Date of Submission

Spring 2015

Academic Programs and Concentrations

Biology

Project Advisor 1

Amy Savage

Abstract/Artist's Statement

Although Caenorhabditis elegans exhibits specific innate immune responses to microbial challenge, pathogen recognition receptors in this nematode remain unidentified. In the absence of traditional pathogen recognition mechanisms, secondary consequences of infection may serve as initiators of immune signaling cascades. An important secondary consequence of Pseudomonas aeruginosa infection in C. elegans is iron deficiency. Genes from several pathways including general stress response (hsf-1, gst-38), non-specific immune response (dkf-2), p38 MAPK (sek-1, clec-74, mul-1), and the DAF-2/DAF-16 insulin-like response (dod-17) were identified from the literature and targeted for this work. Caenorhabditis elegans culture was maintained in conditions of iron deficiency and in the presence of microbial pathogen, P. aeruginosa. Semi-quantitative PCR was used to assay and compare relative gene expression of target genes under conditions of iron deficiency and when challenged by microbial pathogen. Relative gene expression was used to determine the extent of the immune response triggered by iron deficient conditions. A pmk-1 knockout strain of C. elegans was used in conjunction with relative gene expression assays to begin to narrow the possible link between the p38 MAPK pathway and the DAF-2/DAF-16 insulin-like response. Results suggest that iron deficiency in the absence of microbial infection triggers a partial specific immune response as indicated by the expression profiles of dkf-2, sek-1, and dod-17. The altered expression profiles resemble the immune response to P. aeruginosa. These data support the possibility that in the absence of traditional pathogen recognition receptors, C. elegans senses secondary consequences of infection to stimulate a specific immune response to P. aeruginosa infection. The partial activation of the non-specific immune response and p38 pathway, together with the activation of downstream DAF-2/DAF-16 genes, and the results of the knockout expression assays hint at the possibility of crosstalk between the two pathways upstream of the effector molecules. Further investigation of this link via additional genetic knockout experiments presents a promising avenue for continued research.

Open Access Agreement

On-Campus only

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

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