“In the depths of history, a free-living bacterium was engulfed by a larger cell and was neither digested nor destroyed. Instead, it was domesticated. It forged a unique and fateful partnership with its host, eventually becoming the mitochondria of today.” – Ed Yong, Not Exactly Rocket Science, Discover Magazine

Mitochondria are the parts of our cells that we often call the “powerhouse.” Without them, animal cells wouldn’t have the energy they need to sustain life. A mitochondrion is surrounded by two membrane layers, kind of like a little pillow encased in two pillowcases. The inner pillowcase is where most of the action takes place. It’s ruffled, which provides more surface area for the series of chemical reactions that generate ATP, the cell’s currency. Like money, you have to have ATP in order to do things. Cells can cash in ATP to divide, make new proteins, process cellular waste, store fat or do anything else they need to survive (see DNA 101 and Proteins 101).

Because of their role in maintaining a cell’s fuel and energy balance, mitochondria are the subject of intense scrutiny by scientists interested in the molecular underpinnings of metabolism, obesity, diabetes and cancer. But mitochondria also play a role in cell death. Some cells are long-lived (like neurons in the brain), while others turn over quickly (think skin cells). Either way, the process of cellular suicide – called apoptosis – has to be carefully managed in order to both avoid untimely demise and prevent cells from living too long. When called upon, mitochondrial proteins leak out through the outer membrane and into the cell’s cytosol, where they remove the molecular brakes that normally promote survival and activate caspases, enzymes that execute apoptosis. When mitochondrial function or apoptosis go awry, disease can develop – too much cell death causes neurodegenerative diseases like Alzheimer’s, while too little allows cancer cells to avoid destruction.