Fig. 1 Look familiar? An animal cell, showing the mitochondria in its home environment
If your high school biology class was like mine, you learned that mitochondria are little sacks inside eukaryotic cells that are responsible for “making energy for the cell.” And that was pretty much the end of it.
Isn’t that mysterious? How does a teeny-tiny sack in an itty-bitty cell “make” energy? It turns out that the cells convert the energy from sugars we (or any other species, really) consume into a molecule that the cell knows how to use for energy, adenosine triphosphate (commonly referred to as ATP). Mitochondria are able to make this important molecule through an efficient process known as oxidative phosphorylation.This process is more important in cells that need lots of energy (think nerves and muscular cells) and so these cells tend to have more mitochondria. This is also why when a person or animal has some sort disease affecting their mitochondria, or mitochondrial myopathy, the symptoms affect these organ systems. Such conditions can result in in neuromuscular symptoms such as muscular weakness, fatigue, and loss of hearing and other senses.
The mitochondrion, upon first inspection, can seem less important or interesting than other organelles, such as the nucleus. If you don’t remember, the nucleus is heralded as “the brain of the cell.” To be fair, the nucleus is important; it houses the blueprints of the entire organism, the DNA. However, mitochondria actually have DNA of their own, and are able to replicate independently from the rest of the cell. This is believed to be a result of a cell early in the evolutionary tree engulfing another cell which was adept at ATP production, and thus was beneficial to the host cell. This is known as the endosymbiotic theory. For me, it’s fun to think about ancient cells collecting tools that made them better and stronger, and leading life on Earth to where it is today.
Where mitochondria become even more interesting is in the ability of the organelles to signal to the nucleus and change how it is expressing genes. This process is known as retrograde signaling (1), because the pathway from the mitochondria to the nucleus is reversed from how many people have been conditioned to think about subcellular signaling.
The fascinating aspects of the organelle aren’t something only overlooked in introductory general biology courses-but have also historically been ignored by much of the scientific community. With increasing recognition that mitochondria are central to health – and that some of our parasitic enemies have strange mitochondria we can potentially target with drugs, there has been a newfound push to better understand this curious organelle. My personal favorite example of such an organism are the trypanosomes, which are parasitic protists that have a single, long, and funky mitochondrion known as a kinetoplast. Because the kinetoplast is so different from the host’s mitochondria, it is often proposed as a drug target for taking care of the infection from such microbes. It seems like a promising avenue, but there are many questions to be answered before it can become a reality. In the meantime we can sit back in awe at the mini machines that make us work.
 Jazwinski, S. Michal. “The retrograde response: when mitochondrial quality control is not enough.” Biochimica et Biophysica Acta (BBA)-Molecular Cell Research 1833.2 (2013): 400-409.
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