Cell death during Drosophila melanogaster early oogenesis is mediated through autophagy
Open accessAbstract
Autophagy is a physiological and evolutionarily conserved process maintaining homeostatic functions, such as protein degradation and organelle turnover. Accumulating data provide evidence that autophagy also contributes to cell death under certain circumstances, but how this is achieved is not well known. Herein, we report that autophagy occurs during developmentally-induced cell death in the female germline, observed in the germarium and during middle developmental stages of oogenesis in Drosophila melanogaster. Degenerating germline cells exhibit caspase activation, chromatin condensation, DNA fragmentation and punctate staining of mCherry-DrAtg8a, a novel marker for monitoring autophagy in Drosophila. Genetic inhibition of autophagy, by removing atg1 or atg7 function, results in significant reduction of DNA fragmentation, suggesting that autophagy acts genetically upstream of DNA fragmentation in this tissue. This study provides new insights into the mechanisms that regulate cell death in vivo during development.
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During Drosophila oogenesis, the autophagic apparatus acts upstream of DNA fragmentation by promoting IAP degradation and caspase activation.
“while the autophagic apparatus acts upstream of DNA fragmentation by promoting IAP degradation and caspase activation [845, 846].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [846]
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- Authors
- Nezis, I. P., Lamark, T., Velentzas, A. D., Rusten, T. E., Bjørkøy, G., Johansen, T., Papassideri, I. S., Stravopodis, D. J., Margaritis, L. H., Stenmark, H., & Brech, A.
- Affiliations
- University of Oslo (NO)
- UiT The Arctic University of Norway (NO)
- National and Kapodistrian University of Athens (GR)
- Corresponding author
- Stenmark, Harald
- Brech, Andreas
- ORCID
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2009-04
- Volume
- 5
- Issue
- 3
- Pages
- 298-302
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- OpenAlex
- W2123112488
- Cited by
- 132
- References
- 27
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 9 · 2023: 9 · 2022: 4 · 2021: 6 · 2020: 5 · 2019: 8 · 2018: 4 · 2017: 4 · 2016: 9 · 2015: 11 · 2014: 10 · 2013: 12 · 2012: 9
- FWCI
- 6.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Autophagy (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Norges Forskningsråd
- Hartmann Fonden
- European Social Fund
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cell death, Drosophila melanogaster, oogenesis, female germline, germarium, DNA fragmentation, caspase activation, Atg1, ATG7, developmental cell death
- MeSH terms
- Autophagy-Related Protein-1 Homolog, Autophagy-Related Protein 7, Animals, Autophagy, Chromatin, Drosophila melanogaster, Enzyme Activation, Female, Germ Cells, Male, Models, Biological, Models, Genetic, Oogenesis, Developmental Biology, Protein Serine-Threonine Kinases, Caspases, Drosophila Proteins, DNA Fragmentation
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