Date of Award

Spring 2019

Document Type

Restricted Thesis

Terms of Use

© 2019 Serena W. Sung-Clarke. All rights reserved. Access to this work is restricted to users within the Swarthmore College network and may only be used for non-commercial, educational, and research purposes. Sharing with users outside of the Swarthmore College network is expressly prohibited. For all other uses, including reproduction and distribution, please contact the copyright holder.

Degree Name

Bachelor of Arts

Department

Biology Department

First Advisor

Elizabeth Ann Vallen

Abstract

Coral-algal symbiosis is an essential process for the health and growth of coral reefs. Although the host immune system is implicated in symbiosis, immune pathways in corals and other cnidaria are poorly understood. In the sea anemone Aiptasia pallida, a model for cnidarian symbiosis, we characterized Toll/IL-1 Receptor (TIR) domain proteins, which have a conserved role initiating the immune TLR pathway. Through genomic and transcriptomic analysis and literature review, we failed to identify canonical Toll-like receptors or the pathway’s kinase, IRAK, while we were able to identify many other components of the pathway. A novel splice variant of the key signaling protein, MyD88, was found in the transcriptome. MyD88t is truncated at the TIR domain-containing C-terminus. Protein interactions involving the two splice variants were characterized using a yeast two-hybrid assay. From this, it was found that MyD88 can interact with itself strongly, MyD88t interacts with itself more weakly, and that a MyD88-MyD88t interaction appeared the weakest. This suggests that MyD88t does not sequester MyD88. Other potential interactions were identified, notably between MyD88t (but not MyD88) and the transcription factors NF-κB and p52. Further confirmation of this interaction is needed, but if biologically relevant, MyD88t could be a dominant negative regulator of the MyD88-dependent NF-κB activation pathway through sequestering NF-κB.

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