Promoting Drp1-mediated mitochondrial fission in midlife prolongs healthy lifespan of Drosophila melanogaster
Open accessAbstract
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.
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Positive regulation of DRP1 in midlife extends the lifespan and health of Drosophila by inducing mitochondrial fission and reducing the accumulation of dysfunctional mitochondria in aged flight muscle.
“Although positive regulation of DRP1 in midlife extends the lifespan and health of Drosophila by inducing mitochondrial fission and reducing the accumulation of dysfunctional mitochondria in aged flight muscle (Rana et al., 2017)”
From Aging promotes an increase in mitochondrial fragmentation in astrocytes (2024) · cites this paper as Rana et al., 2017
Rebalancing of mitochondrial dynamics rescues the phenotype of certain diseases associated with alterations of mitochondrial fusion or fission.
“Several reports have shown that rebalancing of mitochondrial dynamics rescues the phenotype of certain diseases associated with alterations of mitochondrial fusion or fission [119, 194, 195, 214]”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [214]
DRP1 overexpression in muscles of Drosophila slows aging sarcopenia by ameliorating mitochondrial morphology, function, and mitophagy.
“In line with this report, DRP1 overexpression in muscles of Drosophila slows aging sarcopenia by ameliorating mitochondrial morphology, function, and mitophagy [214].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [214]
Boosting mitophagy by overexpressing PINK1, Parkin, DRP1, or p62 in Drosophila muscles improves age-dependent muscle function deterioration and extends lifespan.
“Boosting mitophagy by overexpressing PINK1, Parkin, DRP1, or p62 in Drosophila muscles improves the age-dependent muscle function deterioration and extends lifespan [214, 236, 237].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [214]
A subset of mitochondria in aged Drosophila indirect flight muscles are ubiquitylated.
“FK2 positive puncta are colocalized or intercalated with mitoGFP, suggesting a subset of mitochondria were ubiquitylated in muscles.”
From Overexpression of pink1 or parkin in indirect flight muscles promotes mitochondrial proteostasis and extends lifespan in Drosophila melanogaster (2019) · cites this paper as [15]
Enhanced Drp1-dependent fission in midlife promotes a healthy lifespan in D. melanogaster.
“Enhanced Drp1-dependent fission in midlife promotes a healthy lifespan in D. melanogaster [193].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [193]
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Aging promotes an increase in mitochondrial fragmentation in astrocytes
Araujo, A. P. B., Vargas, G., Hayashide, L. D. S., Matias, I., Andrade, C. B. V., de Carvalho, J. J., Gomes, F. C. A., & Diniz, L. P. (2024) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1496163 · Cited by 43 · see citing works
Holzscheck, N., Söhle, J., Kristof, B., Grönniger, E., Gallinat, S., Wenck, H., Winnefeld, M., Falckenhayn, C., & Kaderali, L. (2020) · Aging · doi:10.18632/aging.103499 · Cited by 40 · see citing works
Si, H., Ma, P., Liang, Q., Yin, Y., Wang, P., Zhang, Q., Wang, S., & Deng, H. (2019) · PLOS ONE · doi:10.1371/journal.pone.0225214 · Cited by 37 · see citing works
- Authors
- Rana, A., Oliveira, M. P., Khamoui, A. V., Aparicio, R., Rera, M., Rossiter, H. B., & Walker, D. W.
- Affiliations
- University of California, Los Angeles (US)
- Universidade Federal do Rio de Janeiro (BR)
- The Lundquist Institute (US)
- University of Leeds (GB)
- Corresponding author
- Walker, David W.
- Venue
- Nature Communications
- Published
- 2017-09-06
- Volume
- 8
- Issue
- 1
- Pages
- 448-448
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC5587646
- OpenAlex
- W2752071018
- Cited by
- 294
- References
- 74
- Citations by year
- 2026: 17 · 2025: 32 · 2024: 32 · 2023: 40 · 2022: 44 · 2021: 44 · 2020: 36 · 2019: 26 · 2018: 20 · 2017: 2
- FWCI
- 9.79
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- White Rose Research Online (University of Leeds, The University of Sheffield, University of York) (acceptedVersion)
- HAL (submittedVersion, other-oa)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- Ellison Medical Foundation
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- National Institutes of Health (NIH P40OD018537, P40OD018537)
- National Institute on Aging (R01AG040288, R01AG049157, R01AG037514)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- Drp1, mitochondrial fission, mitochondrial dynamics, mitophagy, aging, lifespan extension, healthspan, mitochondrial dysfunction, flight muscle, mitochondrial respiratory function, proteostasis, autophagy, Drosophila melanogaster
- MeSH terms
- Animals, Cytoskeletal Proteins, Drosophila melanogaster, Female, Hormone Antagonists, Longevity, Male, Mitochondria, Time Factors, Mifepristone, Gene Expression, Microscopy, Confocal, GTP-Binding Proteins, Reverse Transcriptase Polymerase Chain Reaction, Animals, Genetically Modified, Mitochondrial Dynamics, Mitophagy
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