Mitochondria are the cellular power plants, but bigger power plants are not always a good thing. Defects in the regulation of mitochondrial size and dynamics can cause neurodegenerative diseases such as Alzheimer’s disease. Today’s image is from a paper describing an important player in mitochondrial division, or fission.
Mitochondria serve as the cellular power plants due to their production of ATP, the cell’s energy source, and are quite dynamic, with fusion and fission events occurring regularly. Mitochondrial fission is how mitochondria divide, but fission also plays an important role in apoptosis and ridding the cell of damaged mitochondrial components. In current models of fission, the GTPase dynamin (Drp1) forms a ring around and constricts the mitochondrial membranes. A recent paper describes the importance of the myosin II, an actin motor, in Drp1-mediated fission. Korobova and colleagues found that inhibition of myosin II resulted in abnormally long mitochondria. This inhibition of myosin II also affected the presence of Drp1 at mitochondria. In the images above, the use of blebbistatin, a myosin II chemical inhibitor, resulted in long mitochondria (right), compared to control mitochondria (left).
Korobova, F., Gauvin, T., & Higgs, H. (2014). A Role for Myosin II in Mammalian Mitochondrial Fission Current Biology, 24 (4), 409-414 DOI: 10.1016/j.cub.2013.12.032
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