ArticleCell death and differentiation2011
Mitochondrial fusion is regulated by Reaper to modulate Drosophila programmed cell death.
Article in Cell death and differentiation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Causal roles of mitochondrial dynamics in longevity and healthy aging.EMBO reports · 2019Review
- Drosophila as a Model System to Study Cell Signaling in Organ Regeneration.BioMed research international · 2018Review
- Organelles - understanding noise and heterogeneity in cell biology at an intermediate scale.Journal of cell science · 2017Review
- Programmed cell death acts at different stages of Drosophila neurodevelopment to shape the central nervous system.FEBS letters · 2016Review
- Article
- Rapid selection against arbovirus-induced apoptosis during infection of a mosquito vector.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Regulation of Cell Death by IAPs and Their Antagonists.Current topics in developmental biology · 2015Review
- Diversity of cell death pathways: insight from the fly ovary.Trends in cell biology · 2013Review
- Screening of candidate proteins interacting with IE-2 of Bombyx mori nucleopolyhedrovirus.Molecular biology reports · 2013Article
- Huntington's disease induced cardiac amyloidosis is reversed by modulating protein folding and oxidative stress pathways in the Drosophila heart.PLoS genetics · 2013Article
- Identification of NCF2/p67phox as a novel p53 target gene.Cell cycle (Georgetown, Tex.) · 2012Article
- Review
- Article
- Mitochondria in apoptosis: Bcl-2 family members and mitochondrial dynamics.Developmental cell · 2011Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
In most multicellular organisms, the decision to undergo programmed cell death in response to cellular damage or developmental cues is typically transmitted through mitochondria. It has been suggested that an exception is the apoptotic pathway of Drosophila melanogaster, in which the role of mitochondria remains unclear. Although IAP antagonists in Drosophila such as Reaper, Hid and Grim may induce cell death without mitochondrial membrane permeabilization, it is surprising that all three localize to mitochondria. Moreover, induction of Reaper and Hid appears to result in mitochondrial fragmentation during Drosophila cell death. Most importantly, disruption of mitochondrial fission can inhibit Reaper and Hid-induced cell death, suggesting that alterations in mitochondrial dynamics can modulate cell death in fly cells. We report here that Drosophila Reaper can induce mitochondrial fragmentation by binding to and inhibiting the pro-fusion protein MFN2 and its Drosophila counterpart dMFN/Marf. Our in vitro and in vivo analyses reveal that dMFN overexpression can inhibit cell death induced by Reaper or γ-irradiation. In addition, knockdown of dMFN causes a striking loss of adult wing tissue and significant apoptosis in the developing wing discs. Our findings are consistent with a growing body of work describing a role for mitochondrial fission and fusion machinery in the decision of cells to die.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.