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dc.contributor.authorNandy, Anubhab
dc.contributor.authorLin, Lin
dc.contributor.authorVelentzas, Panagiotis D.
dc.contributor.authorWu, Louisa P.
dc.contributor.authorBaehrecke, Eric H.
dc.contributor.authorSilverman, Neal S.
dc.date2022-08-11T08:09:51.000
dc.date.accessioned2022-08-23T16:46:19Z
dc.date.available2022-08-23T16:46:19Z
dc.date.issued2018-11-20
dc.date.submitted2018-12-21
dc.identifier.citation<p>Cell Rep. 2018 Nov 20;25(8):2110-2120.e3. doi: 10.1016/j.celrep.2018.10.076. <a href="https://doi.org/10.1016/j.celrep.2018.10.076">Link to article on publisher's site</a></p>
dc.identifier.issn2211-1247 (Electronic)
dc.identifier.doi10.1016/j.celrep.2018.10.076
dc.identifier.pmid30463009
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40858
dc.description.abstractMacroautophagy and cell death both contribute to innate immunity, but little is known about how these processes integrate. Drosophila larval salivary glands require autophagy for developmentally programmed cell death, and innate immune signaling factors increase in these dying cells. Here, we show that the nuclear factor kappaB (NF-kappaB) factor Relish, a component of the immune deficiency (Imd) pathway, is required for salivary gland degradation. Surprisingly, of the classic Imd pathway components, only Relish and the PGRP receptors were involved in salivary gland degradation. Significantly, Relish controls salivary gland degradation by regulating autophagy but not caspases. In addition, expression of either Relish or PGRP-LC causes premature autophagy induction and subsequent gland degradation. Relish controls autophagy by regulating the expression of Atg1, a core component and activator of the autophagy pathway. Together these findings demonstrate that a NF-kappaB pathway regulates autophagy during developmentally programmed cell death.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=30463009&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsThis is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectDrosophila
dc.subjectNF-κB
dc.subjectautophagy
dc.subjectcell death
dc.subjectCell Biology
dc.subjectCells
dc.subjectCellular and Molecular Physiology
dc.subjectHemic and Immune Systems
dc.subjectImmunity
dc.titleThe NF-kappaB Factor Relish Regulates Atg1 Expression and Controls Autophagy
dc.typeJournal Article
dc.source.journaltitleCell reports
dc.source.volume25
dc.source.issue8
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4675&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3663
dc.identifier.contextkey13525552
refterms.dateFOA2022-08-23T16:46:20Z
html.description.abstract<p>Macroautophagy and cell death both contribute to innate immunity, but little is known about how these processes integrate. Drosophila larval salivary glands require autophagy for developmentally programmed cell death, and innate immune signaling factors increase in these dying cells. Here, we show that the nuclear factor kappaB (NF-kappaB) factor Relish, a component of the immune deficiency (Imd) pathway, is required for salivary gland degradation. Surprisingly, of the classic Imd pathway components, only Relish and the PGRP receptors were involved in salivary gland degradation. Significantly, Relish controls salivary gland degradation by regulating autophagy but not caspases. In addition, expression of either Relish or PGRP-LC causes premature autophagy induction and subsequent gland degradation. Relish controls autophagy by regulating the expression of Atg1, a core component and activator of the autophagy pathway. Together these findings demonstrate that a NF-kappaB pathway regulates autophagy during developmentally programmed cell death.</p>
dc.identifier.submissionpathoapubs/3663
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pages2110-2120.e3


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This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Except where otherwise noted, this item's license is described as This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).