Anti-fungal innate immunity in C. elegans is enhanced by evolutionary diversification of antimicrobial peptides.

Encounters with pathogens provoke changes in gene transcription that are an integral part of host innate immune responses. In recent years, studies with invertebrate model organisms have given insights into the origin, function, and evolution of innate immunity. Here, we use genome-wide transcriptom...

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Autores principales:	Nathalie Pujol, Olivier Zugasti, Daniel Wong, Carole Couillault, C Léopold Kurz, Hinrich Schulenburg, Jonathan J Ewbank
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2008
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/e7824bf52c8441ebada068056338bb43
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spelling	oai:doaj.org-article:e7824bf52c8441ebada068056338bb432021-11-25T05:46:30ZAnti-fungal innate immunity in C. elegans is enhanced by evolutionary diversification of antimicrobial peptides.1553-73661553-737410.1371/journal.ppat.1000105https://doaj.org/article/e7824bf52c8441ebada068056338bb432008-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18636113/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Encounters with pathogens provoke changes in gene transcription that are an integral part of host innate immune responses. In recent years, studies with invertebrate model organisms have given insights into the origin, function, and evolution of innate immunity. Here, we use genome-wide transcriptome analysis to characterize the consequence of natural fungal infection in Caenorhabditis elegans. We identify several families of genes encoding putative antimicrobial peptides (AMPs) and proteins that are transcriptionally up-regulated upon infection. Many are located in small genomic clusters. We focus on the nlp-29 cluster of six AMP genes and show that it enhances pathogen resistance in vivo. The same cluster has a different structure in two other Caenorhabditis species. A phylogenetic analysis indicates that the evolutionary diversification of this cluster, especially in cases of intra-genomic gene duplications, is driven by natural selection. We further show that upon osmotic stress, two genes of the nlp-29 cluster are strongly induced. In contrast to fungus-induced nlp expression, this response is independent of the p38 MAP kinase cascade. At the same time, both involve the epidermal GATA factor ELT-3. Our results suggest that selective pressure from pathogens influences intra-genomic diversification of AMPs and reveal an unexpected complexity in AMP regulation as part of the invertebrate innate immune response.Nathalie PujolOlivier ZugastiDaniel WongCarole CouillaultC Léopold KurzHinrich SchulenburgJonathan J EwbankPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 4, Iss 7, p e1000105 (2008)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Nathalie Pujol Olivier Zugasti Daniel Wong Carole Couillault C Léopold Kurz Hinrich Schulenburg Jonathan J Ewbank Anti-fungal innate immunity in C. elegans is enhanced by evolutionary diversification of antimicrobial peptides.
description	Encounters with pathogens provoke changes in gene transcription that are an integral part of host innate immune responses. In recent years, studies with invertebrate model organisms have given insights into the origin, function, and evolution of innate immunity. Here, we use genome-wide transcriptome analysis to characterize the consequence of natural fungal infection in Caenorhabditis elegans. We identify several families of genes encoding putative antimicrobial peptides (AMPs) and proteins that are transcriptionally up-regulated upon infection. Many are located in small genomic clusters. We focus on the nlp-29 cluster of six AMP genes and show that it enhances pathogen resistance in vivo. The same cluster has a different structure in two other Caenorhabditis species. A phylogenetic analysis indicates that the evolutionary diversification of this cluster, especially in cases of intra-genomic gene duplications, is driven by natural selection. We further show that upon osmotic stress, two genes of the nlp-29 cluster are strongly induced. In contrast to fungus-induced nlp expression, this response is independent of the p38 MAP kinase cascade. At the same time, both involve the epidermal GATA factor ELT-3. Our results suggest that selective pressure from pathogens influences intra-genomic diversification of AMPs and reveal an unexpected complexity in AMP regulation as part of the invertebrate innate immune response.
format	article
author	Nathalie Pujol Olivier Zugasti Daniel Wong Carole Couillault C Léopold Kurz Hinrich Schulenburg Jonathan J Ewbank
author_facet	Nathalie Pujol Olivier Zugasti Daniel Wong Carole Couillault C Léopold Kurz Hinrich Schulenburg Jonathan J Ewbank
author_sort	Nathalie Pujol
title	Anti-fungal innate immunity in C. elegans is enhanced by evolutionary diversification of antimicrobial peptides.
title_short	Anti-fungal innate immunity in C. elegans is enhanced by evolutionary diversification of antimicrobial peptides.
title_full	Anti-fungal innate immunity in C. elegans is enhanced by evolutionary diversification of antimicrobial peptides.
title_fullStr	Anti-fungal innate immunity in C. elegans is enhanced by evolutionary diversification of antimicrobial peptides.
title_full_unstemmed	Anti-fungal innate immunity in C. elegans is enhanced by evolutionary diversification of antimicrobial peptides.
title_sort	anti-fungal innate immunity in c. elegans is enhanced by evolutionary diversification of antimicrobial peptides.
publisher	Public Library of Science (PLoS)
publishDate	2008
url	https://doaj.org/article/e7824bf52c8441ebada068056338bb43
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Anti-fungal innate immunity in C. elegans is enhanced by evolutionary diversification of antimicrobial peptides.

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