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10.1523/JNEUROSCI.1912-15.2016 http://scihub22266oqcxt.onion/10.1523/JNEUROSCI.1912-15.2016 C4792933!4792933 !26985028     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26985028 &cmd=llinks): Failed to open stream: HTTP request failed! 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Defective Phagocytic Corpse Processing Results in Neurodegeneration and Can Be Rescued by TORC1 Activation |pdf=|usr=}}{{26985028 }} gab.com Text Defective Phagocytic Corpse Processing Results in Neurodegeneration and Can Be Rescued by TORC1 Activation JO: J Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=26985028 #FOAvip 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. Twit Text FOAVip Defective Phagocytic Corpse Processing Results in Neurodegeneration and Can Be Rescued by TORC1 Activation ????J Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=26985028 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26985028 #FOAvip English Wikipedia <ref>{{Cite pmid|26985028 }}</ref> Defective Phagocytic Corpse Processing Results in Neurodegeneration and Can Be Rescued by TORC1 Activation #MMPMID26985028 Etchegaray JI ; Elguero EJ ; Tran JA ; Sinatra V ; Feany MB ; McCall K J Neurosci 2016[Mar]; 36 (11 ): 3170-83 PMID26985028 show ga 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. |Age Factors [MESH] |Animals [MESH] |Animals, Genetically Modified [MESH] |Apoptosis/*physiology [MESH] |Brain/pathology [MESH] |Caenorhabditis elegans Proteins/genetics [MESH] |Drosophila Proteins/genetics/*metabolism [MESH] |Drosophila melanogaster [MESH] |Embryo, Nonmammalian [MESH] |Eukaryotic Initiation Factors/deficiency/genetics [MESH] |Gene Expression Regulation/genetics [MESH] |Larva [MESH] |Membrane Proteins/genetics/metabolism [MESH] |Nerve Degeneration/*genetics/pathology [MESH] |Neuroglia/*pathology/ultrastructure [MESH] |Neurons/metabolism/pathology/ultrastructure [MESH] |Phagocytosis/*physiology [MESH] |RNA Interference/physiology [MESH]Defective Phagocytic Corpse Processing Results in Neurodegeneration an(epmc).pdf DeepDyve Pubget Overpricing