| http://purl.uniprot.org/citations/35058357 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/35058357 | http://www.w3.org/2000/01/rdf-schema#comment | "After injury, severed dendrites and axons expose the "eat-me" signal phosphatidylserine (PS) on their surface while they break down. The degeneration of injured axons is controlled by a conserved Wallerian degeneration (WD) pathway, which is thought to activate neurite self-destruction through Sarm-mediated nicotinamide adenine dinucleotide (NAD+) depletion. While neurite PS exposure is known to be affected by genetic manipulations of NAD+, how the WD pathway coordinates both neurite PS exposure and self-destruction and whether PS-induced phagocytosis contributes to neurite breakdown in vivo remain unknown. Here, we show that in Drosophila sensory dendrites, PS exposure and self-destruction are two sequential steps of WD resulting from Sarm activation. Surprisingly, phagocytosis is the main driver of dendrite degeneration induced by both genetic NAD+ disruptions and injury. However, unlike neuronal Nmnat loss, which triggers PS exposure only and results in phagocytosis-dependent dendrite degeneration, injury activates both PS exposure and self-destruction as two redundant means of dendrite degeneration. Furthermore, the axon-death factor Axed is only partially required for self-destruction of injured dendrites, acting in parallel with PS-induced phagocytosis. Lastly, injured dendrites exhibit a unique rhythmic calcium-flashing that correlates with WD. Therefore, both NAD+-related general mechanisms and dendrite-specific programs govern PS exposure and self-destruction in injury-induced dendrite degeneration in vivo."xsd:string |
| http://purl.uniprot.org/citations/35058357 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.2111818119"xsd:string |
| http://purl.uniprot.org/citations/35058357 | http://purl.uniprot.org/core/author | "Han C."xsd:string |
| http://purl.uniprot.org/citations/35058357 | http://purl.uniprot.org/core/author | "Sarkar A."xsd:string |
| http://purl.uniprot.org/citations/35058357 | http://purl.uniprot.org/core/author | "Wang B."xsd:string |
| http://purl.uniprot.org/citations/35058357 | http://purl.uniprot.org/core/author | "Ji H."xsd:string |
| http://purl.uniprot.org/citations/35058357 | http://purl.uniprot.org/core/author | "Sapar M.L."xsd:string |
| http://purl.uniprot.org/citations/35058357 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
| http://purl.uniprot.org/citations/35058357 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
| http://purl.uniprot.org/citations/35058357 | http://purl.uniprot.org/core/pages | "e2111818119"xsd:string |
| http://purl.uniprot.org/citations/35058357 | http://purl.uniprot.org/core/title | "Phagocytosis and self-destruction break down dendrites of Drosophila sensory neurons at distinct steps of Wallerian degeneration."xsd:string |
| http://purl.uniprot.org/citations/35058357 | http://purl.uniprot.org/core/volume | "119"xsd:string |
| http://purl.uniprot.org/citations/35058357 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/35058357 |
| http://purl.uniprot.org/citations/35058357 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/35058357 |
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