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ATFS-1 plays no repressive role in the regulation of epidermal immune response

Fungal infection triggers the induction of antimicrobial peptide (AMP) genes in the epidermis (Pujol et al, 2008). We previously showed that this effect is suppressed by the mitochondrial unfolded protein response (UPR(mt)), which can be activated by knockdown of select genes including the mitochond...

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Detalles Bibliográficos
Autores principales: Martineau, Celine N, Maynard, Claire A, Pujol, Nathalie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Caltech Library 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8864481/
https://www.ncbi.nlm.nih.gov/pubmed/35224461
http://dx.doi.org/10.17912/micropub.biology.000525
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author Martineau, Celine N
Maynard, Claire A
Pujol, Nathalie
author_facet Martineau, Celine N
Maynard, Claire A
Pujol, Nathalie
author_sort Martineau, Celine N
collection PubMed
description Fungal infection triggers the induction of antimicrobial peptide (AMP) genes in the epidermis (Pujol et al, 2008). We previously showed that this effect is suppressed by the mitochondrial unfolded protein response (UPR(mt)), which can be activated by knockdown of select genes including the mitochondrial metalloprotease spg-7 (Zugasti et al, 2016). Here, we confirm that RNAi against spg-7 triggers the UPR(mt )and blocks AMP induction during infection, whereas infection itself does not trigger the UPR(mt). ATFS-1 is a key factor in the UPR(mt), mediating much of the associated transcriptional response. We find that, surprisingly, ATFS-1 is not required for the suppression of AMP induction provoked by spg-7(RNAi). These data show that the mitochondrial dysfunction that blocks the immune response upon infection or wounding is independent of ATFS-1.
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spelling pubmed-88644812022-02-24 ATFS-1 plays no repressive role in the regulation of epidermal immune response Martineau, Celine N Maynard, Claire A Pujol, Nathalie MicroPubl Biol Negative Result Fungal infection triggers the induction of antimicrobial peptide (AMP) genes in the epidermis (Pujol et al, 2008). We previously showed that this effect is suppressed by the mitochondrial unfolded protein response (UPR(mt)), which can be activated by knockdown of select genes including the mitochondrial metalloprotease spg-7 (Zugasti et al, 2016). Here, we confirm that RNAi against spg-7 triggers the UPR(mt )and blocks AMP induction during infection, whereas infection itself does not trigger the UPR(mt). ATFS-1 is a key factor in the UPR(mt), mediating much of the associated transcriptional response. We find that, surprisingly, ATFS-1 is not required for the suppression of AMP induction provoked by spg-7(RNAi). These data show that the mitochondrial dysfunction that blocks the immune response upon infection or wounding is independent of ATFS-1. Caltech Library 2022-02-22 /pmc/articles/PMC8864481/ /pubmed/35224461 http://dx.doi.org/10.17912/micropub.biology.000525 Text en Copyright: © 2022 by the authors https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Negative Result
Martineau, Celine N
Maynard, Claire A
Pujol, Nathalie
ATFS-1 plays no repressive role in the regulation of epidermal immune response
title ATFS-1 plays no repressive role in the regulation of epidermal immune response
title_full ATFS-1 plays no repressive role in the regulation of epidermal immune response
title_fullStr ATFS-1 plays no repressive role in the regulation of epidermal immune response
title_full_unstemmed ATFS-1 plays no repressive role in the regulation of epidermal immune response
title_short ATFS-1 plays no repressive role in the regulation of epidermal immune response
title_sort atfs-1 plays no repressive role in the regulation of epidermal immune response
topic Negative Result
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8864481/
https://www.ncbi.nlm.nih.gov/pubmed/35224461
http://dx.doi.org/10.17912/micropub.biology.000525
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