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Activated and inactivated immune responses in Caenorhabditis elegans against Photorhabdus luminescens TT01
The Gram-negative bacterium Photorhabdus luminescens which symbiotically associates with the entomopathogenic nematode Heterorhabditis bacteriophora, has a broad insecticidal and nematicidal activity. The virulence of P. luminescens toward the non-mutualistic nematode Caenorhabditis elegans has not...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4171960/ https://www.ncbi.nlm.nih.gov/pubmed/25279274 http://dx.doi.org/10.1186/2193-1801-3-274 |
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author | Sato, Kazuki Yoshiga, Toyoshi Hasegawa, Koichi |
author_facet | Sato, Kazuki Yoshiga, Toyoshi Hasegawa, Koichi |
author_sort | Sato, Kazuki |
collection | PubMed |
description | The Gram-negative bacterium Photorhabdus luminescens which symbiotically associates with the entomopathogenic nematode Heterorhabditis bacteriophora, has a broad insecticidal and nematicidal activity. The virulence of P. luminescens toward the non-mutualistic nematode Caenorhabditis elegans has not been described. We showed that when fed on P. luminescens, the intestinal cells of C. elegans worms become delicate and some crystal-like structure was developed within the intestinal lumen. Next, we examined the requirement of the p38 mitogen-activated protein kinase (MAPK) and insulin/IGF-1 signaling pathway against P. luminescens. Depletion of pmk-1 by RNAi enhances susceptibility to P. luminescens, and numerous downstream targets regulated by the p38 MAPK pathway were induced when fed on P. luminescens. On the other hand, knockdown of daf-16 has no effects on C. elegans lifespan, but knockdown of daf-2 dramatically increased resistance to P. luminescens in a daf-16-dependent manner. We also revealed one of the daf-2 ligands ins-7 was induced and ins-7 deletion mutant survived longer when fed on P. luminescens. These results suggest the p38 MAPK pathway is activated and required for the host defense against P. luminescens. Insulin/IGF-1 signaling pathway is inactivated by P. luminescens through the overexpression of insulin-like gene. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/2193-1801-3-274) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4171960 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-41719602014-10-02 Activated and inactivated immune responses in Caenorhabditis elegans against Photorhabdus luminescens TT01 Sato, Kazuki Yoshiga, Toyoshi Hasegawa, Koichi Springerplus Research The Gram-negative bacterium Photorhabdus luminescens which symbiotically associates with the entomopathogenic nematode Heterorhabditis bacteriophora, has a broad insecticidal and nematicidal activity. The virulence of P. luminescens toward the non-mutualistic nematode Caenorhabditis elegans has not been described. We showed that when fed on P. luminescens, the intestinal cells of C. elegans worms become delicate and some crystal-like structure was developed within the intestinal lumen. Next, we examined the requirement of the p38 mitogen-activated protein kinase (MAPK) and insulin/IGF-1 signaling pathway against P. luminescens. Depletion of pmk-1 by RNAi enhances susceptibility to P. luminescens, and numerous downstream targets regulated by the p38 MAPK pathway were induced when fed on P. luminescens. On the other hand, knockdown of daf-16 has no effects on C. elegans lifespan, but knockdown of daf-2 dramatically increased resistance to P. luminescens in a daf-16-dependent manner. We also revealed one of the daf-2 ligands ins-7 was induced and ins-7 deletion mutant survived longer when fed on P. luminescens. These results suggest the p38 MAPK pathway is activated and required for the host defense against P. luminescens. Insulin/IGF-1 signaling pathway is inactivated by P. luminescens through the overexpression of insulin-like gene. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/2193-1801-3-274) contains supplementary material, which is available to authorized users. Springer International Publishing 2014-06-01 /pmc/articles/PMC4171960/ /pubmed/25279274 http://dx.doi.org/10.1186/2193-1801-3-274 Text en © Sato et al.; licensee Springer. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. |
spellingShingle | Research Sato, Kazuki Yoshiga, Toyoshi Hasegawa, Koichi Activated and inactivated immune responses in Caenorhabditis elegans against Photorhabdus luminescens TT01 |
title | Activated and inactivated immune responses in Caenorhabditis elegans against Photorhabdus luminescens TT01 |
title_full | Activated and inactivated immune responses in Caenorhabditis elegans against Photorhabdus luminescens TT01 |
title_fullStr | Activated and inactivated immune responses in Caenorhabditis elegans against Photorhabdus luminescens TT01 |
title_full_unstemmed | Activated and inactivated immune responses in Caenorhabditis elegans against Photorhabdus luminescens TT01 |
title_short | Activated and inactivated immune responses in Caenorhabditis elegans against Photorhabdus luminescens TT01 |
title_sort | activated and inactivated immune responses in caenorhabditis elegans against photorhabdus luminescens tt01 |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4171960/ https://www.ncbi.nlm.nih.gov/pubmed/25279274 http://dx.doi.org/10.1186/2193-1801-3-274 |
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