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000140635 0247_ $$2doi$$a10.1038/s41418-018-0164-x
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000140635 0247_ $$2pmc$$apmc:PMC6462001
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000140635 0247_ $$2ISSN$$a1476-5403
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000140635 037__ $$aDZNE-2020-06957
000140635 041__ $$aEnglish
000140635 082__ $$a610
000140635 1001_ $$aAalto, Anna L$$b0
000140635 245__ $$aM1-linked ubiquitination by LUBEL is required for inflammatory responses to oral infection in Drosophila.
000140635 260__ $$aLondon$$bMacmillan$$c2019
000140635 264_1 $$2Crossref$$3online$$bSpringer Science and Business Media LLC$$c2018-07-19
000140635 264_1 $$2Crossref$$3print$$bSpringer Science and Business Media LLC$$c2019-05-01
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000140635 3367_ $$2BibTeX$$aARTICLE
000140635 3367_ $$2ORCID$$aJOURNAL_ARTICLE
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000140635 520__ $$aPost-translational modifications such as ubiquitination play a key role in regulation of inflammatory nuclear factor-κB (NF-κB) signalling. The Drosophila IκB kinase γ (IKKγ) Kenny is a central regulator of the Drosophila Imd pathway responsible for activation of the NF-κB Relish. We found the Drosophila E3 ligase and HOIL-1L interacting protein (HOIP) orthologue linear ubiquitin E3 ligase (LUBEL) to catalyse formation of M1-linked linear ubiquitin (M1-Ub) chains in flies in a signal-dependent manner upon bacterial infection. Upon activation of the Imd pathway, LUBEL modifies Kenny with M1-Ub chains. Interestingly, the LUBEL-mediated M1-Ub chains seem to be targeted both directly to Kenny and to K63-linked ubiquitin chains conjugated to Kenny by DIAP2. This suggests that DIAP2 and LUBEL work together to promote Kenny-mediated activation of Relish. We found LUBEL-mediated M1-Ub chain formation to be required for flies to survive oral infection with Gram-negative bacteria, for activation of Relish-mediated expression of antimicrobial peptide genes and for pathogen clearance during oral infection. Interestingly, LUBEL is not required for mounting an immune response against systemic infection, as Relish-mediated antimicrobial peptide genes can be expressed in the absence of LUBEL during septic injury. Finally, transgenic induction of LUBEL-mediated M1-Ub drives expression of antimicrobial peptide genes and hyperplasia in the midgut in the absence of infection. This suggests that M1-Ub chains are important for Imd signalling and immune responses in the intestinal epithelia, and that enhanced M1-Ub chain formation is able to drive chronic intestinal inflammation in flies.
000140635 536__ $$0G:(DE-HGF)POF3-341$$a341 - Molecular Signaling (POF3-341)$$cPOF3-341$$fPOF III$$x0
000140635 542__ $$2Crossref$$i2018-07-19$$uhttps://creativecommons.org/licenses/by/4.0
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000140635 650_2 $$2MeSH$$aAnimals
000140635 650_2 $$2MeSH$$aBacterial Infections: genetics
000140635 650_2 $$2MeSH$$aBacterial Infections: microbiology
000140635 650_2 $$2MeSH$$aDisease Models, Animal
000140635 650_2 $$2MeSH$$aDrosophila: genetics
000140635 650_2 $$2MeSH$$aDrosophila Proteins: genetics
000140635 650_2 $$2MeSH$$aGram-Negative Bacteria: pathogenicity
000140635 650_2 $$2MeSH$$aHumans
000140635 650_2 $$2MeSH$$aImmunity, Innate: genetics
000140635 650_2 $$2MeSH$$aInflammation: genetics
000140635 650_2 $$2MeSH$$aInflammation: microbiology
000140635 650_2 $$2MeSH$$aInhibitor of Apoptosis Proteins: genetics
000140635 650_2 $$2MeSH$$aMouth: microbiology
000140635 650_2 $$2MeSH$$aMouth: pathology
000140635 650_2 $$2MeSH$$aNF-kappa B: genetics
000140635 650_2 $$2MeSH$$aProtein Processing, Post-Translational: genetics
000140635 650_2 $$2MeSH$$aRNA-Binding Proteins: genetics
000140635 650_2 $$2MeSH$$aSignal Transduction: genetics
000140635 650_2 $$2MeSH$$aTranscription Factors: genetics
000140635 650_2 $$2MeSH$$aUbiquitin: genetics
000140635 650_2 $$2MeSH$$aUbiquitin-Protein Ligases: genetics
000140635 650_2 $$2MeSH$$aUbiquitination: genetics
000140635 7001_ $$aMohan, Aravind K$$b1
000140635 7001_ $$0P:(DE-2719)2810987$$aSchwintzer, Lukas$$b2$$udzne
000140635 7001_ $$aKupka, Sebastian$$b3
000140635 7001_ $$aKietz, Christa$$b4
000140635 7001_ $$aWalczak, Henning$$b5
000140635 7001_ $$0P:(DE-2719)2810307$$aBroemer, Meike$$b6$$udzne
000140635 7001_ $$0P:(DE-HGF)0$$aMeinander, Annika$$b7$$eCorresponding author
000140635 77318 $$2Crossref$$3journal-article$$a10.1038/s41418-018-0164-x$$b : Springer Science and Business Media LLC, 2018-07-19$$n5$$p860-876$$tCell Death & Differentiation$$v26$$x1350-9047$$y2018
000140635 773__ $$0PERI:(DE-600)1496681-5$$a10.1038/s41418-018-0164-x$$gVol. 26, no. 5, p. 860 - 876$$n5$$p860-876$$q26:5<860 - 876$$tCell death and differentiation$$v26$$x1350-9047$$y2018
000140635 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC6462001
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000140635 9141_ $$y2019
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