2ef706adaafa0d258
CATEGORIES:Conferences - Seminars
DESCRIPTION:Mario PENDE Institut Necker\, Paris\, France\nSEMINAR SERIES :
   Trends in Physiology and Metabolism (Bio-682)\n\nAbstract:\nIn metazoan
 s\, nutrient and growth factor availability control cell number\, size and
  metabolic homeostasis. We investigate the specific programs underlying th
 ese responses\, and their coordination by signal transduction mechanisms.W
 e focus on two nutrient signal transduction pathways\, the mTOR (mammalian
  Target Of Rapamycin) and the Vps15/Vps34 complex (Vacuolar Protein Sortin
 g15/34). These ancient pathways are present in every eukaryotic cell\, fro
 m unicellular organisms like yeast to humans. They function as essential m
 echanisms that direct how growth and metabolism adapt to nutritional cues.
  mTOR is a Ser/Thr protein kinase\, while the Vps15/Vps34 complex is a lip
 id kinase with phosphatidylinositol 3-kinase activity (class III PI3K). Th
 e transduction mechanisms triggered by mTOR and class III PI3K are complex
 . In mammalian cells\, both kinases are engaged in multiple complexes that
  have different localization\, targets and sensitivities to upstream signa
 ls\, like nutrients and insulin. We have contributed to demonstrate that t
 his crosstalk and differential regulation may explain many physiological r
 esponses to nutrition. For instance\, why nutrients and insulin are synerg
 istic for cell growth\, though nutrients cause resistance to the metabolic
  action of insulin. Or why insulin inhibits autophagy\, though stimulates 
 receptor trafficking. During the past fifteen years we have generated and 
 characterized a wide panel of mouse mutants in the mTOR and class III PI3K
  pathways. We were involved in revealing unique and interesting phenotypes
  that increased our knowledge of mTOR/class III PI3K roles in pathophysiol
 ogy: mutants with small cells (Pende et al.\, Nature\, 2000\; Ohanna et al
 .\, Nature Cell Biol\, 2005)\, mutants resistant to tumorigenesis in speci
 fic tissues and after specific oncogenic insults (Alliouachene et al.\, JC
 I\, 2008\; Panasyuk et al.\, Nature Comm.\, 2012\; Patitucci et al.\, JCI\
 , 2017)\, mutants with muscle disease (Risson et al.\, JCB\, 2009\; Nemaza
 nyy et al.\, EMBO Mol Med\, 2013)\, mutants mimicking caloric restriction 
 and promoting longevity (Aguilar et al.\, Cell Metabolism\, 2007\; Barilar
 i et al.\, EMBO J\, 2017)\, mutants with altered insulin action (Nemazanyy
  et al.\, Nature Comm.\, 2015\; Treins et al.\, Mol Cel Biol\, 2012). I wi
 ll present our progress on the molecular mechanisms of cell size control a
 nd organismal longevity. I will also detail our efforts to understand rare
  human genetic diseases that arise from pathological changes in the activi
 ty of the mTOR/ class III PI3K pathways or that may benefit from therapeut
 ical intervention on these pathways. These diseases include Tuberous Scler
 osis Complex and lysosomal storage diseases.\n\n 
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717
STATUS:CONFIRMED
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