Microbial Friends And Foes: Characterizing The Cnidarian Response To Pathogenic And Mutualistic Microorganisms

Abstract

The ecology and evolution of cnidarians is driven by symbiotic and pathogenic hostmicrobe relationships. Research regarding these relationships is especially timely given the recent decline of coral reef ecosystems, in part due to disruptions in cnidarian-microbe interactions. My dissertation is an experimental analysis of how cnidarians respond to both harmful and beneficial microorganisms and explores the interplay between these two types of interactions. Corals provide a multifaceted habitat that supports a rich bacterial assemblage, and in Chapter 1, I review our current knowledge regarding the diversity, specificity, development, and functions of these assemblages. With a meta-analysis of previous work, I quantitatively analyze what is known regarding the relationship between coral-associated microorganisms and disease. Finally, I examine evidence that these populations could be disrupted by climatic change. One of the most well-known mutualistic relationships is that between cnidarians and unicellular dinoflagellates. To evaluate the molecular mechanisms that underlie the persistence of this relationship, in Chapter 2, I identify differentially expressed transcripts between symbiotic and aposymbiotic individuals of the model sea anemone, Aiptasia pallida. These transcripts include those with potential functions in several metabolic pathways, transport of nutrients between the partners, and host tolerance of the dinoflagellate. To broaden our understanding of the cnidarian response to pathogenic microbes, in Chapter 3, I report the host transcriptome response of aposymbiotic Aiptasia to experimental inoculation with Serratia marcescens. My results suggest that Aiptasia responds to bacterial challenge via the regulation of tumor necrosis factor receptor-associated factor-mediated signaling, apoptosis, and ubiquitination, thus suggesting that lower metazoans respond to immune challenge via highly conserved mechanisms. To determine how the Aiptasia immune response is modulated via the presence of dinoflagellate symbionts, in Chapter 4, I compared gene expression and behavioral assays of S. marcescens-exposed anemones with and without their symbionts. The presence of dinoflagellates greatly alters the number and type of genes expressed in response to bacterial challenge. In addition, symbiotic anemones were less likely to recover from pathogen exposure and had lower survival rates than their aposymbiotic counterparts. These results are consistent with the hypothesis that symbiotic dinoflagellates suppress Aiptasia immunity, perhaps to promote symbiotic homeostasis.