ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016
Defective Phagocytic Corpse Processing Results in Neurodegeneration and Can Be Rescued by TORC1 Activation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 60 citations in OpenAlex.
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- epHero - a tandem-fluorescent probe to track the fate of apoptotic cells during efferocytosis.Cell death discovery · 2024Article
- Defective phagocytosis leads to neurodegeneration through systemic increased innate immune signaling.iScience · 2023Article
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- LC3-associated phagocytosis promotes glial degradation of axon debris after injury in Drosophila models.Nature communications · 2023Article
- Drosophila FGFR/Htl signaling shapes embryonic glia to phagocytose apoptotic neurons.Cell death discovery · 2023Article
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- TM2D genes regulate Notch signaling and neuronal function in Drosophila.PLoS genetics · 2021Article
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- A secreted factor NimrodB4 promotes the elimination of apoptotic corpses by phagocytes in Drosophila.EMBO reports · 2021Article
- Phosphatidylserine synthase plays an essential role in glia and affects development, as well as the maintenance of neuronal function.iScience · 2021Article
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- Neuroimmune cleanup crews in brain injury.Trends in immunology · 2021Review
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6 authors at 2 institutions in 1 country.
Funding
Abstract
The removal of apoptotic cell corpses is important for maintaining homeostasis. Previously, defects in apoptotic cell clearance have been linked to neurodegeneration. However, the mechanisms underlying this are still poorly understood. In this study, we report that the absence of the phagocytic receptor Draper in glia leads to a pronounced accumulation of apoptotic neurons in the brain of Drosophila melanogaster. These dead cells persist in the brain throughout the lifespan of the organism and are associated with age-dependent neurodegeneration. Our data indicate that corpses persist because of defective phagosome maturation, rather than recognition defects. TORC1 activation, or inhibition of Atg1, in glia is sufficient to rescue corpse accumulation as well as neurodegeneration. These results suggest that phagocytosis of apoptotic neurons by glia during development is essential for brain homeostasis in adult flies. Furthermore, it suggests that TORC1 regulates Draper-mediated phagosome maturation. SIGNIFICANCE STATEMENT: Previously, defects in dead cell clearance were linked to neurodegeneration, but the exact mechanisms are not well understood. In this study, we report that the absence of an engulfment receptor leads to a pronounced accumulation of dead neurons in the brain of the fruit fly Drosophila melanogaster. These dead cells persist in the brain throughout the lifespan of the organism and are associated with age-dependent neurodegeneration. Our data indicate that corpses persist because of defective degradation of cells rather than recognition of dead cells.
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