| Citation | Pujol N, Zugasti O, Wong D, Couillault C, Kurz CL, Schulenburg H, Ewbank JJ. Anti-fungal innate immunity in C. elegans is enhanced by evolutionary diversification of antimicrobial peptides. PLoS Pathog, 2008. |
| PubMed ID | 18636113 |
| Short Description | Anti-fungal innate immunity in C. elegans is enhanced by evolutionary diversification of antimicrobial peptides. GEO Record: N.A. Platform: N.A. Download gene-centric, log2 transformed data: WBPaper00032031.ce.mr.csv |
| # of Conditions | 32 |
Full Description
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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. Experimental Details: WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM0 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM1 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM2 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM3 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM4 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM5 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM6 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM7 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM8 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM9 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM10 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM11 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM12 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM13 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM14 WBPaper00032031:N2_12h_DConiospora_vs_N2_12h_control_GEM15 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM16 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM17 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM18 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM19 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM20 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM21 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM22 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM23 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM24 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM25 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM26 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM27 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM28 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM29 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM30 WBPaper00032031:N2_24h_DConiospora_vs_N2_24h_control_GEM31. |
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