| Citation | Tjahjono E, Kirienko NV. A conserved mitochondrial surveillance pathway is required for defense against Pseudomonas aeruginosa. PLoS Genet, 2017. |
| PubMed ID | 28662060 |
| Short Description | A conserved mitochondrial surveillance pathway is required for defense against Pseudomonas aeruginosa. GEO Record: GSE55422 Platform: GPL200 Download gene-centric, log2 transformed data: WBPaper00051448.ce.mr.csv |
| # of Conditions | 21 |
Full Description
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All living organisms exist in a precarious state of homeostasis that requires constant maintenance. A wide variety of stresses, including hypoxia, heat, and infection by pathogens perpetually threaten to imbalance this state. Organisms use a battery of defenses to mitigate damage and restore normal function. Previously, we described a Caenorhabditis elegans-Pseudomonas aeruginosa assay (Liquid Killing) in which toxicity to the host is dependent upon the secreted bacterial siderophore pyoverdine. Although pyoverdine is also indispensable for virulence in mammals, its cytological effects are unclear. We used genetics, transcriptomics, and a variety of pathogen and chemical exposure assays to study the interactions between P. aeruginosa and C. elegans. Although P. aeruginosa can kill C. elegans through at least 5 different mechanisms, the defense responses activated by Liquid Killing are specific and selective and have little in common with innate defense mechanisms against intestinal colonization. Intriguingly, the defense response utilizes the phylogenetically-conserved ESRE (Ethanol and Stress Response Element) network, which we and others have previously shown mitigates damage from a variety of abiotic stresses. This is the first report of this network's involvement in innate immunity, and indicates that host innate immune responses overlap with responses to abiotic stresses. The upregulation of the ESRE network in C. elegans is mediated in part by a family of bZIP proteins (including ZIP-2, ZIP-4, CEBP-1, and CEBP-2) that have overlapping and unique functions. Our data convincingly show that, following infection by P. aeruginosa, the ESRE defense network is activated by mitochondrial damage, and that mitochondrial damage also leads to ESRE activation in mammals. This establishes a role for ESRE in a phylogenetically-conserved mitochondrial surveillance system important for stress response and innate immunity. Experimental Details: WBPaper00051448:glp-4(bn2ts)_OP50_NGM-agar_RepA WBPaper00051448:glp-4(bn2ts)_OP50_NGM-agar_RepB WBPaper00051448:glp-4(bn2ts)_OP50_NGM-agar_RepC WBPaper00051448:glp-4(bn2ts)_OP50_SK-agar_RepA WBPaper00051448:glp-4(bn2ts)_OP50_SK-agar_RepB WBPaper00051448:glp-4(bn2ts)_OP50_SK-agar_RepC WBPaper00051448:glp-4(bn2ts)_OP50_LK_RepA WBPaper00051448:glp-4(bn2ts)_OP50_LK_RepB WBPaper00051448:glp-4(bn2ts)_OP50_LK_RepC WBPaper00051448:glp-4(bn2ts)_PA14_SK-agar_RepA WBPaper00051448:glp-4(bn2ts)_PA14_SK-agar_RepB WBPaper00051448:glp-4(bn2ts)_PA14_SK-agar_RepC WBPaper00051448:glp-4(bn2ts)_PA14_LK_RepA WBPaper00051448:glp-4(bn2ts)_PA14_LK_RepB WBPaper00051448:glp-4(bn2ts)_PA14_LK_RepC WBPaper00051448:glp-4(bn2ts)_OP50_DMSO_RepA WBPaper00051448:glp-4(bn2ts)_OP50_DMSO_RepB WBPaper00051448:glp-4(bn2ts)_OP50_DMSO_RepC WBPaper00051448:glp-4(bn2ts)_OP50_Phe_RepA WBPaper00051448:glp-4(bn2ts)_OP50_Phe_RepB WBPaper00051448:glp-4(bn2ts)_OP50_Phe_RepC. |
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