The NF-kappaB Factor Relish Regulates Atg1 Expression and Controls Autophagy
Velentzas, Panagiotis D.
Wu, Louisa P.
Baehrecke, Eric H.
Silverman, Neal S.
UMass Chan AffiliationsDepartment of Molecular, Cell and Cancer Biology
Department of Medicine, Division of Infectious Diseases and Immunology
Document TypeJournal Article
Cellular and Molecular Physiology
Hemic and Immune Systems
MetadataShow full item record
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.
Cell Rep. 2018 Nov 20;25(8):2110-2120.e3. doi: 10.1016/j.celrep.2018.10.076. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/40858
RightsThis 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/).