Proteasome inhibition triggers tissue-specific immune responses against different pathogens in C. elegans.

Protein quality control pathways play important roles in resistance against pathogen infection. For example, the conserved transcription factor SKN-1/NRF up-regulates proteostasis capacity after blockade of the proteasome and also promotes resistance against bacterial infection in the nematode Caeno...

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Main Authors: Manish Grover, Spencer S Gang, Emily R Troemel, Michalis Barkoulas
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2024-03-01
Series:PLoS Biology
Online Access:https://journals.plos.org/plosbiology/article/file?id=10.1371/journal.pbio.3002543&type=printable
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author Manish Grover
Spencer S Gang
Emily R Troemel
Michalis Barkoulas
author_facet Manish Grover
Spencer S Gang
Emily R Troemel
Michalis Barkoulas
author_sort Manish Grover
collection DOAJ
description Protein quality control pathways play important roles in resistance against pathogen infection. For example, the conserved transcription factor SKN-1/NRF up-regulates proteostasis capacity after blockade of the proteasome and also promotes resistance against bacterial infection in the nematode Caenorhabditis elegans. SKN-1/NRF has 3 isoforms, and the SKN-1A/NRF1 isoform, in particular, regulates proteasomal gene expression upon proteasome dysfunction as part of a conserved bounce-back response. We report here that, in contrast to the previously reported role of SKN-1 in promoting resistance against bacterial infection, loss-of-function mutants in skn-1a and its activating enzymes ddi-1 and png-1 show constitutive expression of immune response programs against natural eukaryotic pathogens of C. elegans. These programs are the oomycete recognition response (ORR), which promotes resistance against oomycetes that infect through the epidermis, and the intracellular pathogen response (IPR), which promotes resistance against intestine-infecting microsporidia. Consequently, skn-1a mutants show increased resistance to both oomycete and microsporidia infections. We also report that almost all ORR/IPR genes induced in common between these programs are regulated by the proteasome and interestingly, specific ORR/IPR genes can be induced in distinct tissues depending on the exact trigger. Furthermore, we show that increasing proteasome function significantly reduces oomycete-mediated induction of multiple ORR markers. Altogether, our findings demonstrate that proteasome regulation keeps innate immune responses in check in a tissue-specific manner against natural eukaryotic pathogens of the C. elegans epidermis and intestine.
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spelling doaj-art-fec3952dc6294cdba47bf1f925fd0cd52024-11-09T05:30:59ZengPublic Library of Science (PLoS)PLoS Biology1544-91731545-78852024-03-01223e300254310.1371/journal.pbio.3002543Proteasome inhibition triggers tissue-specific immune responses against different pathogens in C. elegans.Manish GroverSpencer S GangEmily R TroemelMichalis BarkoulasProtein quality control pathways play important roles in resistance against pathogen infection. For example, the conserved transcription factor SKN-1/NRF up-regulates proteostasis capacity after blockade of the proteasome and also promotes resistance against bacterial infection in the nematode Caenorhabditis elegans. SKN-1/NRF has 3 isoforms, and the SKN-1A/NRF1 isoform, in particular, regulates proteasomal gene expression upon proteasome dysfunction as part of a conserved bounce-back response. We report here that, in contrast to the previously reported role of SKN-1 in promoting resistance against bacterial infection, loss-of-function mutants in skn-1a and its activating enzymes ddi-1 and png-1 show constitutive expression of immune response programs against natural eukaryotic pathogens of C. elegans. These programs are the oomycete recognition response (ORR), which promotes resistance against oomycetes that infect through the epidermis, and the intracellular pathogen response (IPR), which promotes resistance against intestine-infecting microsporidia. Consequently, skn-1a mutants show increased resistance to both oomycete and microsporidia infections. We also report that almost all ORR/IPR genes induced in common between these programs are regulated by the proteasome and interestingly, specific ORR/IPR genes can be induced in distinct tissues depending on the exact trigger. Furthermore, we show that increasing proteasome function significantly reduces oomycete-mediated induction of multiple ORR markers. Altogether, our findings demonstrate that proteasome regulation keeps innate immune responses in check in a tissue-specific manner against natural eukaryotic pathogens of the C. elegans epidermis and intestine.https://journals.plos.org/plosbiology/article/file?id=10.1371/journal.pbio.3002543&type=printable
spellingShingle Manish Grover
Spencer S Gang
Emily R Troemel
Michalis Barkoulas
Proteasome inhibition triggers tissue-specific immune responses against different pathogens in C. elegans.
PLoS Biology
title Proteasome inhibition triggers tissue-specific immune responses against different pathogens in C. elegans.
title_full Proteasome inhibition triggers tissue-specific immune responses against different pathogens in C. elegans.
title_fullStr Proteasome inhibition triggers tissue-specific immune responses against different pathogens in C. elegans.
title_full_unstemmed Proteasome inhibition triggers tissue-specific immune responses against different pathogens in C. elegans.
title_short Proteasome inhibition triggers tissue-specific immune responses against different pathogens in C. elegans.
title_sort proteasome inhibition triggers tissue specific immune responses against different pathogens in c elegans
url https://journals.plos.org/plosbiology/article/file?id=10.1371/journal.pbio.3002543&type=printable
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AT emilyrtroemel proteasomeinhibitiontriggerstissuespecificimmuneresponsesagainstdifferentpathogensincelegans
AT michalisbarkoulas proteasomeinhibitiontriggerstissuespecificimmuneresponsesagainstdifferentpathogensincelegans