By Meghan Bialt-DeCelie ’19

The respiratory function of the mitochondrion, the energy producing organelle found in the cell, can decline over time. This is because of how the mitochondrion enlarge and assume a more elongated shape. Typically, that mitochondrion will eventually break down and get removed processes called mitochondrial fission and mitophagy respectively. Accumulation of the ineffective mitochondria and inability to remove them are major signs of aging.

Researchers led by Anil Rana PhD from the University of California, Los Angeles extended the life of middle aged Drosophila flies by controlling the expression of several genes that mediate mitochondrial dynamics. Specifically, they upregulated Dynamin-related protein 1 (Drp1), a protein responsible for mitochondrial fission, for a week in middle-aged Drosophila. The researchers were also able to extend the lifespan of fruit flies by knocking down genes responsible for Mitofusion proteins (Mfn) which typically allow mitochondria to fuse into larger, dysfunctional morphologies. Atg1, a gene responsible for autophagy of mitochondria, was also studied. The importance of mitochondrial morphology and dynamics were further exhibited when the life-extending effects of increased Drp1 was negated when Atg1 was knocked out. This demonstrated that the expression of some genes and the suppression of others involved in mitochondrial maintenance can impact life span.

These findings will allow the development of drugs that could control mitochondrial fission and autophagy. This will not only increase the number of years a patient can have, but also improve the quality of life of those years.

References:

1. Rana, Anil, et al., Promoting Drp1-mediated mitochondrial fission in midlife prolongs healthy lifespan of Drosophila melanogaster. Nature Communications 8, 448 (2017). doi:10.1038/s41467-017-00525-4.
2. Image retrieved from: https://commons.wikimedia.org/wiki/File:Mitochondria.svg