Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/81549
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dc.contributor.authorPapan, Cyrusen
dc.contributor.authorOsborne, Kathleen Amyen
dc.contributor.authorTorta, Federicoen
dc.contributor.authorShevchenko, Andrejen
dc.contributor.authorSchwudke, Dominiken
dc.contributor.authorKraut, Rachelen
dc.contributor.authorHebbar, Saritaen
dc.contributor.authorSahoo, Ishtapranen
dc.contributor.authorMatysik, Arturen
dc.contributor.authorGarcia, Irene Argudoen
dc.contributor.authorNarayanaswamy, Pradeepen
dc.contributor.authorFun, Xiu Huien
dc.contributor.authorWenk, Markus Ren
dc.date.accessioned2016-01-05T06:02:40Zen
dc.date.accessioned2019-12-06T14:33:31Z-
dc.date.available2016-01-05T06:02:40Zen
dc.date.available2019-12-06T14:33:31Z-
dc.date.issued2015en
dc.identifier.citationHebbar, S., Sahoo, I., Matysik, A., Garcia, I. A., Osborne, K. A., Papan, C., et al. (2015). Ceramides And Stress Signalling Intersect With Autophagic Defects In Neurodegenerative Drosophila blue cheese (bchs) Mutants. Scientific Reports, 5, 15926-.en
dc.identifier.issn2045-2322en
dc.identifier.urihttps://hdl.handle.net/10356/81549-
dc.description.abstractSphingolipid metabolites are involved in the regulation of autophagy, a degradative recycling process that is required to prevent neuronal degeneration. Drosophila blue cheese mutants neurodegenerate due to perturbations in autophagic flux, and consequent accumulation of ubiquitinated aggregates. Here, we demonstrate that blue cheese mutant brains exhibit an elevation in total ceramide levels; surprisingly, however, degeneration is ameliorated when the pool of available ceramides is further increased, and exacerbated when ceramide levels are decreased by altering sphingolipid catabolism or blocking de novo synthesis. Exogenous ceramide is seen to accumulate in autophagosomes, which are fewer in number and show less efficient clearance in blue cheese mutant neurons. Sphingolipid metabolism is also shifted away from salvage toward de novo pathways, while pro-growth Akt and MAP pathways are down-regulated, and ER stress is increased. All these defects are reversed under genetic rescue conditions that increase ceramide generation from salvage pathways. This constellation of effects suggests a possible mechanism whereby the observed deficit in a potentially ceramide-releasing autophagic pathway impedes survival signaling and exacerbates neuronal death.en
dc.description.sponsorshipASTAR (Agency for Sci., Tech. and Research, S’pore)en
dc.description.sponsorshipMOE (Min. of Education, S’pore)en
dc.format.extent18 p.en
dc.language.isoenen
dc.relation.ispartofseriesScientific Reportsen
dc.rights© 2015 Hebbar, S. et al. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/en
dc.subjectBiological Sciencesen
dc.titleCeramides And Stress Signalling Intersect With Autophagic Defects In Neurodegenerative Drosophila blue cheese (bchs) Mutantsen
dc.typeJournal Articleen
dc.contributor.schoolSchool of Biological Sciencesen
dc.identifier.doi10.1038/srep15926en
dc.description.versionPublished versionen
dc.identifier.pmid26639035-
item.fulltextWith Fulltext-
item.grantfulltextopen-
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