Initiation of coral/algal symbioses : the role of cell surface lectin/glycan interactions in recognition and specificity Public Deposited

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  • Mutualistic associations between cnidarians, such as corals, and photosynthetic dinoflagellate algae provide the trophic and structural foundation of coral reef ecosystems. In many cases, this intracellular mutualism is highly specific and must be established anew for each generation of host corals. The ability to maintain partner specificity across generations implies that cellular mechanisms play a role in interpartner recognition. In other mutualisms where these recognition mechanisms have been studied, lectin/glycan interactions have been shown to function in inter-partner recognition during the onset of a stable symbiosis. However, for the majority of symbioses, including the cnidarian/dinoflagellate mutualism, cellular recognition mechanisms that mediate the onset of symbiosis remain largely unknown. How do larval corals and their symbiotic algae discriminate between their preferred partner and other hosts or microbes during the onset of symbiosis? I hypothesized that cell surface lectin/glycan interactions act as one mechanism of recognition and specificity during initial contact between the partners. Chapter one reviews the biology of cnidarian/algal symbioses and discusses the literature to date concerning molecular mechanisms of recognition and specificity during the onset of cnidarian/algal symbioses and how the cnidarian/algal system compares with other horizontally-transmitted mutualisms. Chapter two and three explore the role of algal cell surface glycans during the onset of symbiosis between the Hawai'ian solitary coral Fungia scutaria and its dinoflagellate symbiont, Symbiodinium clade C1f. To determine whether lectin/glycan interactions function during infection, I modified the glycans on the cell surface of algal symbionts (C1f and C31, found in nature in adult F. scutaria and Montipora capitata, respectively), introduced the modified symbionts to F. scutaria larvae, and then looked for changes in infection success. After cell surface modification, infection rates of native C1f algae decreased. In contrast, cell surface modification of non-native C31 algae resulted in higher infection rates compared to unmodified, control C31 algae. These data suggest that the algal cell surface signals to the host F. scutaria larvae identifying it as either a native C1f symbiont or non-native C31 algae. These chapters also investigate the variability of glycans present on the cell surface of several closely-related clade C symbionts to determine if each algal subclade contains a unique cell surface glycan profile. I found that cell surface glycan profiles were different for each symbiont tested, supporting their classification into different subclades. I hypothesize that this subclade specific glycan profile creates the cell surface signal that identifies the symbiont to its host coral. Chapter four describes the complex array of C-type lectins, a type of glycan receptor, in the anemone Nematostella vectensis genome. The diversity of glycan profiles on symbiont cell surfaces and C-type lectins in cnidarians suggests that these interactions could relay a signal for recognition and specificity between symbiotic partners. Chapter five concludes with a brief discussion that places my results in the context of cnidarian innate immunity and parallels between the onset of mutualistic symbioses and the process of infection in parasitic relationships. I close by suggesting future experiments that continue to explore the role of cell surface lectin/glycan interaction in recognition and specificity during the onset of cnidarian/algal symbioses.
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