Gross 2023 MiP2023

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Gross 2023 MiP2023

Gross Atan
M(a)TCH2-ing up metabolism and apoptosis at the MOMbrane.

Link: MiP2023 Obergurgl AT

Gross Atan (2023)

Event: MiP2023 Obergurgl AT

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. Many of our studies are focused on a novel mitochondrial protein named mitochondrial carrier homolog 2 (MTCH2) that mediates the response of mitochondria to stress signals initiating at the plasma membrane or at the nucleus. In the TNF/Fas-death receptor pathway, MTCH2 acts as a receptor-like protein for BH3-only BID, 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. More recently, we revealed that MTCH2 also plays a role in regulating mitochondrial metabolism in skeletal muscle, protecting from diet-induced obesity, and a role in regulating mitochondrial fusion/elongation, which is important in driving the exit from naΓ―ve pluripotency in embryonic stem cells (ESCs). Thus, MTCH2 is an important regulator of mitochondria morphology and metabolism acting at the interface between homeostasis and apoptosis. Determining MTCH2’s exact mechanism of action may lead to deciphering the mechanism by which BID, and perhaps other BCL-2 family members, regulate apoptosis.


Affiliation

Gross Atan
Department of Immunology and Regenerative Biology, Weizmann Institute of Science, Rehovot 76100, Israel
Corresponding author: atan.gross@weizmann.ac.il

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Event: Oral 


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