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Differential patterns of apoptosis in response to aging in Drosophila
Open accessAbstract
Several lines of evidence suggest that programmed cell death may play a role in the aging process and the age-related functional declines of multicellular organisms. To pave the way for the use of Drosophila to rigorously test this hypothesis in a genetic model organism, this work examines the pattern of apoptosis in the adult fly during aging. The analysis across the lifespan of caspase activity and DNA fragmentation shows that apoptosis occurs in adult flies at all ages and that it is linked to physiological age. The results establish that under normal conditions, fly aging is coupled with a lifelong gradual increase of apoptosis within muscle cells and an activation of apoptosis in fat cells of old flies. The nervous system does not show signs of apoptosis. These time- and tissue-specific changes indicate that aging influences the levels and the nature of the cells that commit to apoptosis. The comparison with the apoptotic response to starvation and oxidative stresses strongly suggests that the lifelong increase in flight and leg muscles results from the accumulation of oxidative damage associated with aging. This finding presents an attractive mechanism to account for the decline of locomotor functions and muscle loss in the elderly and opens the way for the genetic analysis of sarcopenia in Drosophila.
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“Increased PCD-like events were observed during aging in muscle tissue and in fat tissue, as indicated by DNA fragmentation and caspase activity (Zheng et al., 2005).”
From Programmed cell death in aging (2015) · cites this paper as Zheng et al., 2005
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Metadata
- Authors
- Zheng, J., Edelman, S. W., Tharmarajah, G., Walker, D. W., Pletcher, S. D., & Seroude, L.
- Affiliations
- California Institute of Technology (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2005-08-12
- Volume
- 102
- Issue
- 34
- Pages
- 12083-12088
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC1189317
- OpenAlex
- W2137068591
- Cited by
- 100
- References
- 53
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 6 · 2022: 3 · 2021: 9 · 2020: 5 · 2019: 4 · 2018: 3 · 2017: 1 · 2016: 3 · 2015: 5 · 2014: 8 · 2013: 7 · 2012: 3
- FWCI
- 1.57
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion)
- Funders
- Queen's University
- Canadian Institutes of Health Research
- Natural Sciences and Engineering Research Council of Canada
- 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 › Cell death mechanisms and regulation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurobiology and Insect Physiology Research
- Keywords
- apoptosis, aging, Drosophila, caspase activity, DNA fragmentation, muscle cells, adipocytes, nervous system, oxidative stress, starvation, sarcopenia, tissue-specific aging
- MeSH terms
- Adipose Tissue, Age Factors, Aging, Animals, Drosophila, Muscles, Apoptosis, DNA Primers, Oxidative Stress, Reverse Transcriptase Polymerase Chain Reaction, Caspases, In Situ Nick-End Labeling, DNA Fragmentation
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