Mitochondria are highly dynamic organelles that play fundamental roles in pivotal cellular processes, and their dysfunction results in the development of many types of diseases. Fusion and fission of mitochondria (termed mitochondrial dynamics) play a critical role in regulating many mitochondrial activities, including metabolism, apoptosis and mitochondria-to-nucleus communications. Thus, the “freedom” of mitochondria to change their morphology - mitochondria plasticity – is fundamental for regulating the fate of our cells. Many of the studies in our laboratory are focused on a novel mitochondrial protein named mitochondrial carrier homolog 2 (MTCH2) and its ligand BID that play important roles in regulating apoptosis, metabolism, and mitochondrial dynamics (Kamer et al, Cell 2005; Zaltsman et al, Nat Cell Biol 2010; Maryanovich et al, Nat Cell Biol 2012, Buzaglo et al, Cell Rep 2016; Bahat et al, Nat Comm 2018). MTCH2 knockout in mice results in embryonic lethality at embryonic day 7.5, and conditional knockout of MTCH2 in several different mouse tissues results in significant alterations to mitochondria function and morphology leading to changes in cell fate and disease outcome. Thus, the mission of our laboratory is to determine the exact function of MTCH2 and its partners in regulating mitochondrial plasticity, and to use our findings to combat the many diseases resulting from mitochondrial dysfunction

Energy supply is important for any undertaking, but in stem cells, energy-producing structures sometimes determine the very fate of the cell. A study from our lab, reported in Nature Communications, reveals how cellular power plants called the mitochondria can wake up blood-forming stem cells from their sleep, causing them to proliferate and mature into different cell types (Maryanovich et al Nat Comm 2015). 

Many people would love to eat to their heart’s content and stay slim. That’s just what happened to genetically engineered mice in a study from our lab published in Cell Reports: The mice stayed impressively lean despite eating more than usual and consuming a great deal of high-fat food. Not only that, the mice were more athletic than the controls and their heart function was found to be increased (Buzaglo-Azriel et al. Cell Reports 2016).

What is the role of mitochondria in the brain? To answer this question from the angle of our lab we knocked out MTCH2 in the mice’s forebrains. Like the MTCH2 muscle-knock-out mice, these mice had high metabolism rates and were more active than normal. But all was not right with these mice: They began failing navigation tests in mazes; their learning and memory were affected. The resulting collaboration between our lab and the lab of Prof. Menahem Segal from the Neurobiology Department, may lead to new directions in the study of neurodegenerative diseases, particularly Alzheimer’s (Ruggiero et al. Scientific Reports 2017).

Shiri Tal (Davidson Institute of Science Education), Shahar Biniamini & Shani Garfinkel (former dancers at the Batsheva Dance Company; see details below), and Prof Atan Gross, have initiated a course at the Feinberg Graduate School (Academic year 2013/14; 1st semester) entitled “Between Movement & Science”. This course has emerged from a successful pilot session that took place at the Weizmann in July 2013 and included 25 students and group leaders from different disciplines.