Promoting Drp1-mediated mitochondrial fission in midlife prolongs healthy lifespan of Drosophila melanogaster

Anil Rana, Matheus P. Oliveira, Andy V. Khamoui, Ricardo Aparicio, Michael Rera, Harry B. Rossiter and David W. Walker ()
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Anil Rana: University of California
Matheus P. Oliveira: University of California
Andy V. Khamoui: Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center
Ricardo Aparicio: University of California
Michael Rera: University of California
Harry B. Rossiter: Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center
David W. Walker: University of California

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: Abstract The accumulation of dysfunctional mitochondria has been implicated in aging, but a deeper understanding of mitochondrial dynamics and mitophagy during aging is missing. Here, we show that upregulating Drp1—a Dynamin-related protein that promotes mitochondrial fission—in midlife, prolongs Drosophila lifespan and healthspan. We find that short-term induction of Drp1, in midlife, is sufficient to improve organismal health and prolong lifespan, and observe a midlife shift toward a more elongated mitochondrial morphology, which is linked to the accumulation of dysfunctional mitochondria in aged flight muscle. Promoting Drp1-mediated mitochondrial fission, in midlife, facilitates mitophagy and improves both mitochondrial respiratory function and proteostasis in aged flies. Finally, we show that autophagy is required for the anti-aging effects of midlife Drp1-mediated mitochondrial fission. Our findings indicate that interventions that promote mitochondrial fission could delay the onset of pathology and mortality in mammals when applied in midlife.

Date: 2017
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DOI: 10.1038/s41467-017-00525-4

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