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Does mitochondria metabolism regulate apoptosis?

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Mitochondria are highly dynamic organelles that play fundamental roles in pivotal cellular processes including energy production, metabolism, and apoptosis. We are interested in understanding how these different mitochondrial processes are coordinated to respond to cellular stress. We are focused on mitochondrial carrier homolog 2 (MTCH2), a non-classical mitochondrial carrier protein, localized to the outer mitochondrial membrane and essential for embryonic development. MTCH2 mediates the response of mitochondria to stress signals initiating at the plasma membrane or at the nucleus. In the TNF α/Fas-death receptor pathway, MTCH2 acts as a receptor-like protein for the pro-apoptotic BID protein, important for cytochrome c release and for Fas-induced liver apoptosis in vivo. On the other hand, in the DNA damage pathway, MTCH2 acts as the down-stream effector of the ATM kinase/BID pathway in haematopoietic stem cells (HSCs), controlling HSC quiescence and survival via regulation of mitochondria metabolism. Moreover, MTCH2 plays an important role in muscle metabolism since loss of muscle MTCH2 increases whole-body energy utilization and protects from 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 an important regulator of mitochondria dynamics and metabolism acting at the interface between homeostasis and apoptosis. Determining MTCH2 ’s exact mechanism of action may lead to deciphering: 1) a new signaling pathway regulating mitochondria metabolism and 2) the mechanism by which mitochondrial metabolism regulates apoptosis.

This talk is part of the MRC Mitochondrial Biology Unit Seminars series.

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