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dc.contributor.authorTracy, Kirsten
dc.contributor.authorVelentzas, Panagiotis D.
dc.contributor.authorBaehrecke, Eric H.
dc.date2022-08-11T08:09:19.000
dc.date.accessioned2022-08-23T16:26:17Z
dc.date.available2022-08-23T16:26:17Z
dc.date.issued2015-11-23
dc.date.submitted2015-11-30
dc.identifier.citationEMBO Rep. 2015 Nov 23. pii: e201541283. [Epub ahead of print] <a href="http://dx.doi.org/10.15252/embr.201541283">Link to article on publisher's site</a>
dc.identifier.issn1469-221X (Linking)
dc.identifier.doi10.15252/embr.201541283
dc.identifier.pmid26598552
dc.identifier.urihttp://hdl.handle.net/20.500.14038/36530
dc.description.abstractAutophagy traffics cellular components to the lysosome for degradation. Ral GTPase and the exocyst have been implicated in the regulation of stress-induced autophagy, but it is unclear whether they are global regulators of this process. Here, we investigate Ral function in different cellular contexts in Drosophila and find that it is required for autophagy during developmentally regulated cell death in salivary glands, but does not affect starvation-induced autophagy in the fat body. Furthermore, knockdown of exocyst subunits has a similar effect, preventing autophagy in dying cells but not in cells of starved animals. Notch activity is elevated in dying salivary glands, this change in Notch signaling is influenced by Ral, and decreased Notch function influences autophagy. These data indicate that Ral and the exocyst regulate autophagy in a context-dependent manner, and that in dying salivary glands, Ral mediates autophagy, at least in part, by regulation of Notch.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=26598552&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.15252/embr.201541283
dc.subjectDrosophila
dc.subjectNotch
dc.subjectRal GTPase
dc.subjectautophagy
dc.subjectcell death
dc.subjectexocyst
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectDevelopmental Biology
dc.titleRal GTPase and the exocyst regulate autophagy in a tissue-specific manner
dc.typeJournal Article
dc.source.journaltitleEMBO reports
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/mccb_pubs/24
dc.identifier.contextkey7884823
html.description.abstract<p>Autophagy traffics cellular components to the lysosome for degradation. Ral GTPase and the exocyst have been implicated in the regulation of stress-induced autophagy, but it is unclear whether they are global regulators of this process. Here, we investigate Ral function in different cellular contexts in Drosophila and find that it is required for autophagy during developmentally regulated cell death in salivary glands, but does not affect starvation-induced autophagy in the fat body. Furthermore, knockdown of exocyst subunits has a similar effect, preventing autophagy in dying cells but not in cells of starved animals. Notch activity is elevated in dying salivary glands, this change in Notch signaling is influenced by Ral, and decreased Notch function influences autophagy. These data indicate that Ral and the exocyst regulate autophagy in a context-dependent manner, and that in dying salivary glands, Ral mediates autophagy, at least in part, by regulation of Notch.</p>
dc.identifier.submissionpathmccb_pubs/24
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology


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