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SUMMARY:Does mitochondria metabolism regulate apoptosis?  - Professor Atan
  Gross\, Weizmann Institute
DTSTART:20220803T140000Z
DTEND:20220803T150000Z
UID:TALK177146@talks.cam.ac.uk
CONTACT:Hannah Burns
DESCRIPTION:Mitochondria are highly dynamic organelles that play fundament
 al roles in pivotal cellular processes including energy production\, metab
 olism\, and apoptosis. We are interested in understanding how these differ
 ent mitochondrial processes are coordinated to respond to cellular stress.
  We are focused on mitochondrial carrier homolog 2 (MTCH2)\, a non-classic
 al mitochondrial carrier protein\, localized to the outer mitochondrial me
 mbrane and essential for embryonic development. MTCH2 mediates the respons
 e of mitochondria to stress signals initiating at the plasma membrane or a
 t the nucleus. In the TNFα/Fas-death receptor pathway\, MTCH2 acts as a r
 eceptor-like protein for the pro-apoptotic BID protein\, important for cyt
 ochrome c release and for Fas-induced liver apoptosis in vivo. On the othe
 r hand\, in the DNA damage pathway\, MTCH2 acts as the down-stream effecto
 r of the ATM kinase/BID pathway in haematopoietic stem cells (HSCs)\, cont
 rolling HSC quiescence and survival via regulation of mitochondria metabol
 ism. Moreover\, MTCH2 plays an important role in muscle metabolism since l
 oss of muscle MTCH2 increases whole-body energy utilization and protects f
 rom diet-induced obesity. More recently\, we revealed that MTCH2 regulates
  mitochondrial fusion/elongation\, which is important in driving the exit 
 from naïve pluripotency in embryonic stem cells (ESCs). Thus\, MTCH2 is a
 n important regulator of mitochondria dynamics and metabolism acting at th
 e interface between homeostasis and apoptosis. Determining MTCH2’s exact
  mechanism of action may lead to deciphering: 1) a new signaling pathway r
 egulating mitochondria metabolism and 2) the mechanism by which mitochondr
 ial metabolism regulates apoptosis. 
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