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@ARTICLE{Aalto:140635,
author = {Aalto, Anna L and Mohan, Aravind K and Schwintzer, Lukas
and Kupka, Sebastian and Kietz, Christa and Walczak, Henning
and Broemer, Meike and Meinander, Annika},
title = {{M}1-linked ubiquitination by {LUBEL} is required for
inflammatory responses to oral infection in {D}rosophila.},
journal = {Cell death and differentiation},
volume = {26},
number = {5},
issn = {1350-9047},
address = {London},
publisher = {Macmillan},
reportid = {DZNE-2020-06957},
pages = {860-876},
year = {2019},
abstract = {Post-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.},
keywords = {Animals / Bacterial Infections: genetics / Bacterial
Infections: microbiology / Disease Models, Animal /
Drosophila: genetics / Drosophila Proteins: genetics /
Gram-Negative Bacteria: pathogenicity / Humans / Immunity,
Innate: genetics / Inflammation: genetics / Inflammation:
microbiology / Inhibitor of Apoptosis Proteins: genetics /
Mouth: microbiology / Mouth: pathology / NF-kappa B:
genetics / Protein Processing, Post-Translational: genetics
/ RNA-Binding Proteins: genetics / Signal Transduction:
genetics / Transcription Factors: genetics / Ubiquitin:
genetics / Ubiquitin-Protein Ligases: genetics /
Ubiquitination: genetics},
cin = {AG Brömer 1},
ddc = {610},
cid = {I:(DE-2719)5000021},
pnm = {341 - Molecular Signaling (POF3-341)},
pid = {G:(DE-HGF)POF3-341},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30026495},
pmc = {pmc:PMC6462001},
doi = {10.1038/s41418-018-0164-x},
url = {https://pub.dzne.de/record/140635},
}