Prof. Atan Gross

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 TNFa/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. Recently we revealed that MTCH2 also plays a role in regulating 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 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.

We are also interested in understanding how mitochondria mal function is involved in the development of neurodegenerative diseases like Parkinson's disease (PD), since I was diagnosed with PD four years ago. Our working hypothesis is that mitochondria exhaustion is a major cause in the death of dopaminergic neurons, the cellular "factories" for producing dopamine in the brain. We are using both mice and cultured cells to determine whether increasing mitochondria function for a long period of time can result in aggregation of alfa-synuclein, which is believed to be a major cause for PD development. If we turn out to be correct then perhaps, strengthening mitochondria at the early stages of PD can slow down the progression of the disease.

We are also interested in exploring the connections between science and dance and in 2013 we initiated a course at the Feinberg Graduate School by the name of TNUDA (TNAaa + maDA) together with the Bat Sheva former dancer and choreographer Shahar Binyamini, which has run for four years. In 2021 we established a continuation course named SENSCIENCE (SENsation + SCIENCE) together with Noam Carmeli and Michael Shachrur, whom are world-experts in movement improvisation and contact improvisation. SENSCIENCE is focused on improvising with body sensations and science, and more details about the course can be found at  Feinberg Graduate School web site at https://erez.weizmann.ac.il/pls/htmldb/f?p=186/30/414344961778//NO//pid_/_pprev/14374_/_0